Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Wenxian Xue"'
Autor:
Jing Li, Jingjing Yu, Wenxian Xue, Huili Huang, Longjun Yan, Fan Sang, Shuangshuang An, Jing Zhang, Mingli Wang, Jun Zhang, Hui Li, Xiukun Cui, Jiang He, Yanzhong Hu
Publikováno v:
BMC Biotechnology, Vol 21, Iss 1, Pp 1-12 (2021)
Abstract Background HSPB5 is an ATP-independent molecular chaperone that is induced by heat shock or other proteotoxic stresses. HSPB5 is cytoprotective against stress both intracellularly and extracellularly. It acts as a potential therapeutic candi
Externí odkaz:
https://doaj.org/article/77a0c955934f4560a18731a931337a14
Autor:
Jun Zhang, Fan Sang, Mingli Wang, Yanzhong Hu, Wenxian Xue, Longjun Yan, Xiukun Cui, Jing Zhang, Hui Li, Shuangshuang An, Jingjing Yu, Huili Huang, Jiang He, Jing Li
Publikováno v:
BMC Biotechnology
BMC Biotechnology, Vol 21, Iss 1, Pp 1-12 (2021)
BMC Biotechnology, Vol 21, Iss 1, Pp 1-12 (2021)
Background HSPB5 is an ATP-independent molecular chaperone that is induced by heat shock or other proteotoxic stresses. HSPB5 is cytoprotective against stress both intracellularly and extracellularly. It acts as a potential therapeutic candidate in i
Autor:
Jun Zhang, Hongmei Mu, Jing Li, Wen-wen Cui, Wenxian Xue, Yuanfang Ma, Yanzhong Hu, Shiyuan Liu, Dan-Dan Wu, Xiukun Cui, Jiuli Han, Jing Zhang, Xiang-Xiang Wang, Fengyan Zhang
Publikováno v:
The international journal of biochemistrycell biology. 105
Dysfunction of HSF4 is associated with congenital cataracts. HSF4 transcription activity is turned on and regulated by phosphorylation during early postnatal lens development. Our previous data suggested that mutation HSF4b/S299A can upregulate HSF4
Autor:
Hui Li, Fengyan Zhang, Hongmei Mu, Ren Yanzhu, Wenxian Xue, Weikang Huang, Xuance Wang, Mengyuan Li, Xiukun Cui, Jing Li, Yanzhong Hu, Xiang-Xiang Wang
Publikováno v:
Experimental Eye Research. 189:107821
Posterior capsule opacification (PCO) is a common complication of cataract surgery, resulting from a combination of proliferation, migration, epithelial-mesenchymal transition (EMT) of residual capsular epithelial cells and fibrosis of myofibroblasts