World Library  
Flag as Inappropriate
Email this Article

Rheb

Article Id: WHEBN0001297298
Reproduction Date:

Title: Rheb  
Author: World Heritage Encyclopedia
Language: English
Subject: Tuberous sclerosis, Tuberous sclerosis protein
Collection:
Publisher: World Heritage Encyclopedia
Publication
Date:
 

Rheb

Ras homolog enriched in brain
PDB rendering based on 1xtq.
Available structures
PDB Ortholog search: RCSB
Identifiers
RHEB Gene
RNA expression pattern

GTP-binding protein Rheb also known as Ras homolog enriched in brain (RHEB) is a protein that in humans is encoded by the RHEB gene.[1]

Function

Rheb is a recently discovered member of the Ras superfamily that may be involved in neural plasticity. This function is novel and not typically associated with the Ras proteins.

This gene is a member of the small GTPase superfamily and encodes a lipid-anchored, cell membrane protein with five repeats of the RAS-related GTP-binding region. This protein is vital in regulation of growth and cell cycle progression due to its role in the insulin / TOR / S6K signaling pathway. The protein has GTPase activity and shuttles between a GDP-bound form and a GTP-bound form, and farnesylation of the protein is required for this activity. Three pseudogenes have been mapped, two on chromosome 10 and one on chromosome 22.[2]

Interactions

RHEB has been shown to interact with C-Raf,[3][4][5] Mammalian target of rapamycin,[3][6][7][8] TSC2,[3][9][10][11][12][13] Ataxia telangiectasia mutated,[3] KIAA1303[3] and Ataxia telangiectasia and Rad3 related.[3]

References

Further reading

External links

  • Medical Subject Headings (MeSH)

This article incorporates text from the United States National Library of Medicine, which is in the public domain.


This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and USA.gov, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for USA.gov and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
 
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
 
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.
 


Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.