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1.
The small chaperone protein Hsp27 confers resistance to apoptosis, and therefore is an attractive anticancer drug target. We report here a novel mechanism underlying the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitizing activity of the small molecule LY303511, an inactive analog of the phosphoinositide 3-kinase inhibitor inhibitor LY294002, in HeLa cells that are refractory to TRAIL-induced apoptosis. On the basis of the fact that LY303511 is derived from LY294002, itself derived from quercetin, and earlier findings indicating that quercetin and LY294002 affected Hsp27 expression, we investigated whether LY303511 sensitized cancer cells to TRAIL via a conserved inhibitory effect on Hsp27. We provide evidence that upon treatment with LY303511, Hsp27 is progressively sequestered in the nucleus, thus reducing its protective effect in the cytosol during the apoptotic process. LY303511-induced nuclear translocation of Hsp27 is linked to its sustained phosphorylation via activation of p38 kinase and MAPKAP kinase 2 and the inhibition of PP2A. Furthermore, Hsp27 phosphorylation leads to the subsequent dissociation of its large oligomers and a decrease in its chaperone activity, thereby further compromising the death inhibitory activity of Hsp27. Furthermore, genetic manipulation of Hsp27 expression significantly affected the TRAIL sensitizing activity of LY303511, which corroborated the Hsp27 targeting activity of LY303511. Taken together, these data indicate a novel mechanism of small molecule sensitization to TRAIL through targeting of Hsp27 functions, rather than its overall expression, leading to decreased cellular protection, which could have therapeutic implications for overcoming chemotherapy resistance in tumor cells. 相似文献
2.
The purpose of this table is to provide the community with a citable record of publications of ongoing genome sequencing projects that have led to a publication in the scientific literature. While our goal is to make the list complete, there is no guarantee that we may have omitted one or more publications appearing in this time frame. Readers and authors who wish to have publications added to subsequent versions of this list are invited to provide the bibliographic data for such references to the SIGS editorial office.
Phylum Crenarchaeota
Phylum Deinococcus-Thermus
Phylum Proteobacteria
- “Achromobacter arsenitoxydans” SY8, sequence accession AGUF00000000 [3]
- Acidovorax sp. Strain NO1, sequence accession AGTS00000000 [4]
- Acinetobacter baumannii AB4857, sequence accession AHAG00000000 [5]
- Acinetobacter baumannii AB5075, sequence accession AHAH00000000 [5]
- Acinetobacter baumannii AB5256, sequence accession AHAI00000000 [5]
- Acinetobacter baumannii AB5711, sequence accession AHAJ00000000 [5]
- Aeromonas salmonicida, sequence accession AGVO00000000 [6]
- Aggregatibacter actinomycetemcomitans RHAA1, sequence accession AHGR00000000 [7]
- Agrobacterium tumefaciens 5A, sequence accession AGVZ00000000 [8]
- Azoarcus sp. Strain KH32C, sequence accession AP012304, AP012305 [9]
- Burkholderia sp. Strain YI23, sequence accession CP003087 (Chromosome 1), CP003088 (Chromosome 2), CP003089 (Chromosome 3), CP003090 (plasmid BYI23_D), CP003091 (plasmid BYI23_E) CP003092 (plasmid BYI23_F) [10]
- Brucella suis VBI22, sequence accession CP003128, CP003129 [11]
- Comamonas testosteroni ATCC 11996, sequence accession AHIL00000000 [12]
- “Commensalibacter intestini” A911T, sequence accession AGFR00000000 [13]
- Edwardsiella ictaluri, sequence accession CP001600.1 [14]
- Enterobacter cloacae subsp. dissolvens SDM, sequence accession AGSY00000000 [15]
- “Gluconobacter morbifer” G707T, sequence accession AGQV00000000 [16]
- Legionella dumoffii TEX-KL, sequence accession AGVT00000000 [17]
- Legionella dumoffii NY-23, sequence accession AGVU00000000 [17]
- Legionella pneumophila serogroup 12 Strain 570-CO-H, sequence accession CP003192 [18]
- Marinobacterium stanieri S30, sequence accession AFPL00000000 [19]
- “Marinobacter manganoxydans” MnI7-9, sequence accession CP001978 to CP001980 [20]
- Mesorhizobium alhagi CCNWXJ12-2T, sequence accession AHAM00000000 [21]
- Mesorhizobium amorphae, sequence accession AGSN00000000 [22]
- Methylomicrobium alcaliphilum 20Z, sequence accession FO082060 and FO082061 [23]
- Mitsuaria sp. Strain H24L5A, sequence accession CAFG01000001 to CAFG01000607 [24]
- Novosphingobium pentaromativorans US6-1, sequence accession AGFM00000000 [25]
- Pantoea ananatis B1-9, sequence accession CAEI01000001 to CAEI01000169 [26]
- Pantoea ananatis LMG 5342, sequence accession HE617160 (chromosome), HE617161 (pPANA10) [27]
- Pantoea ananatis Strain PA13, sequence accession CP003085 and CP003086 [28]
- Pseudomonas aeruginosa, sequence accession AFXI00000000 [29]
- Pseudomonas aeruginosa, sequence accession AFXJ00000000 [29]
- Pseudomonas aeruginosa, sequence accession AFXK00000000 [29]
- Pseudomonas chlororaphis GP72, sequence accession AHAY01000000 [30]
- Pseudomonas fluorescens F113, sequence accession CP003150 [31]
- Pseudomonas fluorescens Wayne 1R, sequence accession CADX01000001 to CADX01000090 [32]
- Pseudomonas fluorescens Wood1R, sequence accession CAFF01000001 to CAFF01001437 [32]
- Pseudomonas psychrotolerans L19, sequence accession AHBD00000000 [33]
- Pseudoalteromonas rubra ATCC 29570T, sequence accession AHCD00000000 [34]
- Pseudomonas stutzeri SDM-LAC, sequence accession AGSX00000000 [35]
- Pseudoxanthomonas spadix BD-a59, sequence accession CP003093 [36]
- Rickettsia slovaca, sequence accession CP002428 [37]
- Salmonella enterica serovar Pullorum RKS5078, sequence accession CP003047 [38]
- Sinorhizobium meliloti CCNWSX0020, sequence accession AGVV00000000 [39]
- Sphingobium sp. Strain SYK-6, sequence accession AP012222 and AP012223 [40]
- Sphingomonas sp. Strain PAMC 26605, sequence accession AHIS00000000 [41]
- Stenotrophomonas maltophilia RR-10, sequence accession AGRB00000000 [42]
- Strain HIMB30, sequence accession AGIG00000000 [43]
- Taylorella equigenitalis, sequence accession CP003059 [44]
- Vibrio campbellii DS40M4, sequence accession AGIE00000000 [45]
- Vibrio fischeri SR5, sequence accession AHIH00000000 [46]
- Yersinia enterocolitica, sequence accession AGQO00000000 [47]
Phylum Tenericutes
- Candidatus Mycoplasma haemominutum, sequence accession HE613254 [48]
