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STAT‐1: a novel regulator of apoptosis
Author(s) -
Stephanou Anastasis,
Latchman David S.
Publication year - 2003
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.0959-9673.2003.00363.x
Subject(s) - stat , transactivation , microbiology and biotechnology , stat4 , phosphorylation , stat protein , biology , transcription factor , apoptosis , signal transduction , chemistry , stat3 , gene , biochemistry
Summary. Extracellular signalling molecules binding to their specific receptors are able to modulate gene expression, leading to changes in development, cell growth and homeostasis. The signal transducers and activators of transcription (STAT) protein family members are among the best studied of the latent cytoplasmic signal‐dependent transcription factors. The STAT factors are activated via phosphorylation on the C‐terminal domain following cytokine signalling or by various stress‐induced stimuli. Recently, STAT‐1 has been implicated in modulating pro‐ and anti‐apoptotic genes following several stress‐induced responses. These effects are dependent on STAT‐1 phosphorylation on serine‐727 and require the C‐terminal transactivation domain of STAT‐1 to enhance its pro‐apoptotic effect or inhibit its anti‐apoptotic effects. The STAT‐1 C‐terminal domain has been demonstrated to be important for protein–protein interaction with other transcriptional activators. The reports that STAT‐1‐deficient mice develop spontaneous and chemically induced tumours more rapidly compared to wild‐type mice and that STAT‐1‐deficient cells are more resistant to agents that induce apoptosis strongly support the argument that STAT‐1 acts as a tumour suppressor.