Abstract:
:Nogo-B/ASY has been characterized as a novel human apoptosis-inducing protein without any known apoptosis-related motifs. However, the validity of Nogo-B/ASY as a physiological apoptotic protein was recently questioned. In present research, we demonstrate that ASY overexpression contributes to ER stress and induces apoptosis through ER Ca2+ depletion and ER-specific pathways. ER stress and the disorder of intracellular calcium trigger the apoptosis induced by ASY overexpression. At the same time, stable transfectants overexpressing high levels of ASY are resistant to ER-stress-associated stimuli, which implies that ASY overexpression activates protective response in response to ER stress. Our results provide a direct apoptotic pathway that ASY overexpression induces apoptosis through ER stress and ER-specific signal pathways.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Kuang E,Wan Q,Li X,Xu H,Zou T,Qi Ydoi
10.1016/j.yexcr.2006.02.024subject
Has Abstractpub_date
2006-07-01 00:00:00pages
1983-8issue
11eissn
0014-4827issn
1090-2422pii
S0014-4827(06)00084-Xjournal_volume
312pub_type
杂志文章abstract::Activated fibroblasts promote physiological wound repair following tissue injury. However, dysregulation of fibroblast activation contributes to the development of fibrosis by enhanced production and contraction of collagen-rich extracellular matrix. At the peak of their activities, fibroblasts undergo phenotypic conv...
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