Stat1 Antibody [G13B13] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IP1:100 IHC1:400 - 1:1600 IF1:400 - 1:1600 CHIP1:50

Application
WB, IP, IHC, IF, ChIP

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
84 kDa, 91 kDa

Datasheet & SDS

Biological Description

Specificity
Stat1 (D4Y6Z) Rabbit mAb detects endogenous levels of total Stat1 protein.

Clone
G13B13

Synonym(s)
Signal transducer and activator of transcription 1-alpha/beta; Transcription factor ISGF-3 components p91/p84; STAT1

Background
STAT1, or Signal Transducer and Activator of Transcription 1, is a key member of the seven-member STAT family of cytokine-inducible transcription factors and plays a central role in mediating interferon (IFN) signaling to regulate gene expression. STAT1 primarily exists as two isoforms: STAT1α (750 amino acids, 91 kDa) and STAT1β (84 kDa splice variant). It is activated in response to type I (IFNα/β), type II (IFNγ), and type III IFNs, as well as IL-27, through JAK kinase-mediated phosphorylation at Tyr701. This activation leads to homodimerization (as GAF in response to IFNγ) or heterotrimerization with STAT2 and IRF9 (forming ISGF3 for type I/III IFNs), nuclear translocation, and binding to gamma-activated sites (GAS; TTCN2-4GAA). STAT1 is composed of an N-terminal domain, a coiled-coil domain (which can harbor mutations such as E235G or K278E), a DNA-binding domain (affected by mutations like P329L or T385M), a linker domain with a conserved motif (W-Ψ-D/E-x-Ψ-Ψ-D/E-Ψ-Ψ-K, with critical residues E559 and E563 for DNA orientation and dissociation, and K567 for GAS recognition via interaction with the DNA phosphodiester backbone), an SH2 domain, and a transactivation domain where Ser727 phosphorylation further enhances transcriptional activity. STAT1 is essential for antiviral and antimycobacterial defence, immune regulation (with Th17 impairment in gain-of-function, or GOF, states), and the transcription of interferon-stimulated genes (ISGs), such as GBP1, IFIT2, IRF1, APOL6, and OAS1. Unphosphorylated STAT1 (U-STAT1) also sustains baseline ISG expression. Dysregulation of STAT1 has significant disease implications: GOF mutations (over 100 identified, typically heterozygous) cause chronic mucocutaneous candidiasis, autoimmunity (including hypothyroidism and cytopenias), vascular problems (like aneurysms), and increased risk of malignancy (such as squamous cell carcinoma), largely via heightened STAT1 phosphorylation, impaired IL-17 responses, and variable ISG induction. Conversely, loss-of-function mutations lead to increased susceptibility to viral and mycobacterial infections. Aberrant STAT1 activation can promote therapy resistance, with phosphorylation at Ser727 (often mediated by p38 MAPK) maximally enhancing gene induction under conditions of cellular stress.

Background

STAT1, or Signal Transducer and Activator of Transcription 1, is a key member of the seven-member STAT family of cytokine-inducible transcription factors and plays a central role in mediating interferon (IFN) signaling to regulate gene expression. STAT1 primarily exists as two isoforms: STAT1α (750 amino acids, 91 kDa) and STAT1β (84 kDa splice variant). It is activated in response to type I (IFNα/β), type II (IFNγ), and type III IFNs, as well as IL-27, through JAK kinase-mediated phosphorylation at Tyr701. This activation leads to homodimerization (as GAF in response to IFNγ) or heterotrimerization with STAT2 and IRF9 (forming ISGF3 for type I/III IFNs), nuclear translocation, and binding to gamma-activated sites (GAS; TTCN2-4GAA). STAT1 is composed of an N-terminal domain, a coiled-coil domain (which can harbor mutations such as E235G or K278E), a DNA-binding domain (affected by mutations like P329L or T385M), a linker domain with a conserved motif (W-Ψ-D/E-x-Ψ-Ψ-D/E-Ψ-Ψ-K, with critical residues E559 and E563 for DNA orientation and dissociation, and K567 for GAS recognition via interaction with the DNA phosphodiester backbone), an SH2 domain, and a transactivation domain where Ser727 phosphorylation further enhances transcriptional activity. STAT1 is essential for antiviral and antimycobacterial defence, immune regulation (with Th17 impairment in gain-of-function, or GOF, states), and the transcription of interferon-stimulated genes (ISGs), such as GBP1, IFIT2, IRF1, APOL6, and OAS1. Unphosphorylated STAT1 (U-STAT1) also sustains baseline ISG expression. Dysregulation of STAT1 has significant disease implications: GOF mutations (over 100 identified, typically heterozygous) cause chronic mucocutaneous candidiasis, autoimmunity (including hypothyroidism and cytopenias), vascular problems (like aneurysms), and increased risk of malignancy (such as squamous cell carcinoma), largely via heightened STAT1 phosphorylation, impaired IL-17 responses, and variable ISG induction. Conversely, loss-of-function mutations lead to increased susceptibility to viral and mycobacterial infections. Aberrant STAT1 activation can promote therapy resistance, with phosphorylation at Ser727 (often mediated by p38 MAPK) maximally enhancing gene induction under conditions of cellular stress.

References
https://pubmed.ncbi.nlm.nih.gov/41394881/ https://pubmed.ncbi.nlm.nih.gov/18574148/

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%