BCL2/Adenovirus E1B 19 kDa Protein-Interacting Protein 3-Like (BNIP3L) Antibody

Este producto es parte de BNIP3 - BCL2 interacting protein 3 (Like)
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169€ (20 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
abx320053
tested applications
ELISA, IHC

Description

BNIP3L Antibody is a Rabbit Polyclonal against BNIP3L.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
BCL2/Adenovirus E1B 19 kDa Protein-Interacting Protein 3-Like (BNIP3L)
Host
Rabbit
Reactivity
Human
Recommended Dilution
IHC: 1/20 - 1/200. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Unconjugated
Isotype
IgG
Purification
Antigen Affinity Chromatography.
Size 1
20 µl
Size 2
50 µl
Size 3
100 µl
Size 4
200 µl
Size 5
1 ml
Form
Liquid
Tested Applications
ELISA, IHC
Buffer
PBS, pH 7.3, containing 0.02% sodium azide and 50% 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
NCBI Accession
NP_001317420.1, NM_001330491.1, NP_004322.1, NM_004331.2
OMIM
605368
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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