Browse our anti-BCL2L1 (BCL2L1) Antibodies

Human BCL2-Like 1 (BCL2L1) interaction partners

1. Examined the roles of BCL2 proteins in the induction of apoptosis in cells upon infection with flaviviruses, such as Japanese encephalitis virus, Dengue virus and Zika virus. Showed that survival of the infected cells depends on BCLXL, a pro-survival BCL2 protein due to suppression of the expression of another pro-survival protein, MCL1.

2. Bcl-xL abrogates the cytotoxic effects of LRRK2 inhibition in a neuroblastoma cell line (SH-SY5Y/Bcl-xL) overexpressing Bcl-xL.

3. E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death.

4. Study shows that multiple ion transporters mediate the rise in pH that increases the rate of Bcl-xL deamidation in response to DNA damage in certain cells. Additionally, deamidation of Bcl-xL is intramolecularly catalyzed in a manner that is dependent upon two conserved histidines near each of the deamidation sites and that they may function together as a pH-sensitive switch.

5. hTERT contains a BH3-like motif, a short peptide sequence found in BCL-2 family proteins, and interacts with anti-apoptotic BCL-2 family proteins MCL-1 and BCL-xL

6. Study demonstrated that lncRNA-HEIH regulates miR-939 expression through transcriptional repression of Bcl-xL promoting colorectal tumorigenesis.

7. Results showed that the expressions of RIP2 and BclxL were positively correlated with the malignant grade of astrocytoma. RIP2 promoted human glioblastoma cell proliferation by inducing expression of BclxL.

8. BCL-XL has a role in modulating RAS signalling to favor breast cancer cell stemness

9. Bcl-xL degradation during endoplasmic reticulum stress-induced apoptosis is mediated by RNF183.RNF183 ubiquitinates Bcl-xL.

10. BCL-XL promotes stemness and contributes to the aggressiveness of both melanoma and glioblastoma.

11. inhibition of the BCL2 family member BCLxL resulted in nanomolar potency against human synovial sarcoma cell lines and 50% tumor reduction in a genetically engineered mouse model

12. In this study, we investigated whether APG-1252-12A inhibits the growth of five leukemia cell lines in a concentration- or time-dependent manner by MTS assay.APG-1252-12A is a Bcl-2 homology (BH)-3 mimetic that specifically binds to Bcl-2 and Bcl-xl, which has shown efficacy in some Bcl-2 dependent hematological cancers

13. inhibition of Bcl-xL induces significantly more apoptosis in IDH1-mutated cells than in wild-type IDH1 cells.

14. 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

15. 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 such as the cancer stem cell and adipocyte niches.

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

17. anti-apoptotic molecules BclxL and Bcl-2 and the pro-apoptotic factors BAD and BID cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L.

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

19. that Ubiquitin-specific peptidase 18 directly bind to BCL2L1 and positively regulated its expression in hepatocellular carcinoma cells

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

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

1. Examined the roles of BCL2 proteins in the induction of apoptosis in cells upon infection with flaviviruses, such as Japanese encephalitis virus, Dengue virus and Zika virus. Showed that survival of the infected cells depends on BCLXL, a pro-survival BCL2 protein due to suppression of the expression of another pro-survival protein, MCL1.

2. Depletion of miR-34a facilitated endothelial cell growth and blocked apoptosis in AS by upregulating Bcl-2, offering a promising avenue for AS therapy.

3. BCL-XL promotes stemness and contributes to the aggressiveness of both melanoma and glioblastoma.

4. targeting BCLxL in human and mouse synovial sarcoma with the small molecule BH3 domain inhibitor, BXI-72, achieved significant cytoreduction and increased apoptotic signaling.

5. GATA-3 participates in the healing of bone fractures via regulating bcl-xL gene expression, owing to its association with Runx2.

6. this study demonstrates that necrosis of Mycobacterium tuberculosis-infected macrophages is dependent on the action of Bcl-xl

7. Mitochondrial Bcl-xL is involved in maintaining mitochondrial respiratory capacity. Its deficiency causes oxidative stress, which is associated with an increased glycolytic capacity and balanced by an increased activity of the pentose phosphate pathway.

8. Proapoptotic proteins BIM and PUMA are not critical for the reticulocyte apoptosis caused by loss of the pro-survival protein BCL-XL.

9. BMP4 promotes survival of neural stem/progenitor cells by enhancing the anti-apoptotic function of Bcl-xL via BMP4-Smad1/5/8-Id1 signaling in the presence of FGF-2.

10. We propose that the GC-induced mitochondrial accumulation of Bax and the interaction between the GR and Bim, Bcl-xL and Bak could play a role in the regulation of thymocyte apoptosis.

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

12. anti-apoptotic molecules BclxL and Bcl-2 and the pro-apoptotic factors BAD and BID cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L.

13. Atherosclerosis-associated endothelial cell apoptosis may partially result from downregulation of Bcl-Xl, through upregulation of miR-876 that binds and suppresses translation of Bcl-Xl mRNA.

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

15. These data show that Mcl-1 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

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

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

18. loss of PUMA had no impact on the loss of platelets caused by loss of BCL-XL. It therefore remains to be established whether other BH3-only 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 and BAX.

19. MLF1 is negatively regulated by 14-3-3 via binding to, and blocking, MLF1's Bcl-2 homology domain 3 and thereby preventing Bcl-XL from associating with MLF1.

20. Genetic and pharmacological inhibition of BCL-W and BCL-XL causes directed elimination of senescent cells.

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. chromosome mapping by in situ hybridization.

3. 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, endothelin ET-1, and apoptotic Bak 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 is induced by warm ischemia; and (3) cryopreservation insult does not alter the apoptotic signals with short tissue preparation time.

4. Data show that cysteine significantly reduced the expression of pro-inflammatory cytokines, including TNF-alpha, IL-6, IL-12p40, IL-1beta, and resulted in increased expression of the apoptosis initiator caspase-8 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-induced apoptosis via activating bcl2L