Escorting STAT5A

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Escorting STAT5A

ome transcription factors take a chaperone to the nuclear dance. On page 469, Williams et al. show that STAT5A gets this escort from the ERBB4 receptor tyrosine kinase. ERBB4 becomes an escort upon activation by growth factors such as heregulin (HRG). The activated receptor is known to recruit and phos-phorylate STAT5A and get cleaved, thus releasing ERBB4's intracellular domain (4ICD). William...

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Escorting Ras

Ras proteins are best known to function on the plasma membrane to mediate growth factor signaling. Controlling the length of time that Ras proteins stay on the plasma membrane is an effective way to properly modulate the intensity and duration of growth factor signaling. It has been shown previously that H- and N-Ras proteins in the GTP-bound state can be ubiquitylated via a K-63 linkage, which...

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Dataset of STAT5A status in breast cancer

We analysed STAT5A gene expression in breast cancer using the Oncomine database. We exemplify four representative studies showing that STAT5A is generally downregulated in breast cancer.

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Structure of the unphosphorylated STAT5a dimer.

STAT proteins have the function of signaling from the cell membrane into the nucleus, where they regulate gene transcription. Latent mammalian STAT proteins can form dimers in the cytoplasm even before receptor-mediated activation by specific tyrosine phosphorylation. Here we describe the 3.21-A crystal structure of an unphosphorylated STAT5a homodimer lacking the N-terminal domain as well as t...

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Constitutively active Stat5A and Stat5B promote adipogenesis.

OBJECTIVE The metabolic syndrome is an important social problem affecting many people in developed countries. Obesity is a leading cause of this syndrome, hence understanding molecular mechanisms underlying obesity is of prime importance for preventive medicine to develop novel methods to alleviate the corresponding social cost as well as for pharmaceutical companies to develop antimetabolic dr...

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ژورنال

عنوان ژورنال: Journal of Cell Biology

سال: 2004

ISSN: 1540-8140,0021-9525

DOI: 10.1083/jcb1673iti1