Disease relevance of Bcl2l1

• Overexpression of Bcl-xl protects septal neurons from prolonged hypoglycemia and from acute ischemia-like stress [1].
• Bcl-xl expression also significantly protected against the hypoglycemic stress (23% intact 24 h post-stress with green fluorescent protein only, compared with 70% with Bcl-xl and green fluorescent protein), but did not protect from hyperglycemia or 3-nitropropionic acid [1].
• METHODS AND RESULTS: Overexpression of the Bcl-xl gene by adenovirus vector resulted in an 11-fold increase in Bcl-xl protein in neonatal rat cardiac myocytes (BCL) compared to that in cells with beta-galactosidase gene transfection (CTL) [2].
• Bcl-2 was up-regulated in both detected regions at 24 h after ischemia, while the increase in Bax and Bcl-xl protein expression had appeared already at 6 h and also 24 h after ischemia [3].
• Chronic hypoxia induces apoptosis in cardiac myocytes: a possible role for Bcl-2-like proteins [4].

Psychiatry related information on Bcl2l1

• This report describes the production of a monoclonal antibody raised against Bcl-xl, and includes an initial study of bcl-xl expression in neuropathology including Alzheimer's disease (AD) [5].

High impact information on Bcl2l1

• The induction of apoptosis coincides with a marked downregulation of bcl-X expression [6].
• A marked decrease in bcl-X expression was detected in the most luminal layers of the media [6].
• High glucose inhibits apoptosis induced by serum deprivation in vascular smooth muscle cells via upregulation of Bcl-2 and Bcl-xl [7].
• Here, we analyzed DP5 gene expression and the specific interaction of DP5 with Bcl-xl during neuronal death induced by amyloid-beta protein (A beta) [8].
• The hormonal control of cell proliferation and cell death correlated with the overall quantity and distribution of the different bcl-X transcripts [9].

Chemical compound and disease context of Bcl2l1

• Using western blotting and immunochemical analysis, we investigated alterations in the expression of the apoptosis-related proteins bcl-2, bax, and bcl-X in colonic adenocarcinomas induced by subcutaneous injection of azoxymethane (AOM) (15 mg/kg body weight weekly for 2 wk) into male Sprague-Dawley rats [10].

Biological context of Bcl2l1

• Moreover, DP5 specifically interacts with Bcl-xl during neuronal apoptosis following exposure to A beta, and its binding could impair the survival-promoting activities of Bcl-xl [8].
• Overexpression of Bcl-xl, a member of the Bcl-2 protein family, is reported to protect from a variety of stresses involving delayed cell death [1].
• Bcl-xl reduces doxorubicin-induced myocardial damage but fails to control cardiac gene downregulation [2].
• Induction of Akt phosphorylation and increased expression of Bcl-xl were observed in the left lobes of insulin-treated animals [11].
• Bcl-xl expression was related to the degree of liver cell damage due to oxidative stress, and estradiol showed a protective action [12].

Anatomical context of Bcl2l1

• In the present study, we further examined whether overexpression of Bcl-xl ameliorates Dox-induced cardiac myocyte damage [2].
• These results indicate that Bcl-xl, Bcl-xs, Bax, and caspase-3 are important regulators of apoptosis in PC12 cells [13].
• Enhanced Bcl-xl signals were found in the non-ischemic striatum 3, 6 and 24 h after clenbuterol treatment, but no change of Bcl-xl expression by clenbuterol was seen in the non-ischemic hippocampus [3].
• Bcl-xl expression in neutrophils was upregulated with thermal injury and inhibited in the presence of wortmannin [14].
• (3) Bcl-xl in Leydig cells was transiently increased after EDS [15].

Associations of Bcl2l1 with chemical compounds

• The effect of Hsp10 and Hsp60 on the abundance of Bcl-xl could not be blocked by cycloheximide [16].
• Our results suggest that high glucose suppresses serum withdrawal-induced apoptosis in VSMCs by upregulating expression of Bcl-2 and Bcl-xl, suggesting that enhanced expression of antiapoptotic proteins may play an important role in the development of macrovascular complications in diabetes [7].
• Augmented Bcl-2 and Bcl-xl levels in the C2-ceramide treated group were associated with a significant decrease in TUNEL-positive cells [17].
• Clenbuterol also increased Bcl-xl level in the ischemic striatum [3].
• After androgen withdrawal, there were no significant changes in the levels of clusterin, Bcl-xl, Bak, and Bad [18].

Regulatory relationships of Bcl2l1

• CONCLUSIONS: Overexpression of Bcl-xl in cardiac myocytes failed to regulate Dox-induced ROS generation and cardiac-specific gene downregulation but inhibited apoptosis accompanied by reduction of Bax protein [2].

Other interactions of Bcl2l1

• Analysis of mitochondria-associated proteins Bax and Bcl-xl in hemin- and CO-exposed rats showed significant responses, revealing interactions with apoptotic pathways [19].
• In the IO, increased expression of bax in neurons and bcl-X in astrocytes after 3AP was significantly reduced by IGF-I treatment [20].

Analytical, diagnostic and therapeutic context of Bcl2l1

• Ad-CD40Ig reduced frequency of TUNEL+ cells and pro-apoptotic Caspase-3, but enhanced antioxidant HO-1 and anti-apoptotic Bcl-2/Bcl-xl expression [21].
• No changes were observed in the protein levels of Bax and Bcl-2, whereas the anti-apoptotic Bcl-xl protein was down-regulated, as judged by western blot analysis [22].
• In the present study, we used quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) to determine the effects of 50mM ethanol and 100nM of ipsapirone, a 5-HT(1A) agonist, on the expression of several NF-kappaB-dependent antiapoptotic genes: X-linked inhibitor of apoptosis protein (XIAP), cIAP1, cIAP2, Bcl-2, and Bcl-xl [23].

References