| Stuart JR |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=6.872 ------>paper_class3=2 ------>paper_class2=1 ------>vol=24 ------>confirm_bywho=None ------>insert_bywho=tsaik ------>Jurnal_Rank=9.8 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=8 ------>paper_class2Letter=None ------>page2=8092 ------>medlineContent= ------>unit=000 ------>insert_date=20080507 ------>iam=3 ------>update_date=None ------>author=??? ------>change_event=2 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Oncogene ------>paper_name=c-Abl regulates early growth response protein (EGR1) in response to oxidative stress ------>confirm_date=None ------>tch_id=096037 ------>pmid=16091742 ------>page1=8085 ------>fullAbstract=c-Abl is a tyrosine kinase that can act as a regulator of cell growth and apoptosis in response to stress. Using cell lines expressing c-Abl in an inducible manner, we identified genes whose expression was regulated by c-Abl kinase activity. Microarray analysis indicated that Early Growth Response-1 (EGR1) gene expression is induced by c-Abl kinase activity, which was confirmed at the message and protein levels. Promoter mapping experiments revealed that c-Abl utilizes three distal serum response elements (SREs) in the EGR1 promoter, which are transactivated by mitogen/extracellular receptor kinase (MEK/ERK) signaling. PD 95089, a specific inhibitor of MEK/ERK signaling, attenuated c-Abl-mediated upregulation of EGR1 expression in a dose-dependent manner. Similar results were obtained by using a dominant-negative mutant of mitogen/extracellular kinase. Significantly, hydrogen peroxide-induced EGR1 expression appears to be mediated by c-Abl, as cells expressing dominant negative c-Abl, and c-Abl-/- murine embryonic fibroblasts, are completely defective in hydrogen peroxide-induced EGR1 expression. In addition, c-Abl-induced apoptosis is partially mitigated by EGR1 activity, as cells devoid of EGR1 expression undergo reduced rates of c-Abl-induced apoptosis. Together, these results indicate that c-Abl promotes the induction of EGR1 through the MEK/ERK pathway in regulating apoptotic response to oxidative stress. ------>tmu_sno=None ------>sno=18540 ------>authors2=Kawai H ------>authors3=Tsai KK ------>authors4=Chuang EY ------>authors5=Yuan ZM ------>authors6= ------>authors6_c= ------>authors=Stuart JR ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=c-Abl regulates early growth response protein (EGR1) in response to oxidative stress. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2005 ------>submit_flag=None ------>publish_month=12 |