# MODULATION OF CELLULAR PHOSPHORYLATION BY TUMOR PROMOTER

> **NIH NIH R01** · UNIVERSITY OF CHICAGO · 1991 · $272,254

## Abstract

Tumor promoters accelerate the process of cellular transformation through
alteration of normal cellular growth and differentiation processes. One
approach that has yielded important information regarding the regulation
of growth factor receptors and the mechanisms by which tumor promoters act
is to study the interaction of tumor promoters with receptor systems.
Thapsigargin is a protein kinase C-independent tumor promoter that has
recently been shown to alter epidermal growth factor (EGF) receptor binding
and kinase activity. Evidence suggests that the response of the receptor
is due to activation by thapsigargin of a kinase that phosphorylates select
sites on the EGF receptor that differ from those phosphorylated by protein
kinase C. We now propose to identify these sites and to directly test their
role in the action of thapsigargin through site-directed mutagenesis
studies of the EGF receptor. We also plan to investigate the mechanism by
which thapsigargin stimulates kinase activation. These studies provide a
new approach to understanding the regulation of cellular receptors by
exogenous agents, and will lead to the elucidation of new signal
transduction pathways in the cell.

## Key facts

- **NIH application ID:** 3173127
- **Project number:** 2R01CA035541-08
- **Recipient organization:** UNIVERSITY OF CHICAGO
- **SAM.gov UEI:** ZUE9HKT2CLC9
- **Principal Investigator:** MARSHA R ROSNER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $272,254
- **Award type:** 2
- **Project period:** 1987-09-01 → 1995-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3173127

## Citation

> US National Institutes of Health, RePORTER application 3173127, MODULATION OF CELLULAR PHOSPHORYLATION BY TUMOR PROMOTER (2R01CA035541-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3173127. Licensed CC0.

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