- Mycoplasma haemocanis strain Illinois, sequence accession CP003199 [49]
- Mycoplasma iowae, sequence accession AGFP00000000 [50]
- Mycoplasma pneumoniae Type 2a Strain 309, sequence accession AP012303 [51]
Phylum Firmicutes
- Bacillus cereus F837/76, sequence accession CP003187 (chromosome) CP003188 (pF837_55kb), CP003189 (pF837_10kb) [52]
- Brevibacillus laterosporus Strain GI-9, sequence accession CAGD01000001 to CAGD01000061 [53]
- Clostridium sporogenes PA 3679, sequence accession AGAH00000000 [54]
- Enterococcus mundtii CRL1656, sequence accession AFWZ00000000.1 [55]
- Geobacillus thermoleovorans CCB_US3_UF5, sequence accession CP003125 [56]
- Lactobacillus curvatus Strain CRL705, sequence accession AGBU01000000 [57]
- Lactobacillus rhamnosus ATCC 8530, sequence accession CP003094 [58]
- Lactobacillus rhamnosus R0011, sequence accession AGKC00000000 [59]
- Lactococcus garvieae TB25, sequence accession AGQX01000000 [60]
- Lactococcus garvieae LG9, sequence accession AGQY01000000 [60]
- Lactococcus lactis subsp. cremoris A76, sequence accession CP003132 (chromosome), CP003136 (pQA505), CP003135 (PQA518), CP003134 (pQA549), CP003133 (pQA554) [61]
- Leuconostoc citreum LBAE C10, sequence accession CAGE00000000 [62]
- Leuconostoc citreum LBAE C11, sequence accession CAGF00000000 [62]
- Leuconostoc citreum LBAE E16, sequence accession CAGG00000000 [62]
- Leuconostoc mesenteroides subsp. mesenteroides Strain J18, sequence accession CP003101 [63]
- Paenibacillus peoriae Strain KCTC 3763T, sequence accession AGFX00000000 [64]
- Pediococcus acidilactici MA18/5M, sequence accession AGKB00000000 [65]
- Pediococcus claussenii ATCC BAA-344T, sequence accession CP003137 (chromosome), CP003138 (pPECL-1), CP003139 (pPECL-2), CP003140 (pPECL-3), CP003141 (pPECL-4), CP003142 (pPECL-5), CP003143 (pPECL-6), CP003144 (pPECL-7), CP003145 (pPECL-8) [66]
- Staphylococcus aureus M013, sequence accession CP003166 [67]
- Staphylococcus aureus subsp. aureus TW20, sequence accession FN433596 [68]
- Weissella confusa LBAE C39-2, sequence accession CAGH00000000 [69]
Phylum Actinobacteria
- Corynebacterium casei, sequence accession CAFW01000001 to CAFW01000106 [70]
- Corynebacterium glutamicum, sequence accession AGQQ00000000 [71]
- Leucobacter chromiiresistens, sequence accession AGCW00000000 [72]
- Mycobacterium abscessus, sequence accession AGQU00000000 [73]
- Propionibacterium acnes ST9, sequence accession CP003195 [74]
- Propionibacterium acnes ST22, sequence accession CP003196 [74]
- Propionibacterium acnes ST27, sequence accession CP003197 [74]
- Saccharomonospora azurea SZMC 14600, sequence accession AHBX00000000 [75]
- Streptomyces sp. Strain TOR3209, sequence accession AGNH00000000 [76]
- Streptomyces sp. Strain W007, sequence accession AGSW00000000 [77]
Phylum Spirochaetes
- Borrelia valaisiana VS116, sequence accession ABCY02000001 (chromosome), CP001439 (plasmid Ip17), CP001437 (Ip25), CP001440 (plasmid Ip 28-3), CP001442 (plasmid Ip28-8), CP001436 (Ip 36), CP001433 (plasmid Ip 54), CP001438 (plasmid cp9), CP001432 (plasmid cp26), CP001441 (plasmid cp32-5), CP001434 (plasmid cp32-7), CP001435 (plasmid cp32-10) [78]
- “Borrelia bissettii” DN127, sequence accession CP002746 (chromosome), CP002756 (plasmid Ip12), CP002757 (plasmid Ip25), CP002758 (plasmid 28-3), CP002759 (plasmid Ip 28-4), CP002760 (Ip28-7), CP002761 (plasmid Ip54), CP002762 (plasmid Ip56), CP002755 (plasmid cp9), CP002747 (plasmid cp26), CP002749 (plasmid cp32-3), CP002750 (plasmid cp32-4), CP002751 (plasmid 32-5), CP002752 (plasmid cp32-6), CP002753 (plasmid cp32-7), CP0027554 (plasmid cp32-9), CP002748 (plasmid cp32-11) [78]
- Borrelia spielmanii A14S, sequence accession ABKB02000001 (chromosome), CP001468 (plasmid Ip17), CP001471 (Ip28-3), CP001470 (plasmid Ip28-4), CP001465 (plasmid Ip28-2), CP001466 (plasmid Ip36), CP001464 (plasmid Ip38), CP001469 (plasmid Ip54), ABKB02000016, ABKB02000020 (plasmid cp9), CP001467 (plasmid cp26), ABKB02000026 (plasmid cp32-3), ABKB02000031 (plasmid 32-5), ABKB02000021 (plasmid cp32-12), ABKB02000014 (unidentified) [78]
Non-Bacterial genomes
- Aspergillus flavus, sequence accession GSE32177 [79]
- Bacteriophage SPN3UB, sequence accession JQ288021 [80]
- Bamboo mitochondria, sequence accession JQ235166 to JQ235179 [81]
- Boea hygrometrica chloroplast, sequence accession JN107811 [82]
- Boea hygrometrica mitochondrial, sequence accession JN107812 [82]
- Canine Picornavirus, sequence accession JN831356 [83]
- Chandipura virus (CHPV) CIN0327, sequence accession GU212856.1 [84]
- Chandipura virus (CHPV) CIN0451, sequence accession GU212857.1 [84]
- Chandipura virus (CHPV) CIN0751, sequence accession GU212858.1 [84]
- Chandipura virus (CHPV) CIN0755, sequence accession GU190711.1 [84]
- Chinese Porcine Parvovirus Strain PPV2010, sequence accession JN872448 [85]
- Common midwife toad megavirus, sequence accession JQ231222 [86]
- Dengue Virus Serotype 4, sequence accession JN983813 [87]
- Duck Tembusu Virus, sequence accession JF270480 [88]
- Duck Tembusu Virus, sequence accession JQ314464 [88]
- Duck Tembusu Virus, sequence accession JQ314465 [88]
- Emiliania huxleyi Virus 202, sequence accession HQ634145 [89]
- Emiliania huxleyi Virus EhV-88, sequence accession JF974310 [89]
- Emiliania huxleyi EhV-201, sequence accession JF974311 [89]
- Emiliania huxleyi EhV-207, sequence accession JF974317 [89]
- Emiliania huxleyi EhV-208, sequence accession JF974318 [89]
- Glarea lozoyensis, sequence accession GUE00000000 [90]
- Nannochloropis gaditana, sequence accession AGNI00000000 [91]
- Oryza sativa cv., sequence accession DRA000499 [92]
- Partetravirus, sequence accession JN990269 [93]
- Porcine Bocavirus PBoV5, sequence accession JN831651 [94]
- Porcine epidemic diarrhea virus, sequence accession JQ282909 [95]
- Pseudomonas aeruginosa lytic bacteriophage PA1Ø, sequence accession HM624080 [96]
- Pseudomonas fluorescens phage OBP, sequence accesssion JN627160 [97]
- RNA Virus from Avocado, sequence accession JN880414 [98]
- Salmonella enterica Serovar Typhimurium Bacteriophage SPN1S, sequence accession JN391180 [99]
- Schistosoma haematobium, sequence accession PRJNA78265 [100]
- Schistosoma mansoni, sequence accession ERP00038 [101]
- Stenopirates sp., sequence accession JN100019 [102]
- T7-Like Virus, sequence accession JN651747 [103]
- Vibrio harveyi siphophage VHS1, sequence accession JF713456 [104]
- Tyrolean ice man, sequence accession ERP001144 [105]
3.
