World Library  
Flag as Inappropriate
Email this Article

V-Src

Article Id: WHEBN0009895213
Reproduction Date:

Title: V-Src  
Author: World Heritage Encyclopedia
Language: English
Subject: Gag-onc fusion protein, Oncogenes, Geldanamycin, Viral transformation
Collection:
Publisher: World Heritage Encyclopedia
Publication
Date:
 

V-Src

src p60-SRC phosphoprotein
Identifiers
Organism
Symbol src
Entrez 1491925
RefSeq (Prot) NP_056888.1
UniProt O92806
Other data
EC number 2.7.10.2
Chromosome viral: 0.01 - 0.01 Mb

v-Src is a gene found in Rous sarcoma virus that encodes a tyrosine kinase that causes a type of cancer in chickens.

The src gene is oncogenic as it triggers uncontrolled growth in abnormal host cells. It was the first retroviral oncogene to be discovered.[1] The src gene was taken up by RSV and incorporated into its genome conferring it with the advantage of being able to stimulate uncontrolled mitosis of host cells, providing abundant cells for fresh infection.

The src gene is not essential for RSV proliferation but it greatly increases virulence when present.

Contents

  • Discovery 1
  • Function 2
  • See also 3
  • References 4

Discovery

Francis Peyton Rous first proposed that viruses can cause cancer. He proved it in 1911 and was later awarded the Nobel prize in 1966. Chickens grow a tumor called a fibrosarcoma. Rous collected and ground up these sarcomas, and then centrifuged them to remove the solid material. Next, the remaining liquid mixture was injected into chicks. The chicks developed sarcomas. The causative agent in the liquid was a virus, this is now called the Rous sarcoma virus (RSV).

Function

Further research done later on by others showed that RSV was a type of retrovirus. It was found that the v-Src gene in RSV is required for the formation of cancer.[2]

A function for Src tyrosine kinases in normal cell growth was first demonstrated with the binding of family member p56lck to the cytoplasmic tail of the CD4 and CD8 co-receptors on T-cells.[3] Src tyrosine kinases also transmit integrin-dependent signals central to cell movement and proliferation. Hallmarks of v-Src induced transformation are rounding of the cell and the formation of actin rich podosomes on the basal surface of the cell. These structures are correlated with increased invasiveness, a process thought to be essential for metastasis.

v-Src lacks the C-terminal inhibitory phosphorylation site (tyrosine-527), and is therefore constitutively active as opposed to normal Src (c-Src) which is only activated under certain circumstances where it is required (e.g. growth factor signaling). v-Src is therefore an instructive example of an oncogene whereas c-Src is a proto-oncogene.

The first sequence of v-Src was published in 1980[4] and the characterization of sites for tyrosine phosphorylation in the transforming protein of Rous sarcoma virus and its normal cellular homologue was published in 1981.[5]

See also

References

  1. ^ Vogt PK (September 2012). "Retroviral oncogenes: a historical primer". Nat. Rev. Cancer 12 (9): 639–48.  
  2. ^ Stehelin D, Fujita DJ, Padgett T, Varmus HE, Bishop JM. (1977). "Detection and enumeration of transformation-defective strains of avian sarcoma virus with molecular hybridization". Virology 76 (2): 675–84.  
  3. ^ Rudd CE, Trevillyan JM, Dasgupta JD, Wong LL, Schlossman SF (July 1988). "The CD4 receptor is complexed in detergent lysates to a protein-tyrosine kinase (pp58) from human T lymphocytes". Proc. Natl. Acad. Sci. U.S.A. 85 (14): 5190–4.  
  4. ^ Czernilofsky AP, Levinson AD, Varmus HE, Bishop JM, Tischer E, Goodman HM (September 1980). "Nucleotide sequence of an avian sarcoma virus oncogene (src) and proposed amino acid sequence for gene product". Nature 287 (5779): 198–203.  
  5. ^ Smart JE, Oppermann H, Czernilofsky AP, Purchio AF, Erikson RL, Bishop JM (October 1981). "Characterization of sites for tyrosine phosphorylation in the transforming protein of Rous sarcoma virus (pp60v-src) and its normal cellular homologue (pp60c-src)". Proc. Natl. Acad. Sci. U.S.A. 78 (10): 6013–7.  
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.