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

Este producto es parte de BNIP3 - BCL2 interacting protein 3 (Like)
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1235€ (100 µg)

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935106861
info@markelab.com
name
Human BCL2/Adenovirus E1B 19 kDa Protein-Interacting Protein 3-Like (BNIP3L) Protein
category
Proteins and Peptides
provider
Abbexa
reference
abx694049
tested applications
SDS-PAGE

Description

Human BNIP3L Protein is a recombinant protein from Human produced in E. coli. A DNA sequence encoding the human BNIP3L (NP_004322.1) (Ser 2-Lys 187) was expressed and purified, with additional two amino acids (Gly & Pro) at the N-terminus.

Documents del producto

Instrucciones
Data sheet
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Product specifications

Category
Proteins and Peptides
Immunogen Target
BNIP3L
Host
E. coli
Origin
Human
Observed MW
Molecular Weight: 20.4 kDa
Sequence Fragment: Ser2-Lys187
Validity: The validity for this protein is 12 months.
Expression
Recombinant
Purity
> 88% (SDS-PAGE)
Size 1
100 µg
Form
 
Tested Applications
SDS-PAGE
Buffer
Lyophilized from sterile 50mM Tris, 150mM NaCl, 1mM DTT, pH 8.0.
Availability
Shipped within 5-15 working days.
Storage
Aliquot and store at -20°C or -80°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
Q7Z465-1
Alias
BNIP3L,BNIP3A,BNIP3H,NIX,Adenovirus E1B19K-binding protein B5,BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like
Background
Protein BNIP3L
Status
RUO
Note
This product is for research use only.   Not for human consumption, cosmetic, therapeutic or diagnostic use.

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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