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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Bcl2 modifying factor

BMF, Bcl2 modifying factor
The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein contains a single BCL2 homology domain 3 (BH3), and has been shown to bind BCL2 proteins and function as an apoptotic activator. This protein is found to be sequestered to myosin V motors by its association with dynein light chain 2, which may be important for sensing intracellular damage and triggering apoptosis. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: bcl-2, Bim, CAN, Bax, LRP
Papers using BMF antibodies
BAFF regulates B cell survival by downregulating the BH3-only family member Bim via the ERK pathway
Clark Edward A. et al., In The Journal of Experimental Medicine, 1999
... Human APRIL, mouse BAFF, and rabbit anti-Bmf serum were purchased from Axxora.
Papers on BMF
Combination Therapy Targeting Ribosome Biogenesis and mRNA Translation Synergistically Extends Survival in MYC-Driven Lymphoma.
Pearson et al., Melbourne, Australia. In Cancer Discov, Jan 2016
CX-5461 induced nucleolar stress and p53 pathway activation, whereas everolimus induced expression of the proapoptotic protein BMF that was independent of p53 and reduced expression of RPL11 and RPL5.
Brca1 deficiency causes bone marrow failure and spontaneous hematologic malignancies in mice.
Churpek et al., Chicago, United States. In Blood, Jan 2016
Mice lacking Brca1 in the bone marrow have baseline cytopenias and develop spontaneous bone marrow failure (BMF) or diverse hematologic malignancies by six months of age.
Type I IFNs Act upon Hematopoietic Progenitors To Protect and Maintain Hematopoiesis during Pneumocystis Lung Infection in Mice.
Meissner et al., Bozeman, United States. In J Immunol, Jan 2016
Although acquired bone marrow failure (BMF) is considered a T cell-mediated autoimmune disease, few studies have considered contributing roles of innate immune deviations following otherwise innocuous infections as a cause underlying the immune defects that lead to BMF.
Fibrogenesis in Primary Myelofibrosis: Diagnostic, Clinical, and Therapeutic Implications.
Daver et al., Cleveland, United States. In Oncologist, Oct 2015
Bone marrow fibrosis (BMF) plays a central role in the pathophysiology of the disease.
Emerging understanding of Bcl-2 biology: Implications for neoplastic progression and treatment.
Kaufmann et al., Rochester, United States. In Biochim Biophys Acta, Jul 2015
Thirty years later we now understand that anti-apoptotic Bcl-2 family members modulate the intrinsic apoptotic pathway by binding and neutralizing the mitochondrial permeabilizers Bax and Bak as well as a variety of pro-apoptotic proteins, including the cellular stress sensors Bim, Bid, Puma, Bad, Bmf and Noxa.
Role of gga-miR-221 and gga-miR-222 during Tumour Formation in Chickens Infected by Subgroup J Avian Leukosis Virus.
Xie et al., Guangzhou, China. In Viruses, 2014
Over-expression of gga-miR-221 and gga-miR-222 promoted the proliferation, migration, and growth of DF-1 cells, and decreased the expression of BCL-2 modifying factor (BMF) making cells more resistant to apoptosis.
Improvement of Expressed Breast Milk in Mothers of Preterm Infants by Recording Breast Milk Pumping Diaries in a Neonatal Center in China.
Liu et al., Shanghai, China. In Plos One, 2014
The ratios of EBM (days of EBM to NICU/hospitalized days), breast milk feeding (BMF) (days of infants fed with exclusive human milk/hospitalized days), mixed feeding (MF) (days of infants fed with partial breast milk and partial formula/hospitalized days), and formula feeding (FF) (days of infants fed with preterm formula/hospitalized days) were evaluated.
eIF4F is a nexus of resistance to anti-BRAF and anti-MEK cancer therapies.
Vagner et al., Villejuif, France. In Nature, 2014
Resistance to treatment and maintenance of eIF4F complex formation is associated with one of three mechanisms: reactivation of MAPK signalling, persistent ERK-independent phosphorylation of the inhibitory eIF4E-binding protein 4EBP1 or increased pro-apoptotic BCL-2-modifying factor (BMF)-dependent degradation of eIF4G.
