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Study reports the interaction of BCL-XL with RASSF6 (zeige RASSF6 Proteine). BCL-XL inhibits the interaction between RASSF6 (zeige RASSF6 Proteine) and MDM2 (zeige MDM2 Proteine) and suppresses p53 (zeige TP53 Proteine) expression. Consequently, BCL-XL antagonizes RASSF6 (zeige RASSF6 Proteine)-mediated apoptosis. Thus, the inhibition of RASSF6 (zeige RASSF6 Proteine)-mediated apoptosis also underlies the prosurvival role of BCL-XL.
anti-apoptotic molecules BclxL and Bcl-2 (zeige BCL2 Proteine) and the pro-apoptotic factors BAD and BID (zeige BID Proteine) cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L (zeige FASL Proteine).
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 (zeige USP18 Proteine) 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 (zeige PRMT2 Proteine) promotes an increase in the BCL-X(L)/BCL-X(s) ratio in TNF-alpha (zeige TNF Proteine) or LPS (zeige IRF6 Proteine) stimulated cells.
Bcl-xL is a driver in colorectal tumorigenesis and cancer progression.
These data show that Mcl-1 (zeige MCL1 Proteine) 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 (zeige BECN1 Proteine)-UVRAG (zeige UVRAG Proteine).
We propose that the GC-induced mitochondrial accumulation of Bax (zeige BAX Proteine) and the interaction between the GR and Bim (zeige BCL2L11 Proteine), Bcl-xL and Bak (zeige BAK1 Proteine) 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 (zeige MLXIP Proteine)-876 that binds and suppresses translation of Bcl-Xl mRNA.
BCL-XL expression promotes survival of immature B cells, expression of BCL-2 (zeige BCL2 Proteine) is important for survival of mature B cells and long-lived plasma cells (PC), and expression of MCL-1 (zeige MCL1 Proteine) 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 (zeige BBC3 Proteine) had no impact on the loss of platelets caused by loss of BCL-XL. It therefore remains to be established whether other BH3-only (zeige BBC3 Proteine) 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 (zeige BAK1 Proteine) and BAX (zeige BAX Proteine).
MLF1 (zeige MLF1 Proteine) is negatively regulated by 14-3-3 (zeige YWHAQ Proteine) via binding to, and blocking, MLF1 (zeige MLF1 Proteine)'s Bcl-2 (zeige BCL2 Proteine) homology domain 3 and thereby preventing Bcl-XL from associating with MLF1 (zeige MLF1 Proteine).
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 (zeige IL6 Proteine), endothelin ET-1 (zeige EDN1 Proteine), and apoptotic Bak (zeige BAK1 Proteine) 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 (zeige BCL2 Proteine) 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 (zeige TNF Proteine), IL-6 (zeige IL6 Proteine), IL-12p40, IL-1beta (zeige IL1B Proteine), and resulted in increased expression of the apoptosis initiator caspase-8 (zeige CASP8 Proteine) 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 (zeige TP53 Proteine)-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