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anti-Human BNIP3 Antibodies:
anti-Mouse (Murine) BNIP3 Antibodies:
anti-Rat (Rattus) BNIP3 Antibodies:
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Human Polyclonal BNIP3 Primary Antibody for IF, IHC (p) - ABIN388117
Kothari, Cizeau, McMillan-Ward, Israels, Bailes, Ens, Kirshenbaum, Gibson: BNIP3 plays a role in hypoxic cell death in human epithelial cells that is inhibited by growth factors EGF and IGF. in Oncogene 2003
Show all 5 Pubmed References
Human Monoclonal BNIP3 Primary Antibody for ICC, IF - ABIN151087
Landes, Emorine, Courilleau, Rojo, Belenguer, Arnauné-Pelloquin: The BH3-only Bnip3 binds to the dynamin Opa1 to promote mitochondrial fragmentation and apoptosis by distinct mechanisms. in EMBO reports 2010
Show all 2 Pubmed References
Human Polyclonal BNIP3 Primary Antibody for ICC, IF - ABIN4284980
Yang, Yang, Guo, Williams, Weissler: PLAGL2 expression-induced lung epithelium damages at bronchiolar alveolar duct junction in emphysema: bNip3- and SP-C-associated cell death/injury activity. in American journal of physiology. Lung cellular and molecular physiology 2009
TUG1 overexpression aggravates hypoxia injury of cardiomyocytes by regulating miR (show MLXIP Antibodies)-145-5p-Bnip3 axis to activate Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) pathways.
In ESCC cells, although BNIP3-induced autophagy is protective, BNIP3 exerts a pro-death function under hypoxia.
Silencing of BNIP3 suppressed free fatty acid synthesis in mesenchymal stem cells. BNIP3 induction by hypoxia stimulates FASN (show FASN Antibodies)-dependent free fatty acid production.
Apoptosis, but not autophagy, that is induced via p21 (show CDKN1A Antibodies)-activated BNIP3 expression accounts for the efficacy of ICMT (show ICMT Antibodies) inhibition in sensitive pancreatic cancer cells in both in vitro and in vivo models. In contrast, cells resistant to ICMT (show ICMT Antibodies) inhibition demonstrated no mitochondria dysfunction or p21 (show CDKN1A Antibodies) signaling changes under ICMT (show ICMT Antibodies) suppression
BNIP3 is a significant contributor to the pathogenesis of inflammation-induced heart failure pathologies [review]
The authors find that KDM3A (show KDM3A Antibodies) promotes anoikis through transcriptional activation of BNIP3 and BNIP3L (show BNIP3L Antibodies), which encode pro-apoptotic proteins.
the results suggest that BNIP3 plays a vital role in regulating PINK1 (show PINK1 Antibodies) mitochondrial outer membrane localization, the proteolytic process of PINK1 (show PINK1 Antibodies) and PINK1 (show PINK1 Antibodies)/parkin (show PARK2 Antibodies)-mediated mitophagy under physiological conditions.
High BNIP3 expression is associated with chronic myelogenous leukemia.
Results suggest that changes in mitochondrial morphology and transmembrane potential, induced by mutant htt (show HTT Antibodies) protein, are dependent and linked to BNip3 and not to Bax (show BAX Antibodies)/Bak (show BAK1 Antibodies) activation.
JNK (show MAPK8 Antibodies) activates Mff (show MFF Antibodies) and Bnip3, contributing to the fatal mitochondrial fission and mitophagy, respectively.
BNIP3 expression was upregulated in hypoxic keratinocytes, and BNIP3 silencing suppressed hypoxia-induced cell migration.
In a neuronal model of dominant optic atrophy, BNIP3 down-regulation reduced autophagy and mitophagy.
Down-regulation of Bcl2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3) by olomoucine, a cyclin (show PCNA Antibodies)-dependent kinasesinhibitor, reduces lipopolysaccharide - and nitric oxide-induced cell death in BV2 (show DNAH9 Antibodies) microglial cells. Olomoucine may protect cells by limiting proinflammatory responses, thereby reducing nitric oxide generation.
data outline Bnip3 as a key effector of PPARgamma (show PPARG Antibodies)-mediated adipose mitochondrial network fragmentation, improving insulin (show INS Antibodies) sensitivity and limiting oxidative stress.
BNIP3 interacts with the mitochondrial outer membrane directly via mitochondrial BAX (show BAX Antibodies).
Data show that TGFbeta (show TGFB1 Antibodies)-activated kinase-1 (TAK1 (show NR2C2 Antibodies)) activated nuclear factor of activated T-cells (NFAT (show NFATC1 Antibodies))/NF-kappa B (NFkappaB (show NFKB1 Antibodies)), downregulated BCL2-adenovirus E1B interacting protein 3 (Bnip3), and inhibited cardiac cell death.
propose that BNIP3 acts as a brake on HIF-1 (show HIF1A Antibodies) activity serving to increase rates of mitophagy in response to hypoxia and to limit production of damaging ROS (show ROS1 Antibodies) that would further amplify HIF-1 (show HIF1A Antibodies) expression and promote tumor progression to metastasis
Results suggest that Bnip3 regulates cardiac gene expression and perhaps myocyte morphology by activating nuclear p300 acetyltransferase and hyperacetylating histones and its selective transcription factors.
This gene is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. It interacts with the E1B 19 kDa protein, which protects cells from virally-induced cell death. The encoded protein also interacts with E1B 19 kDa-like sequences of BCL2, another apoptotic protector. This protein contains a BH3 domain and a transmembrane domain, which have been associated with pro-apoptotic function. The dimeric mitochondrial protein encoded by this gene is known to induce apoptosis, even in the presence of BCL2.
BCL2/adenovirus E1B 19 kDa protein-interacting protein 3
, BCL2/adenovirus E1B 19kD-interacting protein 3
, BCL2/adenovirus E1B 19 kDa-interacting protein 1, NIP3
, BCL2/adenovirus E1B 19kDa-interacting protein 1, NIP3
, BCL2/adenovirus E1B interacting protein 1, NIP3
, BCL2/adenovirus E1B 19 kDa-interacting protein 3