Giuseppe Battaglia Gemma Molinaro Barbara Riozzi Marianna Storto Carla L. Busceti Paola Spinsanti Domenico Bucci Valentina Di Liberto Giuseppina Mudò Corrado Corti Mauro Corsi Ferdinando Nicoletti Natale Belluardo Valeria Bruno 《PloS one》2009,4(8)
Metabotropic glutamate (mGlu) receptors have been considered potential targets
for the therapy of experimental parkinsonism. One hypothetical advantage
associated with the use of mGlu receptor ligands is the lack of the adverse
effects typically induced by ionotropic glutamate receptor antagonists, such as
sedation, ataxia, and severe learning impairment. Low doses of the mGlu2/3
metabotropic glutamate receptor agonist, LY379268 (0.25–3 mg/kg, i.p.)
increased glial cell line-derived neurotrophic factor (GDNF) mRNA and protein
levels in the mouse brain, as assessed by in situ
hybridization, real-time PCR, immunoblotting, and immunohistochemistry. This
increase was prominent in the striatum, but was also observed in the cerebral
cortex. GDNF mRNA levels peaked at 3 h and declined afterwards, whereas GDNF
protein levels progressively increased from 24 to 72 h following LY379268
injection. The action of LY379268 was abrogated by the mGlu2/3 receptor
antagonist, LY341495 (1 mg/kg, i.p.), and was lost in mGlu3 receptor knockout
mice, but not in mGlu2 receptor knockout mice. In pure cultures of striatal
neurons, the increase in GDNF induced by LY379268 required the activation of the
mitogen-activated protein kinase and phosphatidylinositol-3-kinase pathways, as
shown by the use of specific inhibitors of the two pathways. Both in
vivo and in vitro studies led to the conclusion
that neurons were the only source of GDNF in response to mGlu3 receptor
activation. Remarkably, acute or repeated injections of LY379268 at doses that
enhanced striatal GDNF levels (0.25 or 3 mg/kg, i.p.) were highly protective
against nigro-striatal damage induced by
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice, as assessed by
stereological counting of tyrosine hydroxylase-positive neurons in the pars
compacta of the substantia nigra. We speculate that selective mGlu3 receptor
agonists or enhancers are potential candidates as neuroprotective agents in
Parkinson''s disease, and their use might circumvent the limitations
associated with the administration of exogenous GDNF. 相似文献
4.
Yolanda Alvarez Olaya Astudillo Lasse Jensen Alison L. Reynolds Nora Waghorne Derek P. Brazil Yihai Cao John J. O'Connor Breandán N. Kennedy 《PloS one》2009,4(11)
Ocular neovascularisation is a pathological hallmark of some forms of debilitating blindness including diabetic retinopathy, age related macular degeneration and retinopathy of prematurity. Current therapies for delaying unwanted ocular angiogenesis include laser surgery or molecular inhibition of the pro-angiogenic factor VEGF. However, targeting of angiogenic pathways other than, or in combination to VEGF, may lead to more effective and safer inhibitors of intraocular angiogenesis. In a small chemical screen using zebrafish, we identify LY294002 as an effective and selective inhibitor of both developmental and ectopic hyaloid angiogenesis in the eye. LY294002, a PI3 kinase inhibitor, exerts its anti-angiogenic effect in a dose-dependent manner, without perturbing existing vessels. Significantly, LY294002 delivered by intraocular injection, significantly inhibits ocular angiogenesis without systemic side-effects and without diminishing visual function. Thus, targeting of PI3 kinase pathways has the potential to effectively and safely treat neovascularisation in eye disease. 相似文献
5.
Jiseon Yang Jennifer Barrila Kenneth L. Roland Jacquelyn Kilbourne C. Mark Ott Rebecca J. Forsyth Cheryl A. Nickerson 《PLoS neglected tropical diseases》2015,9(6)
A distinct pathovar of Salmonella enterica serovar Typhimurium, ST313, has emerged in sub-Saharan Africa as a major cause of fatal bacteremia in young children and HIV-infected adults. D23580, a multidrug resistant clinical isolate of ST313, was previously shown to have undergone genome reduction in a manner that resembles that of the more human-restricted pathogen, Salmonella enterica serovar Typhi. It has since been shown through tissue distribution studies that D23580 is able to establish an invasive infection in chickens. However, it remains unclear whether ST313 can cause lethal disease in a non-human host following a natural course of infection. Herein we report that D23580 causes lethal and invasive disease in a murine model of infection following peroral challenge. The LD50 of D23580 in female BALB/c mice was 4.7 x 105 CFU. Tissue distribution studies performed 3 and 5 days post-infection confirmed that D23580 was able to more rapidly colonize the spleen, mesenteric lymph nodes and gall bladder in mice when compared to the well-characterized S. Typhimurium strain SL1344. D23580 exhibited enhanced resistance to acid stress relative to SL1344, which may lend towards increased capability to survive passage through the gastrointestinal tract as well as during its intracellular lifecycle. Interestingly, D23580 also displayed higher swimming motility relative to SL1344, S. Typhi strain Ty2, and the ST313 strain A130. Biochemical tests revealed that D23580 shares many similar metabolic features with SL1344, with several notable differences in the Voges-Proskauer and catalase tests, as well alterations in melibiose, and inositol utilization. These results represent the first full duration infection study using an ST313 strain following the entire natural course of disease progression, and serve as a benchmark for ongoing and future studies into the pathogenesis of D23580. 相似文献
6.
DNA sequencing has been revolutionized by the development of high-throughput sequencing technologies. Plummeting costs and the massive throughput capacities of second and third generation sequencing platforms have transformed many fields of biological research. Concurrently, new data processing pipelines made rapid de novo genome assemblies possible. However, high quality data are critically important for all investigations in the genomic era. We used chloroplast genomes of one Oryza species (O. australiensis) to compare differences in sequence quality: one genome (GU592209) was obtained through Illumina sequencing and reference-guided assembly and the other genome (KJ830774) was obtained via target enrichment libraries and shotgun sequencing. Based on the whole genome alignment, GU592209 was more similar to the reference genome (O. sativa: AY522330) with 99.2% sequence identity (SI value) compared with the 98.8% SI values in the KJ830774 genome; whereas the opposite result was obtained when the SI values in coding and noncoding regions of GU592209 and KJ830774 were compared. Additionally, the junctions of two single copies and repeat copies in the chloroplast genome exhibited differences. Phylogenetic analyses were conducted using these sequences, and the different data sets yielded dissimilar topologies: phylogenetic replacements of the two individuals were remarkably different based on whole genome sequencing or SNP data and insertions and deletions (indels) data. Thus, we concluded that the genomic composition of GU592209 was heterogeneous in coding and non-coding regions. These findings should impel biologists to carefully consider the quality of sequencing and assembly when working with next-generation data. 相似文献
7.
The purpose of this table is to provide the community with a citable record of publications of ongoing genome sequencing projects that have led to a publication in the scientific literature. While our goal is to make the list complete, there is no guarantee that we may have omitted one or more publications appearing in this time frame. Readers and authors who wish to have publications added to this subsequent versions of this list are invited to provide the bibliometric data for such references to the SIGS editorial office.
