NUR77 Antibody [J10J24] | Primary Antibodies

Application: Reactivity: Human

Lane 1: HeLa, Lane 2: HeLa (MG-132, 10µM, 6 h)

Usage Information

Dilution
WB1:1000 IP1:30 FCM1:500

Application
WB, IP, FCM

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
64 kDa 32 kDa,38 kDa,60-80 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	Jurkat cells (TPA, 40nM; A-23187, 2uM, 4 h); Jurkat cells (TPA, 40nM, A-23187, 2uM; MG-132, 10uM, 4 h); HeLa cells (MG-132, 10uM, 6h)
Negative Control	HeLa cells; Jurkat cells

Datasheet & SDS

Biological Description

Specificity
NUR77 Antibody [J10J24] detects endogenous levels of total NUR77 protein.

Clone
J10J24

Synonym(s)
GFRP1; HMR; NAK1; NR4A1; Nuclear receptor subfamily 4 group A member 1; Early response protein NAK1; Nuclear hormone receptor NUR/77; Orphan nuclear receptor HMR; Orphan nuclear receptor TR3; ST-59; Testicular receptor 3; Nur77

Background
NUR77 (NR4A1, TR3, NGFI-B) is an orphan nuclear receptor and immediate-early gene product that acts as a ligand-independent transcription factor rapidly induced by stress, growth factors, and apoptotic signals to regulate cell fate decisions in immunity, metabolism, and tumorigenesis. NUR77 has a canonical nuclear receptor architecture with an intrinsically disordered N-terminal A/B transactivation domain (AF-1) rich in phosphorylation sites, a central C-domain DNA-binding domain containing two zinc-finger motifs that recognize NBRE (AAAGGTCA) elements as a monomer or DR5 sites as RXR heterodimers, a flexible D-hinge region with nuclear localization signals, and a C-terminal E/F ligand-binding domain (aa 351–598) that lacks a classical hydrophobic pocket but supports AF-2 coactivator recruitment and homo/heterodimerization. Mechanistically, various kinases (ERK, JNK, PKC) phosphorylate the N-terminal domain to enhance transactivation and promote mitochondrial translocation, where NUR77 exposes a BH3-like motif to convert anti-apoptotic Bcl-2 into a pro-apoptotic conformer that releases cytochrome c and activates caspases. In the nucleus, NUR77 upregulates FasL, TRAIL, and TRAIL receptor expression to amplify extrinsic apoptosis, inhibits NF-κB p65 via direct interaction to suppress inflammation, and coactivates SREBP or PPARγ to balance lipogenesis and β-oxidation in metabolic tissues, while TCR-induced NUR77 enforces T-cell negative selection by sensitizing thymocytes to Bim-mediated apoptosis. NUR77 deficiency accelerates atherosclerosis through unchecked NF-κB-driven inflammation and foam cell formation, promotes autoimmunity by impairing T-cell apoptosis, and enhances chemical hepatocarcinogenesis. Overexpression or ligand activation suppresses tumor growth in prostate, lung, and ovarian cancers by restoring apoptosis.

Background

NUR77 (NR4A1, TR3, NGFI-B) is an orphan nuclear receptor and immediate-early gene product that acts as a ligand-independent transcription factor rapidly induced by stress, growth factors, and apoptotic signals to regulate cell fate decisions in immunity, metabolism, and tumorigenesis. NUR77 has a canonical nuclear receptor architecture with an intrinsically disordered N-terminal A/B transactivation domain (AF-1) rich in phosphorylation sites, a central C-domain DNA-binding domain containing two zinc-finger motifs that recognize NBRE (AAAGGTCA) elements as a monomer or DR5 sites as RXR heterodimers, a flexible D-hinge region with nuclear localization signals, and a C-terminal E/F ligand-binding domain (aa 351–598) that lacks a classical hydrophobic pocket but supports AF-2 coactivator recruitment and homo/heterodimerization. Mechanistically, various kinases (ERK, JNK, PKC) phosphorylate the N-terminal domain to enhance transactivation and promote mitochondrial translocation, where NUR77 exposes a BH3-like motif to convert anti-apoptotic Bcl-2 into a pro-apoptotic conformer that releases cytochrome c and activates caspases. In the nucleus, NUR77 upregulates FasL, TRAIL, and TRAIL receptor expression to amplify extrinsic apoptosis, inhibits NF-κB p65 via direct interaction to suppress inflammation, and coactivates SREBP or PPARγ to balance lipogenesis and β-oxidation in metabolic tissues, while TCR-induced NUR77 enforces T-cell negative selection by sensitizing thymocytes to Bim-mediated apoptosis. NUR77 deficiency accelerates atherosclerosis through unchecked NF-κB-driven inflammation and foam cell formation, promotes autoimmunity by impairing T-cell apoptosis, and enhances chemical hepatocarcinogenesis. Overexpression or ligand activation suppresses tumor growth in prostate, lung, and ovarian cancers by restoring apoptosis.

References
https://pubmed.ncbi.nlm.nih.gov/30272297/ https://pubmed.ncbi.nlm.nih.gov/33634114/

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

Tech Support

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

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%