BNIP3L/NIX Antibody [E12P3] | Primary Antibodies

Application: Reactivity: Human

Lane 1: Raji, Lane 2: K562

Usage Information

Dilution
WB1:1000 - 1:10000 IHC1:100 - 1:250

Application
WB, IHC

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
24 kDa 26-36 kDa,76 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human breast carcinoma tissue; Raji cells; K562 cells ; A549 cells (CoCl2, 0.1mM, 24 h); HeLa cells (CoCl2, 0.1mM, 24 h)
Negative Control

Datasheet & SDS

Biological Description

Specificity
BNIP3L/NIX Antibody [E12P3] detects endogenous levels of total BNIP3L/NIX protein.

Clone
E12P3

Synonym(s)
BNIP3A; BNIP3H; NIX; BNIP3L; BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like; Adenovirus E1B19K-binding protein B5; BCL2/adenovirus E1B 19 kDa protein-interacting protein 3A; NIP3-like protein X; NIP3L

Background
BNIP3L/NIX (BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like), also known as NIP3-like protein X, is a BH3-only member of the BCL-2 family that predominantly localizes to the mitochondrial outer membrane (OMM) through its C-terminal transmembrane ™ domain, but is also found on the endoplasmic and sarcoplasmic reticulum. BNIP3L contains an N-terminal LC3-interacting region (LIR) motif (WTHL, residues 34-37) vital for binding ATG8 family proteins such as LC3 and GABARAP, a central BH3 domain for interactions with anti-apoptotic BCL-2 proteins (e.g., BCL-xL), and a TM domain with a GxxxG motif (Gly204/208) important for SDS-resistant homodimerization. BNIP3L acts as a mitophagy receptor that recruits autophagosome machinery to damaged mitochondria via its LIR motif, enabling selective mitochondrial clearance independently of the PINK1/Parkin pathway, especially during erythroid maturation where it drives mitochondrial elimination for hemoglobinization, reticulocyte formation, and cardiac progenitor cell development. Dimerized BNIP3L, stabilized by hypoxia-induced HIF-1α, exposes the LIR to bind LC3, nucleates phagophores around mitochondria, triggers DRP1-mediated fission, and indirectly enhances autophagy by releasing Beclin-1 from BCL-2. Under severe stress, it can induce apoptosis via BAX/BAK activation and mitochondrial permeability transition, leading to ROS generation and necrosis. Dysregulation of BNIP3L is implicated in cancer (tumor suppression via mitophagy in AML/melanoma, pro-survival in glioblastoma), neurodegenerative diseases (Parkinson’s and Alzheimer’s due to impaired mitophagy), and cardiopathies (ischemia-reperfusion injury).

Background

BNIP3L/NIX (BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like), also known as NIP3-like protein X, is a BH3-only member of the BCL-2 family that predominantly localizes to the mitochondrial outer membrane (OMM) through its C-terminal transmembrane ™ domain, but is also found on the endoplasmic and sarcoplasmic reticulum. BNIP3L contains an N-terminal LC3-interacting region (LIR) motif (WTHL, residues 34-37) vital for binding ATG8 family proteins such as LC3 and GABARAP, a central BH3 domain for interactions with anti-apoptotic BCL-2 proteins (e.g., BCL-xL), and a TM domain with a GxxxG motif (Gly204/208) important for SDS-resistant homodimerization. BNIP3L acts as a mitophagy receptor that recruits autophagosome machinery to damaged mitochondria via its LIR motif, enabling selective mitochondrial clearance independently of the PINK1/Parkin pathway, especially during erythroid maturation where it drives mitochondrial elimination for hemoglobinization, reticulocyte formation, and cardiac progenitor cell development. Dimerized BNIP3L, stabilized by hypoxia-induced HIF-1α, exposes the LIR to bind LC3, nucleates phagophores around mitochondria, triggers DRP1-mediated fission, and indirectly enhances autophagy by releasing Beclin-1 from BCL-2. Under severe stress, it can induce apoptosis via BAX/BAK activation and mitochondrial permeability transition, leading to ROS generation and necrosis. Dysregulation of BNIP3L is implicated in cancer (tumor suppression via mitophagy in AML/melanoma, pro-survival in glioblastoma), neurodegenerative diseases (Parkinson’s and Alzheimer’s due to impaired mitophagy), and cardiopathies (ischemia-reperfusion injury).

References
https://pubmed.ncbi.nlm.nih.gov/34930907/ https://pubmed.ncbi.nlm.nih.gov/40063005/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%