- Phylum Crenarchaeota
- Phylum Euryarchaeota
- Pyrococcus yayanosii CH1, sequence accession CP002779 [1]
- Methanocella paludicola, sequence accession AP011532 [2]
- Halorhabdus tiamatea, sequence accession AFNT00000000 [3]
- Thermococcus sp. Strain 4557, sequence accession CP002920 [4]
- Phylum Chloroflexi
- Phylum Proteobacteria
- Ralstonia solanacearum strain Po82, sequence accession CP002819 (chromosome) and CP002820 (megaplasmid) [5
- Desulfovibrio alaskensis G20, sequence accession CP000112 [6]
- Methylophaga aminisulfidivorans MPT, sequence accession AFIG00000000 [7]
- Acinetobacter sp. P8-3-8, sequence accession AFIE00000000 [8]
- Sphingomonas strain KC8, sequence accession AFMP01000000 [9]
- Brucella pinnipedialis B2/94, sequence accession CP002078 and CP002079 [10]
- Salmonella enterica Serovar Typhimurium UK-1, sequence accession CP002614 (chromosome), CP002615 (plasmid) [11]
- Bordetella pertussis CS, sequence accession CP002695 [12]
- Alteromonas sp. Strain SN2, sequence accession CP002339 [13]
- Escherichia coli O104:H4, sequence accession AFOB00000000 (LB226692) and AFPS00000000 (01-09591) [14]
- Acidithiobacillus caldus, sequence accession CP002573 (Chromosome), CP002574 (pLAtcm), CP002575 (pLAtc1), CP002576 (pLAtc2), CP002577 (pLAtc3) [15]
- Cupriavidus necator N-1, sequence accession CP002877 (chromosome 1), CP002878 (chromosome 2), CP002879 (pBB1), and CP002880 (pBB2) [16]
- Oligotropha carboxidovorans OM4, sequence accession CP002821 (OM4 chromosome), CP002822 (pHCG3b), CP002823 (pOC167B) [17]
- Oligotropha carboxidovorans OM5, sequence accession CP002826 (OM5 chromosome), CP002827 (pHCG3), and CP002828 (pOC167) [17]
- Pantoea ananatis LMG20103, sequence accession CP001875 [18]
- Helicobacter bizzozeronii strain CIII-1, sequence accession FR871757 (chromosome) and FR871758 (HBZ-1) [19]
- Vibrio anguillarum 775, sequence accession CP002284 to CP002285 [20]
- Zymomonas mobilis subsp. pomaceae, sequence accession CP002865 (chromosome), CP002866 (p29192_1), CP002867 (p29192_2) [21]
- Agrobacterium sp. strain ATCC 31749, sequence accession AECL01000000 [22]
- Xanthomonas spp. strain Xrc, sequence accesssion CP002789 [23]
- Xanthomonas spp. strain Xoc, sequence accesssion AAQN00000000 [23]
- Glaciecola sp. Strain 4H-3-7+YE-5, sequence accession CP002526 (chromosome) and CP002527 (plasmid) [24]
- Escherichia coli Strain HM605, sequence accession CADZ01000001 through CADZ01000154 [25]
- Salinisphaera shabanensis, sequence accession AFNV00000000 [26]
- Methyloversatilis universalis FAM5T, sequence accession AFHG00000000 [27]
- Alicycliphilus denitrificans Strain BC, sequence accession CP002449 (chromosome), CP002450 (megaplasmid), CP002451 (plasmid) [28].
- Alicycliphilus denitrificans K601T, sequence accession CP002657 (chromosome) and CP002658 (plasmid) [28]
- Oligotropha carboxidovorans Strain OM4, sequence accession CP002821 (chromosome), CP002822 (pHCG3b), CP002823 (pOC167B) [29]
- Oligotropha carboxidovorans Strain OM5, sequence accession CP002826 (chromosome), CP002827 (pHCG3), and CP002828 (pOC167) [29]
- Bradyrhizobiaceae strain SG-6C, sequence accession AFOF01000000 [30]
- Hyphomicrobium sp. Strain MC1, sequence accession FQ859181 [31]
- Shewanella sp. Strain HN-41, sequence accession AFOZ01000000 [32]
- Myxococcus fulvus HW-1, sequence accession CP002830 [33]
- Nitrosomonas sp. Strain AL212, sequence accession NC_015222 (chromosome), NC_015223 pNAL21201), NC_015221 (pNAL21202) [34]
- Ruegeria sp. Strain KLH11, sequence accession ACCW00000000 [35]
- Acidovorax avenae subsp. avenae RS-1, sequence accession AFPT01000000 [36]
- Escherichia coli (ExPEC), sequence accession AFAT00000000 [37]
- Vibrio mimicus SX-4, sequence accession ADOO01000000 [38]
- Agrobacterium tumefaciens Strain F2, sequence accession AFSD00000000 [39]
- Pasteurella multocida subsp. gallicida AFRR01000001 to AFRR01000489 [40]
- Pseudomonas aeruginosa 138244, sequence accession AEVV00000000 [41]
- Pseudomonas aeruginosa 152504, sequence accession AEVW00000000 [41]
- Campylobacter jejuni strain 305, sequence accession ADHL00000000 [42]
- Campylobacter jejuni strain DFVF1099, sequence accession ADHK00000000 [42]
- Xanthomonas campestris pv. raphani strain 756C, sequence accession CP002789 [43]
- Xanthomonas campestris pv. raphani strain BLS256, sequence accession AAQN01000001 [43]
- Rickettsia heilongjiangensis, sequence accession CP002912 [44]
- Acidiphilium sp. Strain PM (DSM 24941), sequence accession AFPR00000000 [45]
- Pseudomonas putida Strain S16, sequence accession CP002870 [46]
- Acinetobacter lwoffii, sequence accession AFQY01000000 [47]
- Phylum Firmicutes
- Caldalkalibacillus thermarum strain TA2.A1, sequence accession AFCE00000000 [48]
- Listeria monocytogenes Scott A, sequence accession AFGI00000000 [49]
- Lactococcus garvieae 8831, sequence accession AFCD00000000 [50]
- Natranaerobius thermophilus JW/NM-WN-LF, sequence accession CP001034 (chromosome), CP001035 (plasmid) [51]
- Melissococcus plutonius ATCC 35311, sequence accession AP012200 (chromosome) and AP012201 (plasmid) [52]
- Lactobacillus buchneri NRRL B-30929, sequence accession CP002652 (chromosome), CP002653 (plasmid pLBU01), CP002654 (plasmid pLBU02), and CP002655 (plasmid pLBU03) [53]
- Lactobacillus kefiranofaciens ZW3 , sequence accession CP002764 (chromosome), CP002765 (plasmid), and CP002766 (plasmid) [54]
- Bacillus megaterium strain QM B1551, sequence accession CP001983 (chromosome), CP001984 to CP001990 (plasmids pBM100 through pBM700) [55]
- Bacillus megaterium strain DSM319, sequence accession CP001982 (chromosome) [55]
- Listeria monocytogenes serovar 4a strain M7, sequence accession CP002816 [56]
- Bacillus coagulans 2-6, sequence accession CP002472 [57]
- Streptococcus salivarius strain CCHSS3, sequence accession FR873481 [58]
- Paenibacillus elgii B69, sequence accession AFHW01000000 [59]
- Lactobacillus pentosus MP-10, sequence accession FR871759 through FR871848 [60]
- Leuconostoc pseudomesenteroides KCTC 3652, sequence accession AEOQ00000001 through AEOQ00001160 [61]
