# ROLE OF C-SRC IN RETROVIRAL TRANSFORMATION

> **NIH NIH R01** · UNIVERSITY OF VIRGINIA · 1987 · $108,690

## Abstract

An increasing body of evidence suggests that the products of normal
cellular oncogenes (proto-oncogenes) participate in the biochemical
mechanisms by which cells regulate their own growth and differentiation.
The mechanism(s) by which viral oncogene products or structurally altered
cellular oncogene products disrupt the activity and functional interactions
of normal cellular proteins involved in growth regulation remains unclear.
Our preliminary evidence suggests that the activity of the product of the
src proto-oncogene, pp60c-src, is modulated in cells transformed by a
variety of agents, including retroviruses, DNA tumor viruses, and chemical
mutagens.  In addition, a similar modulation of c-src activity is seen when
normal cells are stimulated by growth factors or tumor promoters.  The
experiments outlined in this proposal focus on the function of pp60c-src in
normal growth regulation, and how this function is altered in
transformation.  We propose to utilize cellular-src specific monoclonal
antibodies to measure the tyrosine kinase activity of pp60c-src in cells
transformed by several families of retroviruses, DNA tumor viruses and
chemical agents as well as from transformed cells which have reverted to
the normal phenotype.  To determine the molecular basis for the observed
alterations in c-src activity from various transformed cells, we will
analyze c-src for chemical modifications such as
phosphorylations/dephosphorylations, for formation of complexes with viral
transforming proteins or cellular regulatory proteins, and for changes in
intracellular localization.  We also propose to investigate the effect of
alterations of c-src activity on its cellular substrates, such as
phosphatidyl inositol, and on various cellular target proteins.  Similar
studies will seek to define and analyze the modulation of c-src in cells
treated with growth factors and tumor promoters.  To gain insight into the
sequence of biochemical events which occur in such responses, we propose to
compare the time course of c-src modulation with the time course of
activation of growth factor receptors and protein kinase C, and the
phosphorylation of various intracellular target proteins.  To determine if
c-src plays a role in post-membrane events, we will follow its
intracellular localization as a function of time after stimulation and test
for possible alterations in substrate phosphorylations or substrate
specificities.  It is the ultimate aim of these studies to help define the
function of c-src, particularly as it relates to transmission of growth
signals from the cell membrane to the nucleus.

## Key facts

- **NIH application ID:** 3178410
- **Project number:** 5R01CA039438-03
- **Recipient organization:** UNIVERSITY OF VIRGINIA
- **SAM.gov UEI:** JJG6HU8PA4S5
- **Principal Investigator:** SARAH J PARSONS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $108,690
- **Award type:** 5
- **Project period:** 1985-04-01 → 1988-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3178410

## Citation

> US National Institutes of Health, RePORTER application 3178410, ROLE OF C-SRC IN RETROVIRAL TRANSFORMATION (5R01CA039438-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3178410. Licensed CC0.

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