BNIP3L Antibody / NIX / BCL2/adenovirus E1B 19 kDa-interacting protein 3-like
| 货号:FY13212 | 规格:100 ug | 目录价:¥6488.05 |
产品详情
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产品名称:
BNIP3L Antibody / NIX / BCL2/adenovirus E1B 19 kDa-interacting protein 3-like
产品描述:
BNIP3L antibody detects BCL2/adenovirus E1B 19 kDa-interacting protein 3-like, also known as NIX or NIP3L, a mitochondrial outer membrane protein that regulates apoptosis, mitophagy, and hypoxia adaptation. The UniProt recommended name is BCL2/adenovirus E1B 19 kDa-interacting protein 3-like (BNIP3L). Functionally identical to NIX, this pro-apoptotic factor is a key effector of mitochondrial quality control, mediating the selective autophagic removal of damaged mitochondria under stress conditions.
NIX antibody detects the same 263-amino-acid integral membrane protein localized to the outer mitochondrial membrane. BNIP3L interacts with members of the BCL2 family and contains an LC3-interacting region (LIR) motif that recruits autophagosomes to mitochondria during mitophagy. Under hypoxic conditions, NIX (BNIP3L) expression is upregulated by hypoxia-inducible factor 1-alpha (HIF1A), initiating mitophagy and limiting reactive oxygen species accumulation. This mechanism is vital for maintaining mitochondrial integrity and metabolic adaptation during oxygen deprivation.
The BNIP3L (NIX) gene resides on chromosome 8p21.2 and is expressed in energy-demanding tissues such as heart, skeletal muscle, and brain. Its transcriptional regulation integrates stress and metabolic cues through signaling pathways including HIF1A, FOXO3, and PGC1A, linking mitochondrial turnover with cellular homeostasis and survival responses.
Pathologically, BNIP3L/NIX plays dual roles in determining cell fate: promoting mitophagy and survival under transient stress, but driving apoptosis during sustained hypoxia or mitochondrial damage. Aberrant regulation of this pathway contributes to cardiomyopathy, neurodegeneration, and tumor resistance to therapy. In cancer biology, elevated NIX (BNIP3L) expression enhances mitochondrial clearance, supporting metabolic flexibility within hypoxic tumor microenvironments. Research using BNIP3L antibody and NIX antibody supports investigations in apoptosis, autophagy, and mitochondrial signaling mechanisms.
This antibody is validated for western blotting, immunofluorescence, and flow cytometry to detect mitophagy-related proteins. NSJ Bioreagents provides BNIP3L/NIX antibody reagents optimized for studies in hypoxia signaling, mitochondrial biology, and programmed cell death.
Structurally, BCL2/adenovirus E1B 19 kDa-interacting protein 3-like (NIX) contains a C-terminal transmembrane domain for mitochondrial localization, a BH3-like domain mediating interactions with BCL2 family members, and an LIR motif enabling autophagosome docking. This antibody supports exploration of BNIP3L/NIX function in balancing mitophagy and apoptosis during cellular stress.
NIX antibody detects the same 263-amino-acid integral membrane protein localized to the outer mitochondrial membrane. BNIP3L interacts with members of the BCL2 family and contains an LC3-interacting region (LIR) motif that recruits autophagosomes to mitochondria during mitophagy. Under hypoxic conditions, NIX (BNIP3L) expression is upregulated by hypoxia-inducible factor 1-alpha (HIF1A), initiating mitophagy and limiting reactive oxygen species accumulation. This mechanism is vital for maintaining mitochondrial integrity and metabolic adaptation during oxygen deprivation.
The BNIP3L (NIX) gene resides on chromosome 8p21.2 and is expressed in energy-demanding tissues such as heart, skeletal muscle, and brain. Its transcriptional regulation integrates stress and metabolic cues through signaling pathways including HIF1A, FOXO3, and PGC1A, linking mitochondrial turnover with cellular homeostasis and survival responses.
Pathologically, BNIP3L/NIX plays dual roles in determining cell fate: promoting mitophagy and survival under transient stress, but driving apoptosis during sustained hypoxia or mitochondrial damage. Aberrant regulation of this pathway contributes to cardiomyopathy, neurodegeneration, and tumor resistance to therapy. In cancer biology, elevated NIX (BNIP3L) expression enhances mitochondrial clearance, supporting metabolic flexibility within hypoxic tumor microenvironments. Research using BNIP3L antibody and NIX antibody supports investigations in apoptosis, autophagy, and mitochondrial signaling mechanisms.
This antibody is validated for western blotting, immunofluorescence, and flow cytometry to detect mitophagy-related proteins. NSJ Bioreagents provides BNIP3L/NIX antibody reagents optimized for studies in hypoxia signaling, mitochondrial biology, and programmed cell death.
Structurally, BCL2/adenovirus E1B 19 kDa-interacting protein 3-like (NIX) contains a C-terminal transmembrane domain for mitochondrial localization, a BH3-like domain mediating interactions with BCL2 family members, and an LIR motif enabling autophagosome docking. This antibody supports exploration of BNIP3L/NIX function in balancing mitophagy and apoptosis during cellular stress.
反应种属:
Human, Mouse, Rat
宿主来源:
Rabbit
实验应用:
WB, ICC/IF, FACS
同种型:
Rabbit IgG
免疫原:
A synthetic peptide corresponding to a sequence in the middle region of human BNIP3L was used as the immunogen for the BNIP3L antibody.
克隆性:
Polyclonal (rabbit origin)
纯化方式:
Immunogen affinity purified
保存温度:
After reconstitution, the BNIP3L antibody can be stored for up to one month at 4oC. For long-term, aliquot and store at -20oC. Avoid repeated freezing and thawing.
产品形式:
Lyophilized
存储溶液:
Adding 0.2 ml of distilled water will yield a concentration of 500 ug/ml
产地:
美国
促销活动
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