# HUMAN MYELOID CHEMOTACTIC RECEPTOR: STRUCTURE-FUNCTION

> **NIH NIH R01** · DUKE UNIVERSITY · 1988 · $182,339

## Abstract

The leukocyte form peptide receptor recognizes a product of bacterial
metabolism and mediates leukocyte responses to microbial invasion.  The
long term objective is to define the biochemical pathway of this response.
This proposal will focus on signal transduction via the formyl peptide
receptor.  Activation of phospholipase C appears to be the earliest
measurable biochemical consequence of receptor occupancy.  Diacylglycerol
and inositol trisphosphate are generated; the former activates protein
kinase C, the latter releases Ca2+ from intracellular stores.  We have
developed a novel assay to measure absolute levels of diacylglycerol in
biological samples.  This assay will be used to measure diacylglycerol
levels in leukocytes after stimulation with formyl peptides and other
agonists.  The fatty acid composition, subcellular location and metabolism
of the diacylglycerols will be determined.  The role of diacylglycerol in
receptor desensitization will be explored.  An assay will be developed for
measuring formyl peptide-stimulated diacylglycerol production in membranes
and the role of a GTP binding protein in this process will be investigated.
Synthetic dioctanoylglycerol causes both degranulation and oxidative burst,
while didecanoylglycerol causes only degranulation.  We will compare these
compounds with regard to C kinase translocation and [32P] phosphoprotein
changes induced in intact leukocytes.  This may allow distinction between
phosphoproteins involved in each response.  The formyl peptide receptor
will be purified by established techniques and the purified product
compared with the receptor identified by affinity labeling.  The proposal
is health related because defects in leukocyte function result in recurrent
infections.  Many other cell surface receptors utilize diacylglycerol as a
second messenger, so information obtained from these studies will have wide
application to mechanisms of neoplastic transformation, wound healing and
vascular disease.

## Key facts

- **NIH application ID:** 3127834
- **Project number:** 5R01AI018308-08
- **Recipient organization:** DUKE UNIVERSITY
- **SAM.gov UEI:** TP7EK8DZV6N5
- **Principal Investigator:** JAMES E NIEDEL
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $182,339
- **Award type:** 5
- **Project period:** 1981-08-01 → 1991-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3127834

## Citation

> US National Institutes of Health, RePORTER application 3127834, HUMAN MYELOID CHEMOTACTIC RECEPTOR: STRUCTURE-FUNCTION (5R01AI018308-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3127834. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*