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1.
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.
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
4.
Haibin Wu Jinxia Qin Jun Han Xiaojie Zhao Shuhong Ouyang Yong Liang Dong Zhang Zhenzhong Wang Qiuhong Wu Jingzhong Xie Yu Cui Huiru Peng Qixin Sun Zhiyong Liu 《PloS one》2013,8(12)
The wax (glaucousness) on wheat leaves and stems is mainly controlled by two sets of genes: glaucousness loci (W1 and W2) and non-glaucousness loci (Iw1 and Iw2). The non-glaucousness (Iw) loci act as inhibitors of the glaucousness loci (W). High-resolution comparative genetic linkage maps of the wax inhibitors Iw1 originating from Triticum dicoccoides, and Iw2 from Aegilops tauschii were developed by comparative genomics analyses of Brachypodium, sorghum and rice genomic sequences corresponding to the syntenic regions of the Iw loci in wheat. Eleven Iw1 and eight Iw2 linked EST markers were developed and mapped to linkage maps on the distal regions of chromosomes 2BS and 2DS, respectively. The Iw1 locus mapped within a 0.96 cM interval flanked by the BE498358 and CA499581 EST markers that are collinear with 122 kb, 202 kb, and 466 kb genomic regions in the Brachypodium 5S chromosome, the sorghum 6S chromosome and the rice 4S chromosome, respectively. The Iw2 locus was located in a 4.1 to 5.4-cM interval in chromosome 2DS that is flanked by the CJ886319 and CJ519831 EST markers, and this region is collinear with a 2.3 cM region spanning the Iw1 locus on chromosome 2BS. Both Iw1 and Iw2 co-segregated with the BF474014 and CJ876545 EST markers, indicating they are most likely orthologs on 2BS and 2DS. These high-resolution maps can serve as a framework for chromosome landing, physical mapping and map-based cloning of the wax inhibitors in wheat. 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.
Zihao Pan Jiale Ma Wenyang Dong Wenchao Song Kaicheng Wang Chengping Lu Huochun Yao 《Applied and environmental microbiology》2015,81(3):976-985
Streptococcus suis is an emerging zoonotic pathogen causing severe infections in pigs and humans. In previous studies, 33 serotypes of S. suis have been identified using serum agglutination. Here, we describe a novel S. suis strain, CZ130302, isolated from an outbreak of acute piglet meningitis in eastern China. Strong pathogenicity of meningitis caused by strain CZ130302 was reproduced in the BALB/c mouse model. The strain showed a high fatality rate (8/10), higher than those for known virulent serotype 2 strains P1/7 (1/10) and 9801 (2/10). Cell adhesion assay results with bEnd.3 and HEp2 cells showed that CZ130302 was significantly close to P1/7 and 9801. Both the agglutination test and its complementary test showed that strain CZ130302 had no strong cross-reaction with the other 33 S. suis serotypes. The multiplex PCR assays revealed no specified bands for all four sets used to detect the other 33 serotypes. In addition, genetic analysis of the whole cps gene clusters of all serotypes was performed in this study. The results of comparative genomics showed that the cps gene cluster of CZ130302, which was not previously reported, showed no homology to the gene sequences of the other strains. Especially, the wzy, wzx, and acetyltransferase genes of strain CZ130302 are phylogenetically distinct from strains of the other 33 serotypes. Therefore, this study suggested that strain CZ130302 represents a novel variant serotype of S. suis (designated serotype Chz) which has a high potential to be virulent and associated with meningitis in animals. 相似文献
7.
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
8.
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]
9.
10.
