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BNIP3 is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. Additionally we are shipping BNIP3 Antibodies (117) and BNIP3 Proteins (3) and many more products for this protein.
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Hypoxia-induced autophagy contributes to the invasion of salivary adenoid cystic carcinoma through the HIF-1alpha (show HIF1A ELISA Kits)/BNIP3 signaling pathway.
The data indicated that BNIP3 plays a vital role in the tumorigenesis of adenoid cystic carcinoma and could be a new target for gene therapy of adenoid cystic carcinoma.
BNIP3 deletion can be used as a prognostic (show HIF1A ELISA Kits)marker of tumor progression to metastasis in human triple-negative breast cancer
BNIP3 expression was found to be regulated by Sp3 (show SP3 ELISA Kits) in prostate cancer.
phosphorylation of these C-terminal BNIP3 residues blocks cell death without preventing autophagy, providing evidence that the two functional roles of BNIP3 can be regulated independently
Bnip3 dual-functionality and crosstalk between mitophagy and apoptosis pathways is presented here.
these findings revealed that silibinin induced autophagic cell death through ROS (show ROS1 ELISA Kits)-dependent mitochondrial dysfunction and ATP depletion involving BNIP3 in MCF7 cells.
The findings of the present study reveal a novel survival pathway that functionally couples the unique glycolytic phenotype in cancer cells to hypoxia resistance via a PDK2 (show PDK2 ELISA Kits)-dependent mechanism that switches Bnip3 from cell death to survival.
Mevalonate depletion through HMG-CoA reductase (show HMGCR ELISA Kits) inhibition impairs the viability of primary human mesenchymal stells via NF-kappaB (show NFKB1 ELISA Kits)/Bnip3 signaling.
protective role of BNIP3 in the form of autophagy inducer to reduce the misfolded proteins directly and prevention of neurodegenerative diseases indirectly
propose that BNIP3 acts as a brake on HIF-1 (show HIF1A ELISA Kits) activity serving to increase rates of mitophagy in response to hypoxia and to limit production of damaging ROS (show ROS1 ELISA Kits) that would further amplify HIF-1 (show HIF1A ELISA Kits) 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.
regulates mitophagy during hypoxia, whereas NIX (show BNIP3L ELISA Kits) is required for mitophagy during development of the erythroid lineage.
BNIP3 primarily regulates basal level of mitophagy in physiological conditions, whereas BNIP3 exclusively activates excessive mitophagy leading to cell death.
Bnip3 generation, mediated by PARP1 (show PARP1 ELISA Kits), causes mitochondrial damage and neuron death.
Suggest pro-tumorigenic role of BNIP3 driving melanoma cell's aggressive features, like migration and vasculogenic mimicry.
BNIP3 has a protective effect against UVB-induced apoptosis in keratinocytes
The BNIP3 cell death pathway may be a new target for protecting oligodendrocytes from death after stroke
Bnip3 is a required downstream effector of FoxO (show FOXO3 ELISA Kits)-driven autophagic flux in mechanically unloaded failing myocardium.
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