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Mouse (Murine) BCL2L1 ELISA Kit for Sandwich ELISA - ABIN427597
Guo, Hsia, Hsiung, Chen: Supplementation with Selenium yeast on the prooxidant-antioxidant activities and anti-tumor effects in breast tumor xenograft-bearing mice. in The Journal of nutritional biochemistry 2015
Bcl-xL is a driver in colorectal tumorigenesis and cancer progression.
These data show that Mcl-1 (show MCL1 ELISA Kits) 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
BCL-XL expression promotes survival of immature B cells, expression of BCL-2 (show BCL2 ELISA Kits) is important for survival of mature B cells and long-lived plasma cells (PC), and expression of MCL-1 (show MCL1 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) and BAX (show BAX ELISA Kits).
MLF1 (show MLF1 ELISA Kits) is negatively regulated by 14-3-3 (show YWHAQ ELISA Kits) via binding to, and blocking, MLF1 (show MLF1 ELISA Kits)'s Bcl-2 (show BCL2 ELISA Kits) homology domain 3 and thereby preventing Bcl-XL from associating with MLF1 (show MLF1 ELISA Kits).
Genetic and pharmacological inhibition of BCL-W (show BCL2L2 ELISA Kits) and BCL-XL causes directed elimination of senescent cells.
Valproic acid sensitized TRAIL-resistant papillary thyroid carcinoma cells to apoptotic cell death through involvement of Nrf2 (show NFE2L2 ELISA Kits) and Bcl-xL.
The influence of chronic ethanol consumption on the expression of the Bdnf (show BDNF ELISA Kits), Bax (show BAX ELISA Kits), Bcl-xL, and CASP3 (show CASP3 ELISA Kits) genes was studied in the brain structures of B6-1473C (C/C) and B6-1473G (G/G) mice that had been obtained on the base of the C57BL/6 strain.
despite its role in Bax (show BAX ELISA Kits) inhibition, Bcl-xL also primes mitochondria to permeabilization and cytochrome c (show CYCS ELISA Kits) release.
that Ubiquitin-specific peptidase 18 (show USP18 ELISA Kits) 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 ELISA Kits) promotes an increase in the BCL-X(L)/BCL-X(s) ratio in TNF-alpha (show TNF ELISA Kits) or LPS (show IRF6 ELISA Kits) stimulated 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-UVRAG.
The combination of 2-deoxyglucose (2-DG) and ABT-199 initiated cell death through the reduction of myeloid cell leukemia sequence 1 protein (Mcl-1 (show MCL1 ELISA Kits)) expression and c-Jun N-terminal kinase 1 (JNK1 (show MAPK8 ELISA Kits)) activation and subsequent Bcl-xL protein degradation.
Bcl-xL is an exosomal caspase-3 (show CASP3 ELISA Kits) substrate and that this processing is required for the uptake of exosomes by recipient cells.
dynamic Bcl-xL(S49) and (S62) phosphorylation/dephosphorylation cycles are important in the maintenance of chromosome integrity during mitosis in normal cells
interleukin-6 (show IL6 ELISA Kits), endothelin ET-1 (show EDN1 ELISA Kits), and apoptotic Bak (show BAK1 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits), IL-6 (show IL6 ELISA Kits), IL-12p40, IL-1beta (show IL1B ELISA Kits), and resulted in increased expression of the apoptosis initiator caspase-8 (show CASP8 ELISA Kits) and bcl2L1.
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.
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 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
, anti-apoptotic Bcl-xL
, BCL2-like protein 1
, BCLX protein
, apoptosis regulator R11