Shuanglin Peng Yujin Gao Sirong Shi Dan Zhao Huayue Cao Ting Fu Xiaoxiao Cai Jingang Xiao 《Cell proliferation》2022,55(1)
ObjectivesBone tissue engineering based on adipose‐derived stem cells (ASCs) is expected to become a new treatment for diabetic osteoporosis (DOP) patients with bone defects. However, compared with control ASCs (CON‐ASCs), osteogenic potential of DOP‐ASCs is decreased, which increased the difficulty of bone reconstruction in DOP patients. Moreover, the cause of the poor osteogenesis of ASCs in a hyperglycemic microenvironment has not been elucidated. Therefore, this study explored the molecular mechanism of the decline in the osteogenic potential of DOP‐ASCs from the perspective of epigenetics to provide a possible therapeutic target for bone repair in DOP patients with bone defects.Materials and methodsAn animal model of DOP was established in mice. CON‐ASCs and DOP‐ASCs were isolated from CON and DOP mice, respectively. AK137033 small interfering RNA (SiRNA) and an AK137033 overexpression plasmid were used to regulate the expression of AK137033 in CON‐ASCs and DOP‐ASCs in vitro. Lentiviruses that carried shRNA‐AK137033 or AK137033 cDNA were used to knockdown or overexpress AK137033, respectively, in CON‐ASCs and DOP‐ASCs in vivo. Hematoxylin and eosin (H&E), Masson''s, alizarin red, and alkaline phosphatase (ALP) staining, micro‐computed tomography (Micro‐CT), flow cytometry, qPCR, western blotting, immunofluorescence, and bisulfite‐specific PCR (BSP) were used to analyze the functional changes of ASCs.ResultsThe DOP mouse model was established successfully. Compared with CON‐ASCs, AK137033 expression, the DNA methylation level of the sFrp2 promoter region, Wnt signaling pathway markers, and the osteogenic differentiation potential were decreased in DOP‐ASCs. In vitro experiments showed that AK137033 silencing inhibited the Wnt signaling pathway and osteogenic ability of CON‐ASCs by reducing the DNA methylation level in the sFrp2 promoter region. Additionally, overexpression of AK137033 in DOP‐ASCs rescued these changes caused by DOP. Moreover, the same results were obtained in vivo.ConclusionsLncRNA‐AK137033 inhibits the osteogenic potential of DOP‐ASCs by regulating the Wnt signaling pathway via modulating the DNA methylation level in the sFrp2 promoter region. This study provides an important reference to find new targets for the treatment of bone defects in DOP patients. 相似文献
11.
12.
Barbara L. Bernardo Timothy S. Wachtmann Patricia G. Cosgrove Max Kuhn Alan C. Opsahl Kyle M. Judkins Thomas B. Freeman John R. Hadcock Nathan K. LeBrasseur 《PloS one》2010,5(6)
Background
Interventions for T2DM have in part aimed to mimic exercise. Here, we have compared the independent and combined effects of a PPARδ agonist and endurance training mimetic (GW501516) and a myostatin antibody and resistance training mimetic (PF-879) on metabolic and performance outcomes in obese insulin resistant mice.Methodology/Principal Findings
Male ob/ob mice were treated for 6 weeks with vehicle, GW501516, PF-879, or GW501516 in combination with PF-879. The effects of the interventions on body composition, glucose homeostasis, glucose tolerance, energy expenditure, exercise capacity and metabolic gene expression were compared at the end of study. GW501516 attenuated body weight and fat mass accumulation and increased the expression of genes of oxidative metabolism. In contrast, PF-879 increased body weight by driving muscle growth and altered the expression of genes involved in insulin signaling and glucose metabolism. Despite their differences, both interventions alone improved glucose homeostasis. Moreover, GW501516 more effectively improved serum lipids, and PF-879 uniquely increased energy expenditure, exercise capacity and adiponectin levels. When combined the robust effects of GW501516 and/or PF-879 on body weight, adiposity, muscle mass, glycemia, serum lipids, energy expenditure and exercise capacity were highly conserved.Conclusions/Significance
The data, for the first time, demonstrate postnatal inhibition of myostatin not only promotes gains in muscle mass similar to resistance training,but improves metabolic homeostasis. In several instances, these effects were either distinct from or complimentary to those of GW501516. The data further suggest that strategies to increase muscle mass, and not necessarily oxidative capacity, may effectively counter insulin resistance and T2DM. 相似文献13.
A novel isolate belonging to the genus Streptomyces, strain SL-4T, was isolated from soil sample collected from a sanitary landfill, New Delhi, India. The taxonomic status of this isolate was studied by polyphasic approach including morphological, physiological and chemo-taxonomic characterization. Spore chains of SL-4T were open loops, hooks or extended spirals of wide diameter (retinaculiperti). The cell wall peptidoglycan of the isolate SL-4T contained L,L-diaminopimelic acid, suggesting that the strain has a cell wall of chemotype-I. The polar lipid profile of the isolate was of Type II, with phosphatidylglycerol, phosphatidylethanolamine, phosphatidylinositol and phosphatidylinositol mannosides. The 16SrRNA gene sequence similarity between SL-4T and its phylogenetic relatives Streptomyces atrovirens NRRLB 16357T (DQ026672), S. albogriseolus NRRLB 1305T (AJ494865), S viridodiastaticus NBRC 13106T (AB184317), S. caelestis NRRL 2418T (X80824), S. flavoviridis NBRC 12772T (AB184842), S. pilosus NBRC 12807T (AB184161) and S. longispororuber NBRC 13488T (AB184440) was 99.65, 99.65, 99.64, 99.23, 99.15, 99.14 and 99.13 % respectively. Subsequent DNA–DNA hybridization experiments with the test strain and its clade members showed 55.27, 44.27, 36.86, and 15.65 % relatedness between SL-4T and its relatives S. atrovirens,S. albogriseolus, S. viridodiastaticus and S. longispororuber respectively. The genotypic and phenotypic data was analyzed to verify possibility of the isolate SL-4T representing novel member of the genus Streptomyces, for which the name S. antibioticalis is being proposed. The type strain is SL-4T (=CCM 7434T=MTCC 8588T). 相似文献
14.
