NFAT3 Antibody [H15F22] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Lane 1: A204, Lane 2: A10, Lane 3: Hela

Usage Information

Dilution
WB1:1000

Application
WB

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

Predicted MW
120-140 kDa

Positive Control	A204 cells; A10 cells; HeLa cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
NFAT3 Antibody [H15F22] detects endogenous levels of total NFAT3 protein.

Clone
H15F22

Synonym(s)
Nuclear factor of activated T-cells, cytoplasmic 4; NF-ATc4; NFATc4; T-cell transcription factor NFAT3; NFATC4; NFAT3

Background
NFAT3 (NFATc4), a nuclear factor of activated T-cells (NFAT) family transcription factor predominantly expressed in T cells, B cells, and cardiac myocytes, contains an intrinsically disordered N-terminal regulatory domain with serine-rich regions (SRR) and SP-repeat motifs that serve as calcineurin docking sites, a central Rel homology region (RHR) immunoglobulin-like fold with a DNA-binding domain recognizing GGAAA consensus sequences and a nuclear localization signal (NLS), and a C-terminal transactivation domain (TAD) that recruits CBP/p300 coactivators. Upon T cell receptor (TCR) or GPCR stimulation, increased cytosolic Ca2+ activates calmodulin-bound calcineurin, which dephosphorylates 14 conserved serine residues in the SRR/SP regions, exposing the NLS and enabling nuclear translocation of NFAT3. In the nucleus, NFAT3 homodimerizes or cooperates with partners like AP-1 (c-Fos/c-Jun), GATA3, or MEF2 to transactivate cytokine genes (IL-2, IL-4, TNF-α) and FasL at composite NFAT:AP-1 sites, while in cardiomyocytes, it drives pathological hypertrophy by inducing BNP and MHCα gene expression. Nuclear export and cytoplasmic sequestration are restored by rephosphorylation through GSK3β, CK1, or PKA. Uniquely, NFAT3 represses cell cycle progression and promotes apoptosis in neurons via Trim17 induction, in contrast to the pro-death role of NFAT4; deficiency of NFAT3 impairs Th2 differentiation and IgE responses. Dysregulated nuclear hyperactivation of NFAT3 contributes to rheumatoid arthritis synovial inflammation, cardiac hypertrophy and failure under pressure overload, and B cell lymphomas through constitutive IL-2 signaling.

Background

NFAT3 (NFATc4), a nuclear factor of activated T-cells (NFAT) family transcription factor predominantly expressed in T cells, B cells, and cardiac myocytes, contains an intrinsically disordered N-terminal regulatory domain with serine-rich regions (SRR) and SP-repeat motifs that serve as calcineurin docking sites, a central Rel homology region (RHR) immunoglobulin-like fold with a DNA-binding domain recognizing GGAAA consensus sequences and a nuclear localization signal (NLS), and a C-terminal transactivation domain (TAD) that recruits CBP/p300 coactivators. Upon T cell receptor (TCR) or GPCR stimulation, increased cytosolic Ca2+ activates calmodulin-bound calcineurin, which dephosphorylates 14 conserved serine residues in the SRR/SP regions, exposing the NLS and enabling nuclear translocation of NFAT3. In the nucleus, NFAT3 homodimerizes or cooperates with partners like AP-1 (c-Fos/c-Jun), GATA3, or MEF2 to transactivate cytokine genes (IL-2, IL-4, TNF-α) and FasL at composite NFAT:AP-1 sites, while in cardiomyocytes, it drives pathological hypertrophy by inducing BNP and MHCα gene expression. Nuclear export and cytoplasmic sequestration are restored by rephosphorylation through GSK3β, CK1, or PKA. Uniquely, NFAT3 represses cell cycle progression and promotes apoptosis in neurons via Trim17 induction, in contrast to the pro-death role of NFAT4; deficiency of NFAT3 impairs Th2 differentiation and IgE responses. Dysregulated nuclear hyperactivation of NFAT3 contributes to rheumatoid arthritis synovial inflammation, cardiac hypertrophy and failure under pressure overload, and B cell lymphomas through constitutive IL-2 signaling.

References
https://pubmed.ncbi.nlm.nih.gov/9143705/ https://pubmed.ncbi.nlm.nih.gov/27100893/

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%