GRIM19 Antibody [J7L19] | Primary Antibodies

Application: Reactivity: Human

Lane 1: Daudi, Lane 2: TT, Lane 3: HepG2, Lane 4: VCaP

Usage Information

Dilution
WB1:1000

Application
WB

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
16 kDa

Datasheet & SDS

Biological Description

Specificity
GRIM19 Antibody [J7L19] detects endogenous levels of total GRIM19 protein.

Clone
J7L19

Synonym(s)
NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 13; Gene associated with retinoic and interferon-induced mortality 19 protein; GRIM-19; NDUFA13

Background
GRIM19, also known as NDUFA13, serves as an integral nuclear-encoded subunit of mitochondrial complex I within the NADH:ubiquinone oxidoreductase assembly, essential for electron transfer from NADH to ubiquinone during oxidative phosphorylation and maintenance of mitochondrial membrane potential. The protein adopts a compact helical bundle structure anchored peripherally to the matrix arm of complex I, positioning its LYR motif to stabilize the Q-module and facilitate conformational coupling between FMN reduction and quinone binding pocket dynamics that drive proton pumping across the inner membrane. Upregulation by type I interferons and retinoic acid through IRF/STAT promoter elements recruits GRIM19 to antagonize STAT3 dimerization by direct binding to its phosphotyrosine tail, blocking nuclear translocation and transcriptional activation of survival genes like c-Myc and Bcl-xL while sensitizing cells to apoptosis via Bax oligomerization. GRIM19 coordinates iron-sulfur cluster relay from the N-module through conformational gating that prevents ROS leakage during reverse electron transport, intersecting with NLRP3 inflammasome regulation, where its depletion elevates mtROS to activate caspase-1 and gasdermin D pore formation, amplifying IL-1β/IL-33 secretion in macrophages and hepatocytes. Loss disrupts fetal hematopoietic stem cell differentiation and adult quiescence through SHP-1/TGF-β axis impairment, while in parietal cells, GRIM19 deficiency triggers ROS-NRF2-HO-1-NF-κB signaling to license NLRP3-dependent spasmolytic polypeptide-expressing metaplasia. Overexpression promotes brown adipose differentiation by shifting PPARγ coactivator-1α toward thermogenic programs, countering diet-induced obesity.

Background

GRIM19, also known as NDUFA13, serves as an integral nuclear-encoded subunit of mitochondrial complex I within the NADH:ubiquinone oxidoreductase assembly, essential for electron transfer from NADH to ubiquinone during oxidative phosphorylation and maintenance of mitochondrial membrane potential. The protein adopts a compact helical bundle structure anchored peripherally to the matrix arm of complex I, positioning its LYR motif to stabilize the Q-module and facilitate conformational coupling between FMN reduction and quinone binding pocket dynamics that drive proton pumping across the inner membrane. Upregulation by type I interferons and retinoic acid through IRF/STAT promoter elements recruits GRIM19 to antagonize STAT3 dimerization by direct binding to its phosphotyrosine tail, blocking nuclear translocation and transcriptional activation of survival genes like c-Myc and Bcl-xL while sensitizing cells to apoptosis via Bax oligomerization. GRIM19 coordinates iron-sulfur cluster relay from the N-module through conformational gating that prevents ROS leakage during reverse electron transport, intersecting with NLRP3 inflammasome regulation, where its depletion elevates mtROS to activate caspase-1 and gasdermin D pore formation, amplifying IL-1β/IL-33 secretion in macrophages and hepatocytes. Loss disrupts fetal hematopoietic stem cell differentiation and adult quiescence through SHP-1/TGF-β axis impairment, while in parietal cells, GRIM19 deficiency triggers ROS-NRF2-HO-1-NF-κB signaling to license NLRP3-dependent spasmolytic polypeptide-expressing metaplasia. Overexpression promotes brown adipose differentiation by shifting PPARγ coactivator-1α toward thermogenic programs, countering diet-induced obesity.

References
https://pubmed.ncbi.nlm.nih.gov/15367666/ https://pubmed.ncbi.nlm.nih.gov/27659873/

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%