排序方式: 共有202条查询结果,搜索用时 31 毫秒
91.
Yusuke Aoki Akira Tsujimura Kazuhiro Kaseda Masaru Okabe Keizo Tokuhiro Tomoe Ohta Moira K O'Bryan Hidenobu Okuda Kouichi Kitamura Yukiko Ogawa Tsukasa Fujiki Morimasa Wada Shigeo Horie Yoshitake Nishimune Hiromitsu Tanaka 《Molecular reproduction and development》2020,87(5):534-541
Haprin (TRIM36) is a ubiquitin‐protein ligase that mediates ubiquitination and subsequent proteasomal degradation of target proteins. It is expressed in the testes in both mice and humans and is thought to be involved in spermiogenesis, the acrosome reaction, and fertilization. However, the functional role of Haprin is poorly understood. The aim of this study was to investigate the physiological role of Haprin in fertility. Homozygous haprin‐deficient mice were generated and these mice, and their spermatozoa, were analyzed to detect morphological and fertility‐related abnormalities. In these models, normal spermatogenesis was observed but sperm quality was reduced with haprin‐deficient mice having poorer sperm morphology and motility than wild‐type mice. Interestingly, haprin‐deficient mice showed normal in vivo fertility but could not fertilize oocytes under standard in vitro fertilization conditions. In conclusion, this study demonstrated that Haprin deficiency causes morphological abnormalities in spermatozoa, indicating that Haprin is involved in spermiogenesis. 相似文献
92.
Flaviviruses are a genus of mostly arthropod-borne RNA viruses that cause a range of pathologies in humans. Basic knowledge on flaviviruses is rapidly expanding, partly due to their status as frequent emerging or re-emerging pathogens.Flaviviruses include the dengue, Zika, West Nile, tick-borne encephalitis and yellow fever viruses(DENV, ZIKV, WNV,TBEV and YFV, respectively). As is the case with other families of viruses, the success of productive infection of human cells by flaviviruses depends in part on the antiviral activity of a heterogeneous group of cellular antiviral proteins called restriction factors. Restriction factors are the effector proteins of the cell-autonomous innate response against viruses, an immune pathway that also includes virus sensors as well as intracellular and extracellular signal mediators such as type I interferons(IFN-I). In this review, I summarize recent progress toward the identification and characterization of flavivirus restriction factors. In particular, I focus on IFI6, Schlafen 11, FMRP, OAS-RNase L, RyDEN, members of the TRIM family of proteins(TRIM5α, TRIM19, TRIM56, TRIM69 and TRIM79α) and a new mechanism of action proposed for viperin. Recent and future studies on this topic will lead to a more complete picture of the flavivirus restrictome, defined as the ensemble of cellular factors with demonstrated anti-flaviviral activity. 相似文献
93.
Patricia L. Weng Amar J. Majmundar Kamal Khan Tze Y. Lim Shirlee Shril Gina Jin John Musgrove Minxian Wang Dina F. Ahram Vimla S. Aggarwal Louise E. Bier Erin L. Heinzen Ana C. Onuchic-Whitford Nina Mann Florian Buerger Ronen Schneider Konstantin Deutsch Thomas M. Kitzler Simone Sanna-Cherchi 《American journal of human genetics》2021,108(2):357-367
94.
95.
96.
97.
Ryu YS Lee Y Lee KW Hwang CY Maeng JS Kim JH Seo YS You KH Song B Kwon KS 《The Journal of biological chemistry》2011,286(29):25729-25738
TRIM32, which belongs to the tripartite motif (TRIM) protein family, has the RING finger, B-box, and coiled-coil domain structures common to this protein family, along with an additional NHL domain at the C terminus. TRIM32 reportedly functions as an E3 ligase for actin, a protein inhibitor of activated STAT y (PIASy), dysbindin, and c-Myc, and it has been associated with diseases such as muscular dystrophy and epithelial carcinogenesis. Here, we identify a new substrate of TRIM32 and propose a mechanism through which TRIM32 might regulate apoptosis. Our overexpression and knockdown experiments demonstrate that TRIM32 sensitizes cells to TNFα-induced apoptosis. The RING domain is necessary for this pro-apoptotic function of TRM32 as well as being responsible for its E3 ligase activity. TRIM32 colocalizes and directly interacts with X-linked inhibitor of apoptosis (XIAP), a well known cancer therapeutic target, through its coiled-coil and NHL domains. TRIM32 overexpression enhances XIAP ubiquitination and subsequent proteasome-mediated degradation, whereas TRIM32 knockdown has the opposite effect, indicating that XIAP is a substrate of TRIM32. In vitro reconstitution assay reveals that XIAP is directly ubiquitinated by TRIM32. Our novel results collectively suggest that TRIM32 sensitizes TNFα-induced apoptosis by antagonizing XIAP, an anti-apoptotic downstream effector of TNFα signaling. This function may be associated with TRIM32-mediated tumor suppressive mechanism. 相似文献
98.
99.
Liu Tingjun Tong Jing Shao Chen Qu Junyan Wang Hua Shi Yi Lin Yajing Liu Yun Shao Shihe Shen Hongxing 《中国病毒学》2021,36(6):1585-1599
Virologica Sinica - Viral myocarditis (VM) is an inflammatory disease of the myocardium associated with heart failure, which is caused by common viral infections. A majority of the infections are... 相似文献
100.
Yuanqing Feng Hongzhan Xu Jinghao Liu Ning Xie Lei Gao Yanyun He Yuan Yao Fengxiang Lv Yan Zhang Jian Lu Wei Zhang Chuan-Yun Li Xinli Hu Ziheng Yang Rui-Ping Xiao 《Molecular biology and evolution》2021,38(7):2930
Cis-regulatory elements play important roles in tissue-specific gene expression and in the evolution of various phenotypes, and mutations in promoters and enhancers may be responsible for adaptations of species to environments. TRIM72 is a highly conserved protein that is involved in energy metabolism. Its expression in the heart varies considerably in primates, with high levels of expression in Old World monkeys and near absence in hominids. Here, we combine phylogenetic hypothesis testing and experimentation to demonstrate that mutations in promoter are responsible for the differences among primate species in the heart-specific expression of TRIM72. Maximum likelihood estimates of lineage-specific substitution rates under local-clock models show that relative to the evolutionary rate of introns, the rate of promoter was accelerated by 78% in the common ancestor of Old World monkeys, suggesting a role for positive selection in the evolution of the TRIM72 promoter, possibly driven by selective pressure due to changes in cardiac physiology after species divergence. We demonstrate that mutations in the TRIM72 promoter account for the differential myocardial TRIM72 expression of the human and the rhesus macaque. Furthermore, changes in TRIM72 expression alter the expression of genes involved in oxidative phosphorylation, which in turn affects mitochondrial respiration and cardiac energy capacity. On a broader timescale, phylogenetic regression analyses of data from 29 mammalian species show that mammals with high cardiac expression of TRIM72 have high heart rate, suggesting that the expression changes of TRIM72 may be related to differences in the heart physiology of those species. 相似文献