We have updated our privacy policy. If you have any question, contact us at privacy@scicrunch.org. Dismiss and don't show again

Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Regulation of STAT3 by direct binding to the Rac1 GTPase.

Science (New York, N.Y.) | Oct 6, 2000

The signal transducers and activators of transcription (STAT) transcription factors become phosphorylated on tyrosine and translocate to the nucleus after stimulation of cells with growth factors or cytokines. We show that the Rac1 guanosine triphosphatase can bind to and regulate STAT3 activity. Dominant negative Rac1 inhibited STAT3 activation by growth factors, whereas activated Rac1 stimulated STAT3 phosphorylation on both tyrosine and serine residues. Moreover, activated Rac1 formed a complex with STAT3 in mammalian cells. Yeast two-hybrid analysis indicated that STAT3 binds directly to active but not inactive Rac1 and that the interaction occurs via the effector domain. Rac1 may serve as an alternate mechanism for targeting STAT3 to tyrosine kinase signaling complexes.

Pubmed ID: 11021801 RIS Download

Mesh terms: Amino Acid Substitution | Animals | COS Cells | Cell Line | Cercopithecus aethiops | DNA-Binding Proteins | Enzyme Activation | Epidermal Growth Factor | Gene Expression Regulation | Genes, Reporter | Genetic Vectors | Guanine Nucleotide Exchange Factors | Humans | Janus Kinase 2 | Mutation | Neoplasm Proteins | Phosphorylation | Phosphoserine | Phosphotyrosine | Protein-Tyrosine Kinases | Proteins | Proto-Oncogene Proteins | Rats | STAT3 Transcription Factor | Signal Transduction | Trans-Activators | Transfection | Two-Hybrid System Techniques | rac1 GTP-Binding Protein

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIGMS NIH HHS, Id: GM-54304
  • Agency: NHLBI NIH HHS, Id: K08-HL-03547
  • Agency: NIDDK NIH HHS, Id: P30-DK34928

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.