Browse our anti-BCL2L1 (BCL2L1) Antibodies

Human BCL2-Like 1 (BCL2L1) interaction partners

1. CCAT1 is upregulated in docetaxel-resistant lung adenocarcinoma cells; its oncogenic function depends on sponging of let-7c, which releases Bcl-xl, promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes

2. In the epithelial ovarian cancer stem cells, 40% knock-down of Bclxl expression was sufficient to induce the full activation of caspases. Bclxl expression levels in EOC cells is dynamic and can be regulated by microenvironments that are enriched with the pro-inflammatory cytokine IL-6 (show IL6 Antibodies) such as the cancer stem cell and adipocyte niches.

3. Study reports the interaction of BCL-XL with RASSF6 (show RASSF6 Antibodies). BCL-XL inhibits the interaction between RASSF6 (show RASSF6 Antibodies) and MDM2 (show MDM2 Antibodies) and suppresses p53 (show TP53 Antibodies) expression. Consequently, BCL-XL antagonizes RASSF6 (show RASSF6 Antibodies)-mediated apoptosis. Thus, the inhibition of RASSF6 (show RASSF6 Antibodies)-mediated apoptosis also underlies the prosurvival role of BCL-XL.

4. anti-apoptotic molecules BclxL and Bcl-2 (show BCL2 Antibodies) and the pro-apoptotic factors BAD and BID (show BID Antibodies) cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L (show FASL Antibodies).

5. These results show that mRNA expression in centenarians is unique and reveals that Bcl-xL plays an important role in exceptional aging.

6. that Ubiquitin-specific peptidase 18 (show USP18 Antibodies) directly bind to BCL2L1 and positively regulated its expression in hepatocellular carcinoma cells

7. High BCL-XL expression is associated with breast cancer.

8. The the expression of the full-length, wildtype form of PRMT2 (show PRMT2 Antibodies) promotes an increase in the BCL-X(L)/BCL-X(s) ratio in TNF-alpha (show TNF Antibodies) or LPS (show IRF6 Antibodies) stimulated cells.

9. Bcl-xL is a driver in colorectal tumorigenesis and cancer progression.

10. These data show that Mcl-1 (show MCL1 Antibodies) 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

Mouse (Murine) BCL2-Like 1 (BCL2L1) interaction partners

1. Proapoptotic proteins BIM (show BCL2L11 Antibodies) and PUMA (show BBC3 Antibodies) are not critical for the reticulocyte apoptosis caused by loss of the pro-survival protein BCL-XL.

2. BMP4 (show BMP4 Antibodies) promotes survival of neural stem/progenitor cells by enhancing the anti-apoptotic function of Bcl-xL via BMP4 (show BMP4 Antibodies)-Smad1 (show SMAD1 Antibodies)/5/8-Id1 (show ID1 Antibodies) signaling in the presence of FGF-2 (show FGF2 Antibodies).

3. We propose that the GC-induced mitochondrial accumulation of Bax (show BAX Antibodies) and the interaction between the GR and Bim (show BCL2L11 Antibodies), Bcl-xL and Bak (show BAK1 Antibodies) could play a role in the regulation of thymocyte apoptosis.

4. Bcl-xL is required for survival of post mitotic neurons throughout the developing spinal cord.

5. anti-apoptotic molecules BclxL and Bcl-2 (show BCL2 Antibodies) and the pro-apoptotic factors BAD and BID (show BID Antibodies) cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L (show FASL Antibodies).

6. Atherosclerosis-associated endothelial cell apoptosis may partially result from downregulation of Bcl-Xl, through upregulation of miR (show MLXIP Antibodies)-876 that binds and suppresses translation of Bcl-Xl mRNA.

7. Bcl-xL is a driver in colorectal tumorigenesis and cancer progression.

8. These data show that Mcl-1 (show MCL1 Antibodies) 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

9. BCL-XL expression promotes survival of immature B cells, expression of BCL-2 (show BCL2 Antibodies) is important for survival of mature B cells and long-lived plasma cells (PC), and expression of MCL-1 (show MCL1 Antibodies) is important for survival throughout B-cell development.

10. Bcl-xL deficiency induced apoptosis in a select population of differentiated neurons and led to severe neurobehavioral abnormalities.

Cow (Bovine) BCL2-Like 1 (BCL2L1) interaction partners

1. amplification and characterization of partial regions of exons 2 and 3 of the bovine BCL2L1 gene

2. Data show that Bcl-x(L) expression is increased in the pulmonary artery undergoing chronic pulmonary vascular remodeling.

Pig (Porcine) BCL2-Like 1 (BCL2L1) interaction partners

1. interleukin-6 (show IL6 Antibodies), endothelin ET-1 (show EDN1 Antibodies), and apoptotic Bak (show BAK1 Antibodies) and Bcl-XL genes have roles in small bowel transplantation, in a swine model of ischemia and reperfusion injury

2. 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

3. CONCLUSION(S): (1) Apoptosis is involved in follicular atresia; (2) Bcl-2 (show BCL2 Antibodies) is induced by warm ischemia; and (3) cryopreservation insult does not alter the apoptotic signals with short tissue preparation time.

4. Bcl-Xl deamidation and methylation has a role in protein isoaspartate methyltransferase prevention of apoptosis induced by oxidative stress in endothelial cells

5. Data show that cysteine significantly reduced the expression of pro-inflammatory cytokines, including TNF-alpha (show TNF Antibodies), IL-6 (show IL6 Antibodies), IL-12p40, IL-1beta (show IL1B Antibodies), and resulted in increased expression of the apoptosis initiator caspase-8 (show CASP8 Antibodies) and bcl2L1.

Rabbit BCL2-Like 1 (BCL2L1) interaction partners

1. This study leads to conclude that BCLXL peak expression at the zygotic genome activation phase may be a requirement for embryo development

2. In this study evidence is provided that exogenous PGF2alpha differentially modulates luteal expression of BCL2L1 transcripts and protein depending on luteal stage.

Xenopus laevis BCL2-Like 1 (BCL2L1) interaction partners

1. 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

Zebrafish BCL2-Like 1 (BCL2L1) interaction partners

1. The bcl2l gene operates in the inhibition of cell death under direct regulation of a thyroid specific set of transcription factors

2. Zebrafish anti-apoptotic gene Bcl-xL can prevent aquatic birnavirus-induced cell death in fish cells without affecting expression of viral proteins.

3. 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

4. Bcl-xL can block post-apoptotic necrosis processes thereby rescuing betanodavirus-infected cells

5. Delta113p53 functions to antagonize p53 (show TP53 Antibodies)-induced apoptosis via activating bcl2L