Signal transduction by Ras and intervention by the Rap1A tumor suppressor gene

Jonathan Trent, H. N. Ananthaswamy

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

IN TUMORIGENESIS, c-ras gene alterations occur in the form of constitutively activating point mutations that uncouple the signal transduction pathway from external stimuli, resulting in a constant proliferative signal. Normal c-ras is activated by pathways consisting of growth factors, growth factor receptors, adapter molecules, and guanine nucleotide-releasing factors. Activated c-ras then recruits raf-1 to the plasma membrane resulting in its activation and initiation of the mitogen- activated protein (MAP) kinase cascade. Concurrent with the identification of pathway molecules, investigators have identified a number of methods to inhibit the effects of c-ras in tumor cells, including the rap1A tumor suppressor gene and dominant negative rasN17. Further identification of intracellular signaling molecules and methods to manipulate these pathways will be essential in the quest to develop effective anticancer agents.

Original languageEnglish
Pages (from-to)140-151
Number of pages12
JournalCancer Bulletin
Volume47
Issue number2
StatePublished - Jan 1 1995
Externally publishedYes

Fingerprint

Tumor Suppressor Genes
Signal Transduction
Guanine Nucleotide Exchange Factors
ras Genes
Growth Factor Receptors
Mitogen-Activated Protein Kinases
Point Mutation
Antineoplastic Agents
Intercellular Signaling Peptides and Proteins
Research Personnel
Cell Membrane
Neoplasms

ASJC Scopus subject areas

  • Cancer Research

Cite this

Signal transduction by Ras and intervention by the Rap1A tumor suppressor gene. / Trent, Jonathan; Ananthaswamy, H. N.

In: Cancer Bulletin, Vol. 47, No. 2, 01.01.1995, p. 140-151.

Research output: Contribution to journalArticle

Trent, J & Ananthaswamy, HN 1995, 'Signal transduction by Ras and intervention by the Rap1A tumor suppressor gene', Cancer Bulletin, vol. 47, no. 2, pp. 140-151.
Trent, Jonathan ; Ananthaswamy, H. N. / Signal transduction by Ras and intervention by the Rap1A tumor suppressor gene. In: Cancer Bulletin. 1995 ; Vol. 47, No. 2. pp. 140-151.
@article{d2531b82da30443fa4c7ef76de68c16f,
title = "Signal transduction by Ras and intervention by the Rap1A tumor suppressor gene",
abstract = "IN TUMORIGENESIS, c-ras gene alterations occur in the form of constitutively activating point mutations that uncouple the signal transduction pathway from external stimuli, resulting in a constant proliferative signal. Normal c-ras is activated by pathways consisting of growth factors, growth factor receptors, adapter molecules, and guanine nucleotide-releasing factors. Activated c-ras then recruits raf-1 to the plasma membrane resulting in its activation and initiation of the mitogen- activated protein (MAP) kinase cascade. Concurrent with the identification of pathway molecules, investigators have identified a number of methods to inhibit the effects of c-ras in tumor cells, including the rap1A tumor suppressor gene and dominant negative rasN17. Further identification of intracellular signaling molecules and methods to manipulate these pathways will be essential in the quest to develop effective anticancer agents.",
author = "Jonathan Trent and Ananthaswamy, {H. N.}",
year = "1995",
month = "1",
day = "1",
language = "English",
volume = "47",
pages = "140--151",
journal = "Cancer Bulletin",
issn = "0008-5448",
publisher = "Medical Arts Publishing",
number = "2",

}

TY - JOUR

T1 - Signal transduction by Ras and intervention by the Rap1A tumor suppressor gene

AU - Trent, Jonathan

AU - Ananthaswamy, H. N.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - IN TUMORIGENESIS, c-ras gene alterations occur in the form of constitutively activating point mutations that uncouple the signal transduction pathway from external stimuli, resulting in a constant proliferative signal. Normal c-ras is activated by pathways consisting of growth factors, growth factor receptors, adapter molecules, and guanine nucleotide-releasing factors. Activated c-ras then recruits raf-1 to the plasma membrane resulting in its activation and initiation of the mitogen- activated protein (MAP) kinase cascade. Concurrent with the identification of pathway molecules, investigators have identified a number of methods to inhibit the effects of c-ras in tumor cells, including the rap1A tumor suppressor gene and dominant negative rasN17. Further identification of intracellular signaling molecules and methods to manipulate these pathways will be essential in the quest to develop effective anticancer agents.

AB - IN TUMORIGENESIS, c-ras gene alterations occur in the form of constitutively activating point mutations that uncouple the signal transduction pathway from external stimuli, resulting in a constant proliferative signal. Normal c-ras is activated by pathways consisting of growth factors, growth factor receptors, adapter molecules, and guanine nucleotide-releasing factors. Activated c-ras then recruits raf-1 to the plasma membrane resulting in its activation and initiation of the mitogen- activated protein (MAP) kinase cascade. Concurrent with the identification of pathway molecules, investigators have identified a number of methods to inhibit the effects of c-ras in tumor cells, including the rap1A tumor suppressor gene and dominant negative rasN17. Further identification of intracellular signaling molecules and methods to manipulate these pathways will be essential in the quest to develop effective anticancer agents.

UR - http://www.scopus.com/inward/record.url?scp=0029035532&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029035532&partnerID=8YFLogxK

M3 - Article

VL - 47

SP - 140

EP - 151

JO - Cancer Bulletin

JF - Cancer Bulletin

SN - 0008-5448

IS - 2

ER -