- Lactobacillus mali KCTC 3596, sequence accession BACP01000001 through BACP01000122 [62]
- Paenibacillus polymyxa Type Strain ATCC 842T, sequence accession AFOX01000000 [63]
- Streptococcus salivarius strain JIM8777, sequence accssion FR873482 [64]
- Lactobacillus cypricasei KCTC 13900, sequence accession BACS01000001 to BACS01000487 [65]
- Lactobacillus zeae KCTC 3804, sequence accession BACQ01000001 to BACQ101000113 [66]
- Listeria monocytogenes Serovar 4a Strain M7, sequence accession CP002816 [67]
- Lactobacillus salivarius GJ-24, sequence accession AFOI00000000 [68]
- Lactobacillus johnsonii PF01, sequence accession AFQJ01000000 [69]
- Clostridium acetobutylicum DSM 1731, sequence accession CP002660 through CP002662 [70]
- Lactobacillus suebicus KCTC 3549, sequence accession BACO01000000 [71]
- Brevibacillus laterosporus LMG 15441, sequence accession AFRV00000000 [72]
- Lactobacillus salivarius NIAS840, sequence accession AFMN00000000 [73]
- Bifidobacterium animalis subsp. lactis CNCM I-2494, sequence accession CP002915 [74]
- Megasphaera elsdenii, sequence accession HE576794 [75]
- Lactobacillus versmoldensis KCTC 3814, sequence accession BACR01000001 to BACR01000102 [76]
- Lactobacillus pentosus IG1, sequence accession FR874848 to FR874860 [77]
- Alicyclobacillus acidocaldarius Strain Tc-4-1, sequence accession CP002902 [78]
- Streptococcus thermophilus Strain JIM8232, sequence accession FR875178 [79]
- Streptococcus equi subsp. zooepidemicus Strain ATCC 35246, sequence accession CP002904 [80]
- Bacillus amyloliquefaciens XH7, sequence accession CP002927 [81]
- Leuconostoc kimchii Strain C2, sequence accession CP002898 [82]
- Lactobacillus malefermentans KCTC 3548, sequence accession BACN01000001 to BACN01000172 [83]
- Weissella koreensis KACC 15510, sequence accession CP002900 [84]
- Phylum Tenericutes
- Mycoplasma bovis Strain Hubei-1, sequence accession CP002513 [85]
- Mycoplasma fermentans Strain M64, sequence accession NC_014921 [86]
- Haloplasma contractile, sequence accession AFNU00000000 [87]
- Mycoplasma ovipneumoniae Strain SC01, sequence accession AFHO01000000 [88]
- Phylum Actinobacteria
- Kocuria rhizophila P7-4, sequence accession AFID00000000 [89]
- Streptomyces S4, sequence accession CADY01000000 [90]
- Corynebacterium nuruki S6-4T, sequence accession AFIZ00000000 [91]
- Propionibacterium humerusii, sequence accession AFAM00000000.1 [92]
- Strain JDM601, sequence accession CP002329 [93]
- Streptomyces sp. strain Tü6071, sequence accession AFHJ01000000 [94]
- Bifidobacterium breve UCC2003, sequence accession CP000303 [95]
- Propionibacterium acnes, sequence accession CP002815 [96]
- Amycolicicoccus subflavus DQS3-9A1T, sequence accession CP002786 (chromosome), CP002787 (plasmid pAS9A-1), and CP002788 (plasmid pAS9A-2). [97]
- Gordonia neofelifaecis NRRL B-59395, sequence accession AEUD01000000 [98]
- Pseudonocardia dioxanivorans strain CB1190, sequence accession NC_015312-4 and CP002595-7 [99]
- Bifidobacterium longum subsp. longum KACC 91563, sequence accession CP002794 to CP002796 [100]
- Streptomyces cattleya NRRL 8057, sequence accession FQ859185 (chromosome) and FQ859184 (megaplasmid) [101]
- Rhodococcus sp. Strain R04, sequence accession AFAQ01000000 [102]
- Mycobacterium bovis BCG Moreau, sequence accession [103]
- Saccharopolyspora spinosa NRRL 18395, sequence accession [104]
- Mycobacterium tuberculosis CCDC5079, sequence accession [105]
- Mycobacterium tuberculosis CCDC5180, sequence accession [105]
- Amycolatopsis mediterranei S699, sequence accession CP002896 [106]
- Nesterenkonia sp. Strain F, sequence accession AFRW01000000 [107]
- Streptomyces xinghaiensis NRRL B24674T, sequence accession AFRP01000000 [108]
- Phylum Chlamydiae
- Chlamydophila abortus variant strain LLG, sequence accession AFHM01000000 [109]
- Chlamydia psittaci 6BC, sequence accession CP002586 (chromosome), CP002587 (plasmid) [110]
- Chlamydia psittaci Cal10, sequence accession AEZD00000000 (draft chromosome and plasmid) [110]
- Chlamydia trachomatis, sequence accession CP002024 [111]
- Phylum Spirochaetes
- Spirochaeta thermophila DSM 6192, sequence accession CP001698 [112]
- Brachyspira intermedia, sequence accession CP002874 (chromosome) and CP002875 (plasmid) [113]
- Phylum Fibrobacteres
- Phylum Bacteroidetes
- Porphyromonas gingivalis TDC60, sequence accession AP012203 [114]
- Krokinobacter sp. strain 4H-3-7-5, sequence accession CP002528 [115]
- Lacinutrix sp. strain 5H-3-7-4, sequence accession CP002825 [115]
- Bacterium HQM9, sequence accession AFPB00000000 [116]
- Anaerophaga sp. Strain HS1, sequence accession AFSL00000000 [117]
- Capnocytophaga canimorsus Strain 5, sequence accession CP002113 [118]
- Mesoflavibacter zeaxanthinifaciens strain S86, sequence accession AFOE00000000 [119]
- Phylum Verrucomicrobia
- Phylum Lentisphaerae
- Phylum Thermotogae
- Kosmotoga olearia Strain TBF 19.5.1, sequence accession CP001634 [120]
- Domain Archaea
- "Candidatus Nitrosoarchaeum koreensis" MY1, sequence accession AFPU00000000 [121]
Non-Bacterial genomes
- North-European Cucumber Cucumis sativus L., sequence accession FI132140-FI136208, GS765762-GS766880, GS815969-GS874855 [122]
- Castor bean Ricinus communis organelle genome, sequence accession JF937588(chloroplast), HQ874649 (mitochondria) [123]
- Stretch Lagoon Orbivirus Umatilla, sequence accession HQ842619 through HQ842628 [124]
- Atlantic cod Gadus morhua, sequence accession CAEA01000001 through CAEA01554869 [125]
- Potato Solanum tuberosum L., sequence accession GS025503 through GS026177 [126]
- ΦCA82, sequence accession HQ264138 [127]
- Paramecium caudatumreveals mitochondria, sequence accession NC001324 [128]
- bacteriophage IME08, sequence accession NC_014260 [129]
- virus (ILTV), sequence accession HQ_630064 [130]
- Australian kangaroo Macropus eugenii, sequence accession ABQO000000000 [131]
- Aichi virus, sequence accession FJ890523 [132]
- "Candidatus Tremblaya princeps" Strain PCVAL, sequence accession CP002918 [133]
8.
