Other Name(s): None
Drug Target Analysis Report Drug Target Analysis Report Content

About the Target

Based on the provided context information, key viewpoints regarding STAT1 can be summarized as follows:

Protein expression changes in vSCC tumors: Increased expression of STAT1 and proteasome proteins in vSCC tumors with a pushing morphology leads to activation of a signaling pathway associated with a lymphoplasmacytic stromal response, inhibiting tumor growth and aggressive behavior. In contrast, tumors with an infiltrative morphology have increased collagen expression and activation of integrin signaling, promoting tumor growth and aggressive behavior [1].

Interaction of STAT1beta with STAT1alpha: STAT1 can form different dimers, including alpha:alpha homodimers, beta:beta homodimers, and alpha:beta heterodimers. STAT1beta can bind to STAT1alpha to protect it from degradation, resulting in prolonged half-life of STAT1alpha and increased transcription activity [2].

IFN-gamma signaling and STAT1 involvement: IFN-gamma primes enhancers and promoters via recruitment of STAT1 and interferon regulatory factor 1 (IRF1), leading to increased histone acetylation and chromatin remodeling. IFN-gamma also induces the formation of latent enhancers by inducing transcription factors that cooperate with other proteins to form new enhancers [3].

HCMV-mediated suppression of type I interferon response: HCMV infection disrupts STAT1 phosphorylation and nuclear localization, inhibiting type I interferon signaling. This prevents the transcriptional activation of interferon-stimulated genes (ISGs) and facilitates viral immune escape from type I interferon [4].

ISG regulation by STAT1 and STAT2 in cancer cells: In BCR-ABL-expressing cells, STAT2 is partially phosphorylated, leading to ISG repression and lack of STAT1 induction. In JAK2V617F-positive cells, STAT2 can induce STAT1 expression and is essential for STAT1 phosphorylation upon IFN-alpha stimulation. The equilibrium of STAT1/STAT1 and STAT1/STAT3 dimers also varies depending on the amount of active STAT2 [5].

These key viewpoints present various aspects of STAT1 function and its involvement in different biological processes, such as tumor behavior, dimer formation, IFN-gamma signaling, viral immune evasion, and regulation of ISGs in cancer cells.
Based on the provided context information, some key viewpoints related to STAT1 are as follows:

The expression of STAT1 and UBC in LUAD tissue is significantly lower than in control tissue, and high expression of UBC and STAT1 can inhibit the development of LUAD [6].
During DENV infection, the phosphorylation of STAT1 is reduced, resulting in less viral progeny production. However, in DENV-antibody-dependent enhancement (ADE) infection, STAT1 phosphorylation is attenuated, leading to increased viral progeny production [7].
Hypoxia downregulates the type I IFN pathway, and it is independent of HIF1alpha. This mechanism involves the downregulation of STAT1 [8].
Mutating certain amino acids (Lys511 and Lys652) in STAT1 enhances the IFN-I response in vivo, including STAT1-Tyr701 phosphorylation and ISG expression [9].
PI3K signaling can repress the expression of MHC molecules and their induction by IFN-gamma, potentially through attenuating STAT1 protein levels and phosphorylation. Inhibiting PI3K or loss of PIK3CA can diminish the repressive effects and increase MHC expression, promoting CD4+ and/or CD8+ T-cell activation and anti-tumor immunity [10].

These key viewpoints provide insights into the regulation and function of STAT1 in different contexts, including cancer, viral infection, hypoxia, and immune response.

Figure [1]

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