BCL2/adenovirus E1B 19 KDa Protein-Interacting Protein 3-Like (BNIP3L) Antibody

260€ (50 µl)
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935106861
info@markelab.com
name
BCL2/adenovirus E1B 19 KDa Protein-Interacting Protein 3-Like (BNIP3L) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx212958
tested applications
ELISA, IHC
Description
BNIP3L Antibody is a Rabbit Polyclonal against BNIP3L.
Documents del producto
Instrucciones
Data sheet
Product specifications
Category | Primary Antibodies |
Immunogen Target | BCL2/adenovirus E1B 19 KDa Protein-Interacting Protein 3-Like (BNIP3L) |
Host | Rabbit |
Reactivity | Human, Mouse |
Recommended Dilution | ELISA: 1/2000 - 1/5000, IHC: 1/50 - 1/200. Optimal dilutions/concentrations should be determined by the end user. |
Clonality | Polyclonal |
Conjugation | Unconjugated |
Isotype | IgG |
Purification | Antigen Affinity Chromatography. |
Size 1 | 50 µl |
Size 2 | 100 µl |
Form | Liquid |
Tested Applications | ELISA, IHC |
Buffer | PBS, pH 7.4, containing 0.05% NaN3 and 40% Glycerol. |
Availability | Shipped within 5-10 working days. |
Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
UniProt ID | O60238 |
Gene ID | 665 |
Alias | BNIP3L,BNIP3A,BNIP3H,NIX,Adenovirus E1B19K-binding protein B5,BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like |
Background | Antibody anti-BNIP3L |
Status | RUO |
Descripción
BCL2 Interacting Protein 3 Like (BNIP3L), also known as NIX, is a member of the BCL2 family of proteins and plays a critical role in programmed cell death and mitochondrial quality control. BNIP3L is known to interact with BCL2 and other apoptotic regulators, promoting mitochondrial autophagy (mitophagy), a selective process that removes damaged or dysfunctional mitochondria to maintain cellular homeostasis. Its function is particularly crucial under conditions of hypoxia, where BNIP3L is upregulated, contributing to cell survival by mitigating oxidative stress and preventing the accumulation of damaged mitochondria. In the context of erythroid maturation, BNIP3L is essential for mitophagy-mediated clearance of mitochondria, a necessary step in the development of red blood cells. Dysregulation of BNIP3L has been implicated in various pathologies, including cancer, where its role can vary between promoting cell death in some contexts and contributing to tumor survival and resistance in others. Additionally, alterations in BNIP3L function are associated with neurodegenerative diseases due to impaired mitochondrial dynamics and clearance. This duality highlights the importance of BNIP3L as a potential therapeutic target for addressing diseases linked to apoptosis and mitochondrial dysfunction.
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