9.
Marius R. Robciuc Paulina Skrobuk Andrey Anisimov Vesa M. Olkkonen Kari Alitalo Robert H. Eckel Heikki A. Koistinen Matti Jauhiainen Christian Ehnholm 《PloS one》2012,7(10)
Peroxisome proliferator-activated receptor (PPAR) delta is an important regulator of fatty acid (FA) metabolism. Angiopoietin-like 4 (Angptl4), a multifunctional protein, is one of the major targets of PPAR delta in skeletal muscle cells. Here we investigated the regulation of Angptl4 and its role in mediating PPAR delta functions using human, rat and mouse myotubes. Expression of Angptl4 was upregulated during myotubes differentiation and by oleic acid, insulin and PPAR delta agonist GW501516. Treatment with GW501516 or Angptl4 overexpression inhibited both lipoprotein lipase (LPL) activity and LPL-dependent uptake of FAs whereas uptake of BSA-bound FAs was not affected by either treatment. Activation of retinoic X receptor (RXR), PPAR delta functional partner, using bexarotene upregulated Angptl4 expression and inhibited LPL activity in a PPAR delta dependent fashion. Silencing of Angptl4 blocked the effect of GW501516 and bexarotene on LPL activity. Treatment with GW501516 but not Angptl4 overexpression significantly increased palmitate oxidation. Furthermore, Angptl4 overexpression did not affect the capacity of GW501516 to increase palmitate oxidation. Basal and insulin stimulated glucose uptake, glycogen synthesis and glucose oxidation were not significantly modulated by Angptl4 overexpression. Our findings suggest that FAs-PPARdelta/RXR-Angptl4 axis controls the LPL-dependent uptake of FAs in myotubes, whereas the effect of PPAR delta activation on beta-oxidation is independent of Angptl4. 相似文献
10.
11.
12.
Stephen J. Peterson Dong Hyun Kim Ming Li Vincenzo Positano Luca Vanella Luigi F. Rodella Francesco Piccolomini Nitin Puri Amalia Gastaldelli Claudia Kusmic Antonio L'Abbate Nader G. Abraham 《Journal of lipid research》2009,50(7):1293-1304
We examined mechanisms by which L-4F reduces obesity and diabetes in obese (ob) diabetic mice. We hypothesized that L-4F reduces adiposity via increased pAMPK, pAKT, HO-1, and increased insulin receptor phosphorylation in ob mice. Obese and lean mice were divided into five groups: lean, lean-L-4F-treated, ob, ob-L-4F-treated, and ob-L-4F-LY294002. Food intake, insulin, glucose adipocyte stem cells, pAMPK, pAKT, CB1, and insulin receptor phosphorylation were determined. Subcutaneous (SAT) and visceral adipose tissue (VAT) were determined by MRI and hepatic lipid content by magnetic resonance spectroscopy. SAT and VAT volumes decreased in ob-L-4F-treated animals compared with control. L-4F treatment decreased hepatic lipid content and increased the numbers of small adipocytes (P < 0.05) and phosphorylation of insulin receptors. L-4F decreased CB1 in SAT and VAT and increased pAKT and pAMPK in endothelium. L-4F-mediated improvement in endothelium was prevented by LY294002. Inhibition of pAKT and pAMPK by LY294002 was associated with an increase in glucose levels. Upregulation of HO-1 by L-4F produced adipose remodeling and increased the number of small differentiated adipocytes. The anti-obesity effects of L-4F are manifested by a decrease in visceral fat content with reciprocal increases in adiponectin, pAMPK, pAKT, and phosphorylation of insulin receptors with improved insulin sensitivity. 相似文献
13.
Xiang Li Xiao-Yan Jiang Jin Ge Jing Wang Guo-Jun Chen Liang Xu Duan-Yang Xie Tian-You Yuan Da-Sheng Zhang Hong Zhang Yi-Han Chen 《PloS one》2014,9(1)
Long non-coding RNAs (lncRNAs) are key regulatory molecules involved in a variety of biological processes and human diseases. However, the pathological effects of lncRNAs on primary varicose great saphenous veins (GSVs) remain unclear. The purpose of the present study was to identify aberrantly expressed lncRNAs involved in the prevalence of GSV varicosities and predict their potential functions. Using microarray with 33,045 lncRNA and 30,215 mRNA probes, 557 lncRNAs and 980 mRNAs that differed significantly in expression between the varicose great saphenous veins and control veins were identified in six pairs of samples. These lncRNAs were sub-grouped and mRNAs expressed at different levels were clustered into several pathways with six focused on metabolic pathways. Quantitative real-time PCR replication of nine lncRNAs was performed in 32 subjects, validating six lncRNAs (AF119885, AK021444, NR_027830, G36810, NR_027927, uc.345-). A coding-non-coding gene co-expression network revealed that four of these six lncRNAs may be correlated with 11 mRNAs and pathway analysis revealed that they may be correlated with another 8 mRNAs associated with metabolic pathways. In conclusion, aberrantly expressed lncRNAs for GSV varicosities were here systematically screened and validated and their functions were predicted. These findings provide novel insight into the physiology of lncRNAs and the pathogenesis of varicose veins for further investigation. These aberrantly expressed lncRNAs may serve as new therapeutic targets for varicose veins. The Human Ethnics Committee of Shanghai East Hospital, Tongji University School of Medicine approved the study (NO.: 2011-DF-53). 相似文献
14.
Beate Fuchs Markus Rupp Hossein A Ghofrani Ralph T Schermuly Werner Seeger Friedrich Grimminger Thomas Gudermann Alexander Dietrich Norbert Weissmann 《Respiratory research》2011,12(1):20
Background
Hypoxic pulmonary vasoconstriction (HPV) is an essential mechanism of the lung that matches blood perfusion to alveolar ventilation to optimize gas exchange. Recently we have demonstrated that acute but not sustained HPV is critically dependent on the classical transient receptor potential 6 (TRPC6) channel. However, the mechanism of TRPC6 activation during acute HPV remains elusive. We hypothesize that a diacylglycerol (DAG)-dependent activation of TRPC6 regulates acute HPV.Methods
We investigated the effect of the DAG analog 1-oleoyl-2-acetyl-sn-glycerol (OAG) on normoxic vascular tone in isolated perfused and ventilated mouse lungs from TRPC6-deficient and wild-type mice. Moreover, the effects of OAG, the DAG kinase inhibitor R59949 and the phospholipase C inhibitor U73122 on the strength of HPV were investigated compared to those on non-hypoxia-induced vasoconstriction elicited by the thromboxane mimeticum U46619.Results
OAG increased normoxic vascular tone in lungs from wild-type mice, but not in lungs from TRPC6-deficient mice. Under conditions of repetitive hypoxic ventilation, OAG as well as R59949 dose-dependently attenuated the strength of acute HPV whereas U46619-induced vasoconstrictions were not reduced. Like OAG, R59949 mimicked HPV, since it induced a dose-dependent vasoconstriction during normoxic ventilation. In contrast, U73122, a blocker of DAG synthesis, inhibited acute HPV whereas U73343, the inactive form of U73122, had no effect on HPV.Conclusion
These findings support the conclusion that the TRPC6-dependency of acute HPV is induced via DAG. 相似文献15.
