GATA4 Antibody [J18F23] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Lane 1: Mouse testis, Lane 2: Rat testis

Usage Information

Dilution
WB1:1000 IP1:30 IHC1:500 IF1:50 FCM1:500

Application
WB, IP, IHC, IF, FCM

Reactivity
Human, Mouse, Rat

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

Observed MW
56 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	Mouse testis tissue; Mouse P7 ovary tissue; Rat P7 testis tissue; Rat P7 ovary tissue; Mouse P7 testis tissue; Human testis tissue; Mouse stomach; Rat testis tissue; Mouse testis tissue; Huh7 cells
Negative Control	Mouse colon; Human skeletal muscle tissue; Rat skeletal muscle tissue; Mouse skeletal muscle tissue; HeLa cells

Datasheet & SDS

Biological Description

Specificity
GATA4 Antibody [J18F23] detects endogenous levels of total GATA4 protein.

Clone
J18F23

Synonym(s)
Gata-4; Gata4; Transcription factor GATA-4; GATA-binding factor 4

Background
GATA4 is a zinc finger transcription factor essential for cardiogenesis, endoderm specification, and gonadal development. It contains two adjacent C2H2-type zinc fingers (N-finger: residues 217–241; C-finger: 271–295) that cooperatively recognize the (A/T)GATA(A/G) consensus DNA motif through synergistic hydrogen bonding and base readout. These zinc fingers are flanked by two N-terminal transcriptional activation domains, TAD1 (aa 1–74) and TAD2 (aa 130–177), which recruit CBP/p300 histone acetyltransferases and the MED23 Mediator subunit, as well as a nuclear localization signal (NLS, aa 271–325), and a C-terminal inhibitory region subject to sumoylation at Lys366 for activity modulation. Upon BMP/TGF-β or Wnt signaling, GATA4 forms enhanceosome complexes via C-finger protein-protein interfaces with partners such as NKX2-5, TBX5, GATA6, HAND2, and SRF, driving chromatin looping at cardiac super-enhancers and transactivating target genes like Nppa (ANF), Acta2 (smooth muscle actin), and Myh6 through combinatorial promoter/enhancer occupancy. GSK3β-mediated phosphorylation at Ser105 within TAD1 disrupts DNA binding and triggers CRM1-dependent nuclear export, while PI3K/AKT pathway-driven acetylation at Lys311/318/320/322 by p300/Cdk9 enhances transcriptional synergy. GATA4 cooperates with GATA6 to maintain epithelial integrity via villin and TFF3 expression in primitive endoderm. Heterozygous GATA4 mutations that disrupt zinc finger structure (G296S, V274D) abolish NKX2-5 synergy, resulting in congenital heart defects such as atrial septal defects, tetralogy of Fallot, and dilated cardiomyopathy due to impaired cardiac morphogenesis. Somatic GATA4 amplifications promote gastric cancer progression through GATA6/KLF5 crosstalk and drive hepatic stellate cell activation in fibrosis by enhancing H3K27ac at profibrotic loci.

Background

GATA4 is a zinc finger transcription factor essential for cardiogenesis, endoderm specification, and gonadal development. It contains two adjacent C2H2-type zinc fingers (N-finger: residues 217–241; C-finger: 271–295) that cooperatively recognize the (A/T)GATA(A/G) consensus DNA motif through synergistic hydrogen bonding and base readout. These zinc fingers are flanked by two N-terminal transcriptional activation domains, TAD1 (aa 1–74) and TAD2 (aa 130–177), which recruit CBP/p300 histone acetyltransferases and the MED23 Mediator subunit, as well as a nuclear localization signal (NLS, aa 271–325), and a C-terminal inhibitory region subject to sumoylation at Lys366 for activity modulation. Upon BMP/TGF-β or Wnt signaling, GATA4 forms enhanceosome complexes via C-finger protein-protein interfaces with partners such as NKX2-5, TBX5, GATA6, HAND2, and SRF, driving chromatin looping at cardiac super-enhancers and transactivating target genes like Nppa (ANF), Acta2 (smooth muscle actin), and Myh6 through combinatorial promoter/enhancer occupancy. GSK3β-mediated phosphorylation at Ser105 within TAD1 disrupts DNA binding and triggers CRM1-dependent nuclear export, while PI3K/AKT pathway-driven acetylation at Lys311/318/320/322 by p300/Cdk9 enhances transcriptional synergy. GATA4 cooperates with GATA6 to maintain epithelial integrity via villin and TFF3 expression in primitive endoderm. Heterozygous GATA4 mutations that disrupt zinc finger structure (G296S, V274D) abolish NKX2-5 synergy, resulting in congenital heart defects such as atrial septal defects, tetralogy of Fallot, and dilated cardiomyopathy due to impaired cardiac morphogenesis. Somatic GATA4 amplifications promote gastric cancer progression through GATA6/KLF5 crosstalk and drive hepatic stellate cell activation in fibrosis by enhancing H3K27ac at profibrotic loci.

References
https://pubmed.ncbi.nlm.nih.gov/22449843/ https://pubmed.ncbi.nlm.nih.gov/11585926/

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%