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Stat2 Is a Transcriptional Activator That Requires Sequence-specific Contacts Provided by Stat1 and p48 for Stable Interaction with DNA*
It is shown that Stat2 is capable of forming a stable homodimer that interacts with p48, can be recruited to DNA, and can activate transcription, raising a question of why Stat1 is required. Expand
Combinatorial association and abundance of components of interferon-stimulated gene factor 3 dictate the selectivity of interferon responses.
The IFN gamma response was dependent on the ISRE and was accentuated by preexposure of cells to IFN alpha, a treatment that increases the abundance of ISGF3 components, and ifN gamma-induced activation of this complex, preferentially formed at high concentrations of p48 and STAT91, may explain some of the overlapping responses toIFN alpha and IFN Gamma. Expand
STAT activation and differential complex formation dictate selectivity of interferon responses.
It is hypothesized that other IRF members could serve as adapter proteins for the STATs during IFN responses to redirect them to subsets of ISRE, GAS and/or IRE-containing IFN-stimulated genes (ISGs). Expand
The unique role of STAT2 in constitutive and IFN-induced transcription and antiviral responses.
The unique role of STAT2 is described in differential complex formation of unphosphorylated and phosphorylated ISGF3 components that direct constitutive and IFN-I-stimulated transcriptional responses. Expand
A Positive Feedback Amplifier Circuit That Regulates Interferon (IFN)-Stimulated Gene Expression and Controls Type I and Type II IFN Responses
Predicting the existence of a multifaceted intracellular amplifier circuit that depends on unphosphorylated and phosphorylated ISGF3 and GAF complexes and IRF1 and providing a molecular explanation for the existing overlap between IFn-I and IFN-II activated ISG expression. Expand
Targeted inhibition of STATs and IRFs as a potential treatment strategy in cardiovascular disease
A pipeline approach is proposed that combines comparative in silico docking of STAT-SH2 and IRF-DBD models with in vitro STAT andIRF activation inhibition validation, as a novel tool to screen multi-million compound libraries and identify specific inhibitors for STATs and IRFs. Expand
Expression of pre-selected TMEMs with predicted ER localization as potential classifiers of ccRCC tumors
The massive down-regulation of expression of TMEM family members suggests their importance in the pathogenesis of ccRCC and the bioinformatic analysis ofTMEM topology implies a significant involvement of ER proteins inccRCC pathology. Expand
STAT1-Dependent Signal Integration between IFNγ and TLR4 in Vascular Cells Reflect Pro-Atherogenic Responses in Human Atherosclerosis
This study provides evidence to suggest that in ECs and VSMCs STAT1 orchestrates a platform for cross-talk between IFNγ and TLR4, and identifies a STAT1-dependent gene signature that reflects a pro-atherogenic state in human atherosclerosis. Expand
STAT2/IRF9 directs a prolonged ISGF3-like transcriptional response and antiviral activity in the absence of STAT1
It is proved that IFNα-activated STAT2/IRF9 induces a prolonged ISGF3-like transcriptome and generates an antiviral response in the absence of STAT1, and the existence of ‘STAT2/ IRF9-specific’ target genes predicts a novel role of STAT2 in IFN α signalling. Expand
ISGF3γ p48, a specificity switch for interferon activated transcription factors
Abstract Interferon (IFN) induces gene expression by phosphorylating latent transcription factors of the STAT family. Two different STAT multimeric complexes that bind distinct enhancer elements areExpand