排序方式: 共有34条查询结果,搜索用时 15 毫秒
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Babrzadeh F Jalili R Wang C Shokralla S Pierce S Robinson-Mosher A Nyren P Shafer RW Basso LC de Amorim HV de Oliveira AJ Davis RW Ronaghi M Gharizadeh B Stambuk BU 《Molecular genetics and genomics : MGG》2012,287(6):485-494
The Saccharomyces cerevisiae strains widely used for industrial fuel-ethanol production have been developed by selection, but their underlying beneficial genetic polymorphisms remain unknown. Here, we report the draft whole-genome sequence of the S. cerevisiae strain CAT-1, which is a dominant fuel-ethanol fermentative strain from the sugarcane industry in Brazil. Our results indicate that strain CAT-1 is a highly heterozygous diploid yeast strain, and the ~12-Mb genome of CAT-1, when compared with the reference S228c genome, contains ~36,000 homozygous and ~30,000 heterozygous single nucleotide polymorphisms, exhibiting an uneven distribution among chromosomes due to large genomic regions of loss of heterozygosity (LOH). In total, 58 % of the 6,652 predicted protein-coding genes of the CAT-1 genome constitute different alleles when compared with the genes present in the reference S288c genome. The CAT-1 genome contains a reduced number of transposable elements, as well as several gene deletions and duplications, especially at telomeric regions, some correlated with several of the physiological characteristics of this industrial fuel-ethanol strain. Phylogenetic analyses revealed that some genes were likely associated with traits important for bioethanol production. Identifying and characterizing the allelic variations controlling traits relevant to industrial fermentation should provide the basis for a forward genetics approach for developing better fermenting yeast strains. 相似文献
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Alfredo Floristn Leah Morales Douglas Hanniford Carlos Martinez Elena Castellano‐Sanz Igor Dolgalev Alejandro Ulloa‐Morales Eleazar Vega‐Saenz de Miera Una Moran Farbod Darvishian Iman Osman Tomas Kirchhoff Eva Hernando 《Pigment cell & melanoma research》2020,33(3):466-479
Next‐generation sequencing has enabled genetic and genomic characterization of melanoma to an unprecedent depth. However, the high mutational background plus the limited depth of coverage of whole‐genome sequencing performed on cutaneous melanoma samples make the identification of novel driver mutations difficult. We sought to explore the somatic mutation portfolio in exonic and gene regulatory regions in human melanoma samples, for which we performed targeted sequencing of tumors and matched germline DNA samples from 89 melanoma patients, identifying known and novel recurrent mutations. Two recurrent mutations found in the RPS27 promoter associated with decreased RPS27 mRNA levels in vitro. Data mining and IHC analyses revealed a bimodal pattern of RPS27 expression in melanoma, with RPS27‐low patients displaying worse prognosis. In vitro characterization of RPS27‐high and RPS27‐low melanoma cell lines, as well as loss‐of‐function experiments, demonstrated that high RPS27 status provides increased proliferative and invasive capacities, while low RPS27 confers survival advantage in low attachment and resistance to therapy. Additionally, we demonstrate that 10 other cancer types harbor bimodal RPS27 expression, and in those, similarly to melanoma, RPS27‐low expression associates with worse clinical outcomes. RPS27 promoter mutation could thus represent a mechanism of gene expression modulation in melanoma patients, which may have prognostic and predictive implications. 相似文献
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Poornima Parameswaran Ella Sklan Courtney Wilkins Trever Burgon Melanie A. Samuel Rui Lu K. Mark Ansel Vigo Heissmeyer Shirit Einav William Jackson Tammy Doukas Suman Paranjape Charlotta Polacek Flavia Barreto dos Santos Roxana Jalili Farbod Babrzadeh Baback Gharizadeh Dirk Grimm Mark Kay Satoshi Koike Peter Sarnow Mostafa Ronaghi Shou-Wei Ding Eva Harris Marie Chow Michael S. Diamond Karla Kirkegaard Jeffrey S. Glenn Andrew Z. Fire 《PLoS pathogens》2010,6(2)
We have used multiplexed high-throughput sequencing to characterize changes in small RNA populations that occur during viral infection in animal cells. Small RNA-based mechanisms such as RNA interference (RNAi) have been shown in plant and invertebrate systems to play a key role in host responses to viral infection. Although homologs of the key RNAi effector pathways are present in mammalian cells, and can launch an RNAi-mediated degradation of experimentally targeted mRNAs, any role for such responses in mammalian host-virus interactions remains to be characterized. Six different viruses were examined in 41 experimentally susceptible and resistant host systems. We identified virus-derived small RNAs (vsRNAs) from all six viruses, with total abundance varying from “vanishingly rare” (less than 0.1% of cellular small RNA) to highly abundant (comparable to abundant micro-RNAs “miRNAs”). In addition to the appearance of vsRNAs during infection, we saw a number of specific changes in host miRNA profiles. For several infection models investigated in more detail, the RNAi and Interferon pathways modulated the abundance of vsRNAs. We also found evidence for populations of vsRNAs that exist as duplexed siRNAs with zero to three nucleotide 3′ overhangs. Using populations of cells carrying a Hepatitis C replicon, we observed strand-selective loading of siRNAs onto Argonaute complexes. These experiments define vsRNAs as one possible component of the interplay between animal viruses and their hosts. 相似文献
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Zahra Ansari Farbod Ebadi Fard Azar Nour-Ahmad Latifi 《Biocatalysis and Biotransformation》2017,35(6):434-441
