SRC3 Antibody [G12J12] | Primary Antibodies

Application: Reactivity: Human

Lane 1: Daudi, Lane 2: HeLa, Lane 3: K562

Usage Information

Dilution
WB1:1000 - 1:10000 IHC1:50 - 1:100 IF1:50 - 1:100 FCM1:100 - 1:500

Application
WB, IHC, IF, 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
155 kDa

Positive Control	Human endometrium adenocarcinoma tissue; Daudi cells; HeLa cells; K562 cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
SRC3 Antibody [G12J12] detects endogenous levels of total SRC3 protein.

Clone
G12J12

Synonym(s)
AIB1; BHLHE42; RAC3; TRAM1; NCOA3; Nuclear receptor coactivator 3; NCoA-3; ACTR; Amplified in breast cancer 1 protein; AIB-1; pCIP; bHLHe42; RAC-3; SRC-3; TRAM-1

Background
Steroid receptor coactivator-3 (SRC-3/AIB1/NCoA3), a p160 family member, functions as a master transcriptional coactivator that integrates growth factor signals to potentiate the activity of nuclear receptors (ERα, PR, AR, PPARγ) and non-receptor transcription factors (E2F1, AP-1, NF-κB, STAT3), controlling gene expression in development, metabolism, and oncogenesis. SRC-3 features an N-terminal bHLH/PAS domain for nuclear localization (via a bipartite NLS) and E2F1 binding, a central receptor interaction domain (RID) with three LXXLL motifs forming α-helices for ligand-dependent nuclear receptor binding, and C-terminal AD1/AD2 domains that recruit CBP/p300 (for H3/H4 acetylation via Q-rich motifs and intrinsic HAT activity) and CARM1/PRMT1 (for H3R17/26 methylation), as well as a polyglutamine tract. SRC-3 is regulated by post-translational modifications (PTMs), including Ser503/505 phosphorylation by AKT (for protein stability), Ser736 by CDK7/RSK (for coactivation), and Ser847 by IKK (for cytoplasmic-nuclear shuttling). Upon growth factor stimulation (EGF/IGF-1), MAPK/PI3K cascades phosphorylate SRC-3 in sequence, increasing LXXLL-nuclear receptor affinity and enabling FoxA1/ER intragenic looping for early gene activation. This leads to chromatin opening (via AD1 acetylation), Pol II pause release (via AD2 methylation), mTOR-driven polyribosome translation of oncogenic mRNAs, and 4E-BP1-mediated repression of pro-inflammatory cytokines in macrophages. In regulatory T cells, synergy with Foxp3 reprograms hundreds of genes to promote tumor immunosuppression. The PTM code orchestrates SRC-3 turnover (MAPK priming, AKT stabilization, SCF-mediated ubiquitin degradation).

Background

Steroid receptor coactivator-3 (SRC-3/AIB1/NCoA3), a p160 family member, functions as a master transcriptional coactivator that integrates growth factor signals to potentiate the activity of nuclear receptors (ERα, PR, AR, PPARγ) and non-receptor transcription factors (E2F1, AP-1, NF-κB, STAT3), controlling gene expression in development, metabolism, and oncogenesis. SRC-3 features an N-terminal bHLH/PAS domain for nuclear localization (via a bipartite NLS) and E2F1 binding, a central receptor interaction domain (RID) with three LXXLL motifs forming α-helices for ligand-dependent nuclear receptor binding, and C-terminal AD1/AD2 domains that recruit CBP/p300 (for H3/H4 acetylation via Q-rich motifs and intrinsic HAT activity) and CARM1/PRMT1 (for H3R17/26 methylation), as well as a polyglutamine tract. SRC-3 is regulated by post-translational modifications (PTMs), including Ser503/505 phosphorylation by AKT (for protein stability), Ser736 by CDK7/RSK (for coactivation), and Ser847 by IKK (for cytoplasmic-nuclear shuttling). Upon growth factor stimulation (EGF/IGF-1), MAPK/PI3K cascades phosphorylate SRC-3 in sequence, increasing LXXLL-nuclear receptor affinity and enabling FoxA1/ER intragenic looping for early gene activation. This leads to chromatin opening (via AD1 acetylation), Pol II pause release (via AD2 methylation), mTOR-driven polyribosome translation of oncogenic mRNAs, and 4E-BP1-mediated repression of pro-inflammatory cytokines in macrophages. In regulatory T cells, synergy with Foxp3 reprograms hundreds of genes to promote tumor immunosuppression. The PTM code orchestrates SRC-3 turnover (MAPK priming, AKT stabilization, SCF-mediated ubiquitin degradation).

References
https://pubmed.ncbi.nlm.nih.gov/37711895/ https://pubmed.ncbi.nlm.nih.gov/16539836/

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%