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Study reports the interaction of BCL-XL with RASSF6 (show RASSF6 Proteins). BCL-XL inhibits the interaction between RASSF6 (show RASSF6 Proteins) and MDM2 (show MDM2 Proteins) and suppresses p53 (show TP53 Proteins) expression. Consequently, BCL-XL antagonizes RASSF6 (show RASSF6 Proteins)-mediated apoptosis. Thus, the inhibition of RASSF6 (show RASSF6 Proteins)-mediated apoptosis also underlies the prosurvival role of BCL-XL.
anti-apoptotic molecules BclxL and Bcl-2 (show BCL2 Proteins) and the pro-apoptotic factors BAD and BID (show BID Proteins) cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L (show FASL Proteins).
These results show that mRNA expression in centenarians is unique and reveals that Bcl-xL plays an important role in exceptional aging.
that Ubiquitin-specific peptidase 18 (show USP18 Proteins) directly bind to BCL2L1 and positively regulated its expression in hepatocellular carcinoma cells
High BCL-XL expression is associated with breast cancer.
The the expression of the full-length, wildtype form of PRMT2 (show PRMT2 Proteins) promotes an increase in the BCL-X(L)/BCL-X(s) ratio in TNF-alpha (show TNF Proteins) or LPS (show IRF6 Proteins) stimulated cells.
Bcl-xL is a driver in colorectal tumorigenesis and cancer progression.
These data show that Mcl-1 (show MCL1 Proteins) is dispensable for the regulation of apoptosis during infection with different large DNA viruses.Bcl-XL, on the other hand, can be important to maintain survival of virus-infected cells
BC200 knockout suppresses tumor cell growth in vitro and in vivo by expression of the pro-apoptotic Bcl-xS isoform.
Bcl-xL inhibits GAS-induced autophagy directly by suppressing autophagosome-lysosome fusion and indirectly by suppressing GAS internalization via interaction with Beclin 1 (show BECN1 Proteins)-UVRAG (show UVRAG Proteins).
We propose that the GC-induced mitochondrial accumulation of Bax (show BAX Proteins) and the interaction between the GR and Bim (show BCL2L11 Proteins), Bcl-xL and Bak (show BAK1 Proteins) could play a role in the regulation of thymocyte apoptosis.
Bcl-xL is required for survival of post mitotic neurons throughout the developing spinal cord.
Atherosclerosis-associated endothelial cell apoptosis may partially result from downregulation of Bcl-Xl, through upregulation of miR (show MLXIP Proteins)-876 that binds and suppresses translation of Bcl-Xl mRNA.
BCL-XL expression promotes survival of immature B cells, expression of BCL-2 (show BCL2 Proteins) is important for survival of mature B cells and long-lived plasma cells (PC), and expression of MCL-1 (show MCL1 Proteins) is important for survival throughout B-cell development.
Bcl-xL deficiency induced apoptosis in a select population of differentiated neurons and led to severe neurobehavioral abnormalities.
loss of PUMA (show BBC3 Proteins) had no impact on the loss of platelets caused by loss of BCL-XL. It therefore remains to be established whether other BH3-only (show BBC3 Proteins) proteins play a critical role in induction of apoptosis in platelets or whether their death is controlled solely by the interactions between BCL-XL with BAK (show BAK1 Proteins) and BAX (show BAX Proteins).
MLF1 (show MLF1 Proteins) is negatively regulated by 14-3-3 (show YWHAQ Proteins) via binding to, and blocking, MLF1 (show MLF1 Proteins)'s Bcl-2 (show BCL2 Proteins) homology domain 3 and thereby preventing Bcl-XL from associating with MLF1 (show MLF1 Proteins).
amplification and characterization of partial regions of exons 2 and 3 of the bovine BCL2L1 gene
Data show that Bcl-x(L) expression is increased in the pulmonary artery undergoing chronic pulmonary vascular remodeling.
interleukin-6 (show IL6 Proteins), endothelin ET-1 (show EDN1 Proteins), and apoptotic Bak (show BAK1 Proteins) and Bcl-XL genes have roles in small bowel transplantation, in a swine model of ischemia and reperfusion injury
Bcl-xL was significantly decreased in haploid parthenotes compared with the diploid parthenotes. These results suggest that the haploid state affects apoptosis-related gene expression which results in increased apoptosis
CONCLUSION(S): (1) Apoptosis is involved in follicular atresia; (2) Bcl-2 (show BCL2 Proteins) is induced by warm ischemia; and (3) cryopreservation insult does not alter the apoptotic signals with short tissue preparation time.
Bcl-Xl deamidation and methylation has a role in protein isoaspartate methyltransferase prevention of apoptosis induced by oxidative stress in endothelial cells
Data show that cysteine significantly reduced the expression of pro-inflammatory cytokines, including TNF-alpha (show TNF Proteins), IL-6 (show IL6 Proteins), IL-12p40, IL-1beta (show IL1B Proteins), and resulted in increased expression of the apoptosis initiator caspase-8 (show CASP8 Proteins) and bcl2L1.
This study leads to conclude that BCLXL peak expression at the zygotic genome activation phase may be a requirement for embryo development
In this study evidence is provided that exogenous PGF2alpha differentially modulates luteal expression of BCL2L1 transcripts and protein depending on luteal stage.
repression of radiation-induced apoptosis by overexpression of Bcl-xL during embryonic development depends upon the timing of its expression and post-translational events that enable the protein to become effective
The bcl2l gene operates in the inhibition of cell death under direct regulation of a thyroid specific set of transcription factors
Zebrafish anti-apoptotic gene Bcl-xL can prevent aquatic birnavirus-induced cell death in fish cells without affecting expression of viral proteins.
transgenic overexpression of zfBLP1 or myeloid cell leukemia sequence 1a in zebrafish larvae interrupts regulation of the homeostatic balance between cell proliferation and programmed cell death during hepatogenesis and leads to liver hyperplasia
Bcl-xL can block post-apoptotic necrosis processes thereby rescuing betanodavirus-infected cells
Delta113p53 functions to antagonize p53 (show TP53 Proteins)-induced apoptosis via activating bcl2L
The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The proteins encoded by this gene are located at the outer mitochondrial membrane, and have been shown to regulate outer mitochondrial membrane channel (VDAC) opening. VDAC regulates mitochondrial membrane potential, and thus controls the production of reactive oxygen species and release of cytochrome C by mitochondria, both of which are the potent inducers of cell apoptosis. Two alternatively spliced transcript variants, which encode distinct isoforms, have been reported. The longer isoform acts as an apoptotic inhibitor and the shorter form acts as an apoptotic activator.
apoptosis regulator Bcl-X
, bcl-2-like protein 1
, protein phosphatase 1, regulatory subunit 52
, B-cell leukemia/lymphoma x
, anti-apoptosis regulatory protein
, B cell lymphoma 2 like
, B cell lymphoma like X
, BCL2-like protein 1
, anti-apoptotic Bcl-xL
, BCLX protein
, BCL2-like 1
, apoptosis regulator R11
, Bcl-xL-like protein 1