In this short report, the genome-wide homologous recombination events were re-evaluated for classical swine fever virus (CSFV) strain AF407339. We challenged a previous study which suggested only one recombination event in AF407339 based on 25 CSFV genomes. Through our re-analysis on the 25 genomes in the previous study and the 41 genomes used in the present study, we argued that there should be possibly at least two clear recombination events happening in AF407339 through genome-wide scanning. The reasons for identifying only one recombination event in the previous study might be due to the limited number of available CSFV genome sequences at that time and the limited usage of detection methods. In contrast, as identified by most detection methods using all available CSFV genome sequences, two major recombination events were found at the starting and ending zones of the genome AF407339, respectively. The first one has two parents AF333000 (minor) and AY554397 (major) with beginning and ending breakpoints located at 19 and 607 nt of the genome respectively. The second one has two parents AF531433 (minor) and GQ902941 (major) with beginning and ending breakpoints at 8397 and 11,078 nt of the genome respectively. Phylogenetic incongruence analysis using neighbor-joining algorithm with 1000 bootstrapping replicates further supported the existence of these two recombination events. In addition, we also identified additional 18 recombination events on the available CSFV strains. Some of them may be trivial and can be ignored. In conclusion, CSFV might have relatively high frequency of homologous recombination events. Genome-wide scanning of identifying recombination events should utilize multiple detection methods so as to reduce the risk of misidentification. 相似文献
16.
Xinxing Lu Qiuling Fan Li Xu Lin Li Yuan Yue Yanyan Xu Yan Su Dongcheng Zhang Lining Wang 《PloS one》2015,10(2)
ObjectiveTo investigate the effect of ursolic acid on autophagy mediated through the miRNA-21-targeted phosphoinositide 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway in rat mesangial cells cultured under high glucose (HG) conditions.MethodsRat glomerular mesangial cells were cultured under normal glucose, HG, HG with the PI3K inhibitor LY294002 or HG with ursolic acid conditions. Cell proliferation and hypertrophy were assayed using an MTT assay and the ratio of total protein to cell number, respectively. The miRNA-21 expression was detected using RT-qPCR. The expression of phosphatase and tensin homolog (PTEN)/AKT/mTOR signaling signatures, autophagy-associated protein and collagen I was detected by western blotting and RT-qPCR. Autophagosomes were observed using electron microscopy.ResultsCompared with mesangial cells cultured under normal glucose conditions, the cells exposed to HG showed up-regulated miRNA-21 expression, down-regulated PTEN protein and mRNA expression, up-regulated p85PI3K, pAkt, pmTOR, p62/SQSTMI, and collagen I expression and down-regulated LC3II expression. Ursolic acid and LY294002 inhibited HG-induced mesangial cell hypertrophy and proliferation, down-regulated p85PI3K, pAkt, pmTOR, p62/SQSTMI, and collagen I expression and up-regulated LC3II expression. However, LY294002 did not affect the expression of miRNA-21 and PTEN. Ursolic acid down-regulated miRNA-21 expression and up-regulated PTEN protein and mRNA expression.ConclusionsUrsolic acid inhibits the glucose-induced up-regulation of mesangial cell miRNA-21 expression, up-regulates PTEN expression, inhibits the activation of PI3K/Akt/mTOR signaling pathway, and enhances autophagy to reduce the accumulation of the extracellular matrix and ameliorate cell hypertrophy and proliferation. 相似文献
17.
Abdallah Ahnaou Hilde Lavreysen Gary Tresadern Jose M. Cid Wilhelmus H. Drinkenburg 《PloS one》2015,10(12)
G-protein-coupled receptor (GPCR) agonists are known to induce both cellular adaptations resulting in tolerance to therapeutic effects and withdrawal symptoms upon treatment discontinuation. Glutamate neurotransmission is an integral part of sleep-wake mechanisms, which processes have translational relevance for central activity and target engagement. Here, we investigated the efficacy and tolerance potential of the metabotropic glutamate receptors (mGluR2/3) agonist LY354740 versus mGluR2 positive allosteric modulator (PAM) JNJ-42153605 on sleep-wake organisation in rats. In vitro, the selectivity and potency of JNJ-42153605 were characterized. In vivo, effects on sleep measures were investigated in rats after once daily oral repeated treatment for 7 days, withdrawal and consecutive re-administration of LY354740 (1–10 mg/kg) and JNJ-42153605 (3–30 mg/kg). JNJ-42153605 showed high affinity, potency and selectivity at mGluR2. Binding site analyses and knowledge-based docking confirmed the specificity of JNJ-42153605 at the mGluR2 allosteric binding site. Acute LY354740 and JNJ-42153605 dose-dependently decreased rapid eye movement (REM) sleep time and prolonged its onset latency. Sub chronic effects of LY354740 on REM sleep measures disappeared from day 3 onwards, whereas those of JNJ-42153605 were maintained after repeated exposure. LY354740 attenuated REM sleep homeostatic recovery, while this was preserved after JNJ-42153605 administration. JNJ-42153605 enhanced sleep continuity and efficiency, suggesting its potential as an add-on medication for impaired sleep quality during early stages of treatment. Abrupt cessation of JNJ-42153605 did not induce withdrawal phenomena and sleep disturbances, while the initial drug effect was fully reinstated after re-administration. Collectively, long-term treatment with JNJ-42153605 did not induce tolerance phenomena to its primary functional effects on sleep measures, nor adverse effects at withdrawal, while it promoted homeostatic recovery sleep. From the translational perspective, the present rodent findings suggest that mGluR2 positive allosteric modulation has therapeutic potential based on its superior long term efficacy over agonists in psychiatric disorders, particularly of those commonly occurring with REM sleep overdrive. 相似文献
18.
The purpose of this table is to provide the community with a citable record of publications of ongoing genome sequencing projects that have led to a publication in the scientific literature. While our goal is to make the list complete, there is no guarantee that we may have omitted one or more publications appearing in this time frame. Readers and authors who wish to have publications added to subsequent versions of this list are invited to provide the bibliographic data for such references to the SIGS editorial office.