An enzymatic reaction using glucose oxidase (GOx) was applied for continues production of hydrogen peroxide and organic acid in Phanerochaete chrysosporium cultures for use simultaneously in catalytic cycle of peroxidases. Decolorization efficiency of crystal violet (CV) as a model pollutant was investigated in 16 d old cultures which overproduced manganese peroxidase (MnP) in response to daily GOx addition and control cultures (i.e. no GOx was added). However, the ability of overproduced cultures in decolorization of CV was not increased significantly, through addition of GOx (300?U/L)?+?glucose (10?Mm) to the culture medium at the start of decolorization, the time needed to obtain 87?±?0.5% removal of CV was reduced 10.7-fold in compared with the control culture. The best GOx concentration in culture medium for more efficient decolorization was obtained to be 300?U/L. These findings indicated that GOx in the presence of glucose could increase the degradation of CV not only by inducing ligninolytic activity in cultures but also as a subsidiary source for in situ H2O2 and organic acid production for catalytic activity of peroxidases in P. chrysosporium cultures. 相似文献
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Meder B Huttner IG Sedaghat-Hamedani F Just S Dahme T Frese KS Vogel B Köhler D Kloos W Rudloff J Marquart S Katus HA Rottbauer W 《Molecular and cellular biology》2011,31(16):3424-3435
Integrin-linked kinase (ILK) is an essential component of the cardiac mechanical stretch sensor and is bound in a protein complex with parvin and PINCH proteins, the so-called ILK-PINCH-parvin (IPP) complex. We have recently shown that inactivation of ILK or β-parvin activity leads to heart failure in zebrafish via reduced protein kinase B (PKB/Akt) activation. Here, we show that PINCH proteins localize at sarcomeric Z disks and costameres in the zebrafish heart and skeletal muscle. To investigate the in vivo role of PINCH proteins for IPP complex stability and PKB signaling within the vertebrate heart, we inactivated PINCH1 and PINCH2 in zebrafish. Inactivation of either PINCH isoform independently leads to instability of ILK, loss of stretch-responsive anf and vegf expression, and progressive heart failure. The predominant cause of heart failure in PINCH morphants seems to be loss of PKB activity, since PKB phosphorylation at serine 473 is significantly reduced in PINCH-deficient hearts and overexpression of constitutively active PKB reconstitutes cardiac function in PINCH morphants. These findings highlight the essential function of PINCH proteins in controlling cardiac contractility by granting IPP/PKB-mediated signaling. 相似文献
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Rastegar F Gao JL Shenaq D Luo Q Shi Q Kim SH Jiang W Wagner ER Huang E Gao Y Shen J Yang K He BC Chen L Zuo GW Luo J Luo X Bi Y Liu X Li M Hu N Wang L Luther G Luu HH Haydon RC He TC 《PloS one》2010,5(12):e14182
Background
Osteosarcoma is the most common primary malignancy of bone with poorly characterized molecular pathways important in its pathogenesis. Increasing evidence indicates that elevated lipid biosynthesis is a characteristic feature of cancer. We sought to investigate the role of lysophosphatidic acid acyltransferase β (LPAATβ, aka, AGPAT2) in regulating the proliferation and growth of human osteosarcoma cells. LPAATβ can generate phosphatidic acid, which plays a key role in lipid biosynthesis as well as in cell proliferation and survival. Although elevated expression of LPAATβ has been reported in several types of human tumors, the role of LPAATβ in osteosarcoma progression has yet to be elucidated.Methodology/Principal Findings
Endogenous expression of LPAATβ in osteosarcoma cell lines is analyzed by using semi-quantitative PCR and immunohistochemical staining. Adenovirus-mediated overexpression of LPAATβ and silencing LPAATβ expression is employed to determine the effect of LPAATβ on osteosarcoma cell proliferation and migration in vitro and osteosarcoma tumor growth in vivo. We have found that expression of LPAATβ is readily detected in 8 of the 10 analyzed human osteosarcoma lines. Exogenous expression of LPAATβ promotes osteosarcoma cell proliferation and migration, while silencing LPAATβ expression inhibits these cellular characteristics. We further demonstrate that exogenous expression of LPAATβ effectively promotes tumor growth, while knockdown of LPAATβ expression inhibits tumor growth in an orthotopic xenograft model of human osteosarcoma.Conclusions/Significance
Our results strongly suggest that LPAATβ expression may be associated with the aggressive phenotypes of human osteosarcoma and that LPAATβ may play an important role in regulating osteosarcoma cell proliferation and tumor growth. Thus, targeting LPAATβ may be exploited as a novel therapeutic strategy for the clinical management of osteosarcoma. This is especially attractive given the availability of selective pharmacological inhibitors. 相似文献9.
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Role of myeloid cells in tumor angiogenesis and growth 总被引:5,自引:0,他引:5
Cells of the innate immune system have a key role in maintaining homeostasis by providing the first line of defense against many pathogens. Innate immunity can also modulate the activity of acquired immunity by several mechanisms. However, subsets of myeloid cells can facilitate tumor growth, because these cells produce angiogenic factors and can also prevent the immune system from attacking tumor cells. Recent studies also emphasize the role of myeloid cells in mediating refractoriness to anti-VEGF treatments. This function of myeloid cells occurs through a proangiogenic pathway that is, at least in part, driven by the secreted protein Bv8. This review summarizes recent findings on the complex role of bone marrow-derived cells in tumor growth. 相似文献