Why does the bone marrow fail in Fanconi anemia?
Patel et al., Cambridge, United Kingdom. In Blood, 2014
The inherited bone marrow failure (BMF) syndromes are a rare and diverse group of genetic disorders that ultimately result in the loss of blood production.
Learning from a paradox: recent insights into Fanconi anaemia through studying mouse models.
te Riele et al., Amsterdam, Netherlands. In Dis Model Mech, 2013
Fanconi anaemia (FA) is a rare autosomal recessive or X-linked inherited disease characterised by an increased incidence of bone marrow failure (BMF), haematological malignancies and solid tumours.
Bcl-2-modifying factor induces renal proximal tubular cell apoptosis in diabetic mice.
Chan et al., Montréal, Canada. In Diabetes, 2012
a potential role for Bmf in regulating renal proximal tubular cells (RPTC) apoptosis and tubular atrophy in diabetes.
Intrinsic and extrinsic apoptotic pathway signaling as determinants of histone deacetylase inhibitor antitumor activity.
Johnstone et al., Melbourne, Australia. In Adv Cancer Res, 2011
In many cases, HDACi activate the intrinsic pathway via upregulation of a number of proapoptotic BH3-only Bcl-2 family genes including Bim, Bid, and Bmf.
BCL-2 modifying factor (BMF) is a central regulator of anoikis in human intestinal epithelial cells.
Rogler et al., Zürich, Switzerland. In J Biol Chem, 2011
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
Hypoxia suppression of Bim and Bmf blocks anoikis and luminal clearing during mammary morphogenesis.
Reginato et al., Philadelphia, United States. In Mol Biol Cell, 2010
Data show that hypoxic conditions inhibit anoikis and block expression of proapoptotic BH3-only family members Bim and Bmf in epithelial cells.
AMP-activated protein kinase mediates apoptosis in response to bioenergetic stress through activation of the pro-apoptotic Bcl-2 homology domain-3-only protein BMF.
Prehn et al., Dublin, Ireland. In J Biol Chem, 2010
Studies suggest that overexpression of DN-HNF1A induces bioenergetic stress and activation of AMPK, and this in turn mediates the transcriptional activation of BMF, coupling prolonged energy stress to apoptosis activation.
BH3-only protein Bmf mediates apoptosis upon inhibition of CAP-dependent protein synthesis.
Villunger et al., Innsbruck, Austria. In Cell Death Differ, 2010
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
Identification of a molecular signaling network that regulates a cellular necrotic cell death pathway.
Yuan et al., Boston, United States. In Cell, 2009
Interestingly, Bmf, a BH3-only Bcl-2 family member, is required for death-receptor-induced necroptosis.
Activated intrinsic apoptosis pathway is a key related prognostic parameter in acute myeloid leukemia.
Schuurhuis et al., Amsterdam, Netherlands. In J Clin Oncol, 2007
Forward selection and cross validation revealed the antiapoptotic gene BIRC3 and the proapoptotic genes BAX-(l) and BMF to optimally predict OS.
Hierarchical regulation of mitochondrion-dependent apoptosis by BCL-2 subfamilies.
Cheng et al., Saint Louis, United States. In Nat Cell Biol, 2006
Extensive mutagenesis of BAX-BAK indicates that their activity is not kept in check by BCL-2-BCL-X(L)-MCL-1. Anti-apoptotic BCL-2 members are differentially inactivated by the remaining 'inactivator' BH3-only molecules including BAD, NOXA, BMF, BIK/BLK and HRK/DP5.
Bmf: a proapoptotic BH3-only protein regulated by interaction with the myosin V actin motor complex, activated by anoikis.
Strasser et al., Melbourne, Australia. In Science, 2001
We identified a BH3-only protein, Bmf, and show that its BH3 domain is required both for binding to prosurvival Bcl-2 proteins and for triggering apoptosis.
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