Phylum Euryarchaeota
- Halococcus hamelinensis, sequence accession PRJNA80845 [1]
- “Methanocella conradii” HZ254, sequence accession CP003243 [2]
- Thermococcus litoralis NS-C, sequence accession AHVB00000000 [3]
Phylum Crenarchaeota
- Candidatus Nitrosopumilus salaria” BD31, sequence accession AEXL00000000 [4]
- Candidatus Nitrosoarchaeum limnia, sequence accession AHJG00000000 [5]
Phylum Deinococcus-Thermus
Phylum Proteobacteria
- Aggregatibacter actinomycetemcomitans strain ANH9381, sequence accession CP003099 [7]
- Alishewanella jeotgali, sequence accession AHTH00000000 [8]
- Enterobacter aerogenes KCTC 2190, sequence accession CP002824 [9]
- Escherichia coli O104:H4, sequence accession AFOB02000092 [10]
- Helicobacter pylori strains 17874, sequence accession PRJNA76569 [11]
- Helicobacter pylori strains P79, sequence accession PRJNA76567 [11]
- Janthinobacterium sp. Strain PAMC 25724, sequence accession AHHB00000000 [12]
- Klebsiella oxytoca KCTC 1686, sequence accession CP003218 [13]
- Klebsiella pneumoniae subsp. pneumoniae HS11286, sequence accession CP003200 (chromosome), CP003223 (plasmid pKPHS1), CP003224 (plasmid pKPHS2), CP003225 (plasmid pKPHS3), CP003226 (plasmid pKPHS4), CP003227 (plasmid pKPHS5), CP003228 (plasmid pKPHS6) [14]
- Oceanimonas sp. GK1, sequence accession CP003171 [15]
- “Pseudogulbenkiania ferrooxidans” Strain 2002, sequence accession NZ_ACIS01000000 [16]
- Pseudomonas extremaustralis 14-3b, sequence accession AHIP00000000 [17]
- Pseudomonas sp. Strain PAMC 25886, sequence accession AHHC00000000 [18]
- Psychrobacter, sequence accession AHVZ00000000 [19]
- Rahnella sp. Strain Y9602, sequence accession CP002505 [20]
- Rhizobium sp. Strain PDO1-076, sequence accession AHZC00000000 [21]
- Rhodospirillum photometricum DSM122, sequence accession HE663493 [22]
- “Rickettsia sibirica sibirica”, sequence accession AHIZ00000000 [23]
- Rickettsia sibirica subsp. mongolitimonae strain HA-91, sequence accession AHZB00000000 [24]
- Salmonella enterica subsp. enterica Serotype Enteritidis Strain LA5, sequence accession [25]
- Salmonella enterica subsp. enterica Serotype Senftenberg Strain SS209, sequence accession CAGQ00000000 [26]
- Salmonella enterica subsp. enterica Serovar Typhi P-stx-12, sequence accession CP003278 (chromosome) and CP003279 (plasmid) [27]
- Sphingomonas echinoides ATCC 14820, sequence accession AHIR00000000 [28]
- Strain HIMB55, sequence accession AGIF00000000 [29]
- Vibrio harveyi CAIM 1792, sequence accession AHHQ00000000 [30]
- Wolbachia Strain wAlbB, sequence accession CAGB01000001 to CAGB01000165 [31]
- Xanthomonas axonopodis pv. punicae Strain LMG 859, sequence accession CAGJ01000001 to CAGJ01000217 [32]
Phylum Tenericutes
Phylum Firmicutes
- Bacillus subtilis, sequence accession BGSCID 3A27 through BGSCID 28A4 [34]
- Clostridium difficile Strain CD37, sequence accession AHJJ00000000 [35]
- Clostridium perfringens, sequence accession AFES00000000 [36]
- Lactobacillus fructivorans KCTC 3543, sequence accession AEQY00000000 [37]
- Lactococcus lactis IO-1, sequence accession AP012281 [38]
- Lactobacillus plantarum strain NC8, sequence accession AGRI00000000 [39]
- Paenibacillus dendritiformis C454, sequence accession AHKH00000000 [40]
- Paenibacillus sp. Strain Aloe-11, sequence accession AGFI00000000 [41]
- “Peptoniphilus rhinitidis” 1-13T, sequence accession BAEW01000001 to BAEW01000056 [42]
- Streptococcus macedonicus ACA-DC 198, sequence accession HE613569 and HE613570 [43]
- Staphylococcus aureus VC40, sequence accession CP003033 [44]
- Streptococcus infantarius subsp. infantarius Strain CJ18, sequence accession CP003295 (chromosome), CP003296 (plasmid) [45]
- Streptococcus macedonicus ACA-DC 198, sequence accession HE613569 (chromosome), HE613570 (plasmid pSMA198) [46]
Phylum Actinobacteria
- Actinoplanes sp. SE50/110, sequence accession CP003170 [47]
- Amycolatopsis sp. Strain ATCC 39116, sequence accession [48]
- Nocardia cyriacigeorgica GUH-2, sequence accession FO082843 [49]
- Salinibacterium sp., sequence accession AHWA00000000 [50]
- Streptomyces acidiscabies 84-104, sequence accession AHBF00000000 [51]
Non-Bacterial genomes
- Bluetongue Virus Serotype 2, sequence accession AJ783905 (Seg-6) and JQ681257 (Seg-1), JQ681257 (Seg-1), JQ681258 (Seg-2), JQ681259 (Seg-3), JQ681260 (Seg-4), JQ681261 (Seg-5), JQ681262 (Seg-7), JQ6812563 (Seg-8), JQ6812564 (Seg-9), to JQ681265 (Seg-10) [52]
- Virus Serotype 1, sequence accession AJ585111 (Seg-2), AJ586659 (Seg-6), JQ282770 (Seg-1), JQ282771 (Seg-3), JQ282772 (Seg-4), JQ282773 (Seg-5), JQ282774 (Seg-7), JQ282775 (Seg-8), JQ282776 (Seg-9), and JQ282777 (Seg-10) [52]
- Chloroplast genome of Erycina pusilla, sequence accession JF_746994 [53]
- Danio rerio, sequence accession JQ434101 [54]
- Enterococcal Bacteriophage SAP6, sequence accession JF731128 [55]
- Eubenangee virus, sequence accession JQ070376 through JQ070385 [56]
- Fujian/411-like viruses, sequence accession CY087969 to CY088568 [57]
- Hantavirus Variant of Rio Mamoré Virus, Maripa Virus, sequence accession JQ611712 (segment S), JQ611713 (segment M), and JQ611714 (segment L) [58]
- Pata virus, sequence accession JQ070386 through JQ070395 [59]
- Porcine Circovirus 2, sequence accession JQ413808 [60]
- Porcine Reproductive and Respiratory Syndrome Virus, sequence accession JQ326271 [61]
- Streptococcus mutans Phage M102AD, sequence accession DQ386162 [62]
- Tilligery virus, sequence accession JQ070366 through JQ070375 [63]
19.
Wenxiu Yi Qiang Li Jian Shen Lijie Ren Xiaohui Liu Qi Wang Sudan He Qingyu Wu Hu Hu Xinliang Mao Li Zhu 《PloS one》2014,9(8)
The phosphatidylinositol 3–kinase (PI3K) signaling pathway is critical in modulating platelet functions. In the present study, we evaluated the effect of S14161, a recently identified pan-class I PI3K inhibitor, on platelet activation and thrombus formation. Results showed that S14161 inhibited human platelet aggregation induced by collagen, thrombin, U46619, and ADP in a dose-dependent manner. Flow cytometric studies showed that S14161 inhibited convulxin- or thrombin-induced P-selectin expression and fibrinogen binding of single platelet. S14161 also inhibited platelet spreading on fibrinogen and clot retraction, processes mediated by outside-in signaling. Using a microfluidic chamber we demonstrated that S14161 decreased platelet adhesion on collagen-coated surface by about 80%. Western blot showed that S14161 inhibited phosphorylation of Akt at both Ser473 and Thr308 sites, and GSK3β at Ser9 in response to collagen, thrombin, or U46619. Comparable studies showed that S14161 has a higher potential bioavailability than LY294002, a prototypical inhibitor of pan-class I PI3K. Finally, the effects of S14161 on thrombus formation in vivo were measured using a ferric chloride-induced carotid artery injury model in mice. The intraperitoneal injection of S14161 (2 mg/kg) to male C57BL/6 mice significantly extended the first occlusion time (5.05±0.99 min, n = 9) compared to the vehicle controls (3.72±0.95 min, n = 8) (P<0.05), but did not prolong the bleeding time (P>0.05). Taken together, our data showed that S14161 inhibits platelet activation and thrombus formation without significant bleeding tendency and toxicity, and considering its potential higher bioavailability, it may be developed as a novel therapeutic agent for the prevention of thrombotic disorders. 相似文献