Xun-Li Xia Guang-Xiao Yang Guang-Yuan He 《Physiology and Molecular Biology of Plants》2009,15(1):99-102
A tandem gene cluster CHS-CHI-IFS (rIFS) for secondary metabolites of plant isoflavones was constructed by using the chalcone synthase (CHS), chalcone isomerase (CHI), and isoflavone synthase (IFS) (GenBank accession numbers EU526827, EU526829, EU526830) in a single recombination event with the pET22b vector. The resulting expression vector pET-rIFS was heterogeneously expressed. The highlights of the vector include ease of handling, high efficiency and universal application among diverse plant species. To the best of our knowledge, this is the first attempt at developing a novel method of constructing tandem gene cluster for future research involving secondary metabolism of isoflavones and isoflavones engineering.Key words: Isoflavones biosynthesis, Novel method, Secondary metabolism, Tandem gene cluster 相似文献
15.
The primary objective of this study was to construct an immune-related long noncoding RNAs (IRLs) classifier to precisely predict the prognosis and immunotherapy response of patients with thymic epithelial tumors (TET). Based on univariable Cox regression analysis and Lasso regression, six prognosis-related IRLs (AC004466.3, AC138207.2, AC148477.2, AL450270.1, HOXB-AS1 and SNHG8) were selected to build an IRL classifier. Importantly, results of qRT-PCR validated that higher expression levels of AC138207.2, AC148477.2, AL450270.1 and SNHG8 as well as lower expression levels of AC004466.3, and HOXB-AS1 in TETs samples compared with normal controls. The IRL classifier could effectively classify patients into the low-risk and high-risk groups based on the different survival parameters. In terms of predictive ability and clinical utility, the IRL classifier was superior to Masaoka staging system. Additionally, IRL classifier is significantly associated with immune cells infiltration (dendritic cells, activated CD4 memory T cells and tumor-infiltrating lymphocyte (TIL), T cell subsets in particular), immune microenvironment (immune score and immune checkpoint inhibitors) and immunogenicity (TMB) in TETs, which hints that IRL classifier is tightly correlated with immune characteristics and might guide more effective immunotherapy strategies for TETs patients. Encouragingly, according to TIDE algorithm, there were more immunotherapy responders in the low-risk IRL subgroup and the IRL score was robustly negatively linked to the immunotherapeutic response. To sum up, the IRL classifier was established, which can be used to predict the prognosis, immune infiltration status, immunotherapy response in TETs patients, and may facilitate personalized counseling for immunotherapy. 相似文献
16.
Group I mGluRs (metabotropic glutamate receptors), including mGluR1 and mGluR5, are GPCRs (G-protein coupled receptors) and play important roles in physiology and pathology. Studies on their role in cerebral ischaemia have provided controversial results. In this study, we used a PT (photothrombosis)-induced ischaemia model to investigate whether antagonists to the group I mGluRs may offer acute and long-term protective effects in adult mice. Our results demonstrated that administration with mGluR5 antagonist MPEP [2-methyl-6-(phenylethynyl)-pyridine] or mGluR1 antagonist LY367385 by intraperitoneal injection at 3 h after PT decreased brain infarct volume evaluated one day after ischaemia. Additive effects on infarct volume were observed upon co-injection with MPEP and LY367385. These antagonists also significantly alleviated neurodegeneration and apoptosis in the penumbra. In addition, when evaluated 2 weeks after PT, they reduced infarct volume and tissue loss, attenuated glial scar formation, and inhibited cell proliferation in the penumbra. Importantly, co-injection with MPEP and LY367385 reduced the expression levels of calpain, a Ca2+-activated protease known to mediate ischaemia-induced neuronal death. Injection of calpeptin, a calpain inhibitor, could inhibit neuronal death and brain damage after PT but injection of calpeptin together with MPEP and LY367385 did not further improve the protective effects mediated by MPEP and LY367385. These results suggest that inhibition of group I mGluRs is sufficient to protect ischaemic damage through the calpain pathway. Taken together, our results demonstrate that inhibition of group I mGluRs can mitigate PT-induced brain damage through attenuating the effects of calpain, and improve long-term histological outcomes. 相似文献
17.
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
18.
19.
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
20.
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