ELK Biotechnology Stat1 (Acetyl Lys410/K413) rabbit pAb

Stat1 (Acetyl Lys410/K413) rabbit pAb

제품 정보

세포 내 위치 (Cellular Localization)

Cytoplasm and nucleus. Translocated into the nucleus upon tyrosine phosphorylation and dimerization in response to IFN-gamma and FGFR signaling. Monomethylation at Lys-525 is required for phosphorylation at Tyr-701 and nuclear translocation. Also translocates to the nucleus upon interferon-beta stimulation.

Background

Defects in STAT1 are associated with Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:209950], also known as familial disseminated atypical mycobacterial infection. This condition predisposes to infections by BCG vaccine strains, environmental mycobacteria, and Mycobacterium tuberculosis. In severe cases, patients may die in early childhood due to overwhelming infection, while others develop later, curable tuberculoid granulomas.
STAT1 defects can also cause STAT1 deficiency [MIM:600555], leading to susceptibility to mycobacterial or viral diseases.

Function

STAT1 mediates signaling by interferons (IFNs). Upon IFN-α/β binding, Jak kinases (TYK2, JAK1) activate STAT1 and STAT2 via tyrosine phosphorylation, forming the ISGF3 complex with IRF-9 that translocates to the nucleus and activates interferon-stimulated genes.
In response to IFN-γ, STAT1 is phosphorylated on tyrosine and serine residues, forming a homodimer (GAF) that binds to the GAS element to induce antiviral gene expression.

Post-Translational Modifications (PTM)

• Phosphorylation: On Tyr-701 and Ser-727 upon IFN-α, IFN-γ, PDGF, EGF stimulation.
• Sumoylation: By SUMO1/2/3, enhanced by IFN-γ-induced phosphorylation on Ser-727 and interaction with PIAS proteins.
• Functional impact: Phosphorylation and sumoylation regulate STAT1 activation, nuclear translocation, and transcriptional activity.

Similarity & Structure

• Belongs to the STAT transcription factor family
• Contains one SH2 domain

Subunit Interaction

• Isoform α forms homodimers upon IFN-γ-induced phosphorylation
• Heterodimerizes with STAT2 upon IFN-α/β stimulation
• Interacts with NMI, viral proteins (Sendai virus, Nipah virus, rabies virus), and HCV core protein
• Interacts with PIAS1, which inhibits STAT1 activation upon Ser-727 phosphorylation