anti-Bcl2 Modifying Factor (BMF) Antibodies

Human Bcl2 Modifying Factor (BMF) interaction partners

1. The findings are consistent with rs539846 influencing chronic lymphocytic leukemia (CLL) susceptibility through differential RELA binding, with direct modulation of BMF expression impacting on anti-apoptotic BCL2, a hallmark of oncogenic dependency in CLL.

2. Reciprocal regulation of BMF and BIRC5 is linked to Eomes overexpression in colorectal cancer.

3. Early generated B1 B cells with restricted BCRs become chronic lymphocytic leukemia with continued c-Myc and low Bmf expression

4. these findings suggest that p53-R273H can specifically drive AKT signaling and suppress BMF expression, resulting in enhanced cell survivability and anoikis resistance.

5. On the corresponding BMF gene promoter, loss of HDAC8 was associated with signal transducer and activator of transcription 3 (STAT3)/specificity protein 3 (Sp3) transcription factor exchange and recruitment of p300.

6. Overexpression of ApoL2 did not induce cell death on its own. ApoL2 did not sensitize or protect cells from overexpression of the BH3-only proteins Bmf or Noxa.

7. Diva binds peptides derived from the BH3 domain of several other proapoptotic Bcl-2 proteins, including mouse Harakiri, Bid, Bak and Bmf.

8. BMF is induced in human IEC by the loss of cell attachment and is likely to play an important role in the regulation of IEC survival

9. characterization of the bmf gene locus; molecular basis of the generation of the 2 major isoforms of Bmf; provide evidence that Bmf can act as a sensor for stress that associates with the repression of the conventional CAP-dependent translation machinery

10. Data show that hypoxic conditions inhibit anoikis and block expression of proapoptotic BH3-only family members Bim and Bmf in epithelial cells.

11. Bmf is upregulated by PS-341 and has a crucial role in PS-341-mediated glioma cell death through JNK phosphorylation.

12. Up or downregulation of Bmf isoforms may have a role in regulating growth and survival in B cells and leukemic B-CLL cells

13. There was no somatic mutation of BH3 domains of Bad, Bmf and Bcl-G genes in transitional cell carcinoma samples. The data presented here indicate that BH3 domain mutation of these genes is rare in TCCs and may not contribute to the pathogenesis of TCCs.

14. histone hyperacetylation may enhance ionizing radiation-induced death via activation of Bmf transcription, thereby implying Bmf as a key molecule for HDAC inhibitors (FK228 and CBHA)-mediated enhancing effect on IR-induced cell death

15. Bmf is a central mediator of anoikis in mammary cells and a target of oncogenes that contribute to the progression of glandular epithelial tumors

16. data presented here indicate that BH3 domain mutation of the proapoptotic genes Bad, Bmf and Bcl-G is rare in laryngeal squamous cell carcinoma and may not contribute to the apoptosis-resistance mechanisms of laryngeal squamous cell carcinoma

17. arsenic trioxide upregulated expression of Bmf, Noxa, and Bim. Silencing of Bmf, Noxa, and Bim significantly protected MM cells from ATO-induced apoptosis

18. Our data indicate a synergistic role for both bim and Bmf in an apoptotic pathway leading to the clearance of Neisseria gonorrhoeae -infected cells.

19. Bmf supports Bim in regulating cell death processes in response to many stimuli. Review.

20. MicroRNA-221 targets Bmf in hepatocellular carcinoma and correlates with tumor multifocality.

Mouse (Murine) Bcl2 Modifying Factor (BMF) interaction partners

1. In clinical Esophageal squamous cell carcinoma (ESCC)specimens, BMF expression was upregulated, and negatively correlated with that of miR-125b. In conclusion, miR-125b had an antitumor role in ESCC cells mediated by targeting BMF, which can be potentially useful for tumorigenesis in ESCC

2. demonstrate that this sudden and dramatic loss of primordial follicles is hormonally triggered and identify the pro-apoptotic BH3-only protein, BCL-2 modifying factor (BMF), as essential for this process, implicating the intrinsic apoptotic pathway as a key mechanism.

3. FOXO-dependent BMF expression is repressed in E-cadherin-negative and metastatic breast cancer cells and that expression of BMFis sufficient to inhibit tumour growth and dissemination in mice.

4. BMF loss is associated with germ cell loss during oogenesis.

5. Bcl2 interacting mediator of cell death (Bim) and Bcl2 modifying factor (Bmf), mediate apoptosis in the context of TACI-Ig overexpression that effectively neutralizes BAFF as well as APRIL.

6. Bmf deficiency induced significant protection against oxygen/glucose deprivation injury in cultured neurons.

7. Our findings support an important role for BMF in determining the number of primordial follicles maintained in the ovary throughout adult reproductive life.

8. Bim and Bmf act in concert to prevent autoimmunity and malignant disease

9. Bmf-deficient mice showed normal sensitivity to the convulsant effects of KA, displayed significantly more neuronal death in the hippocampal CA1 and CA3 subfields after SE.

10. deacetylation of p53 suppresses Bmf expression and facilitates autophagy.

11. critical role for Bim and Bmf as regulators of hematopoietic stem and progenitor cell dynamics both during early engraftment and long-term reconstitution

12. our study suggests that Bad and Bmf co-regulate lymphocyte homeostasis and limit spontaneous transformation by mechanisms that may not exclusively be linked to the induction of lymphocyte apoptosis.

13. a potential role for Bmf in regulating renal proximal tubular cells (RPTC) apoptosis and tubular atrophy in diabetes.

14. characterization of the bmf gene locus; molecular basis of the generation of the 2 major isoforms of Bmf; provide evidence that Bmf can act as a sensor for stress that associates with the repression of the conventional CAP-dependent translation machinery

15. Data show that loss of Bmf reduced the pressure to inactivate p53, whereas Bad deficiency did not, identifying Bmf as a novel component of the p53-independent tumor suppressor pathway triggered by c-Myc.

16. Developmental ablation of interdigital webbing on mouse paws and normal lymphocyte homeostasis require the cooperative activity of Bim and Bmf.

17. Study shows, using spectroscopic methods, that the BH3-only proteins Bim, Bad and Bmf are unstructured in the absence of binding partners.

18. TGF beta-induced Bmf and Bim undergo significant expression changes, the combined effect of which is to trigger the cell death program.

19. Bmf is a central mediator of anoikis in mammary cells and a target of oncogenes that contribute to the progression of glandular epithelial tumors

20. Bmf plays a critical role in apoptosis signaling and can function as a tumor suppressor.