# MOLECULAR MECHANISMS FOR LIPOCORTIN GENE EXPRESSION

> **NIH NIH R01** · UNIVERSITY OF FLORIDA · 1988 · $117,330

## Abstract

The formation of prostaglandins is inhibited by anti-inflammatory
steroids in intact cells and isolated organs by specifically
hindering release of polyunsaturated fatty acid precursors, namely
arachidonic acid.  The inhibitory action of steroids is a
consequence of RNA and protein synthesis.  This acute anti-
inflammatory activity has been correlated to steroid- dependent
induction and release of phospholipase inhibitory proteins, which
directly inhibit arachidonic acid release.  Independently isolated
proteins have been shown to be closely related and designated
lipocortin.

Full length cDNAs coding for human lipocortin I and II (also called
calpactin) have recently been isolated.  The purpose of this
research is to undertake a high resolution analysis of the normal
and glucocorticoid-mediated mechanisms which control the
regulation of lipocortin I gene expression in vivo in the mouse,
which offers established genetics, the direct analysis of animal
tissues, and a wide variety of appropriate cell lines.  The primary
strategy of the proposal is as follows:  1) The initial goal is the
isolation and total characterization of a complete murine cDNA
and genomic clone by restriction and DNA sequence analysis; 2)
The evaluation of tissue-specific transcription and the level of
glucocorticoid-mediated transcriptional control; 3) The
delineation of the promoter boundaries via the generation of
deletion mutants of the lipocortin 5' flanking sequence, fusion to a
reporter gene coding sequence, and assaying by transient
expression and/or in stable transformants; 4) The investigation of
lipocortin chromatin structure using DNase I hypersensitive
studies; 5) The study of lipocortin gene regulation at nucleotide
resolution by directly scanning relevant sequences in vivo to
detect protein-DNA interactions using the laboratories expertise
in genomic sequencing.  These studies are also of medical
relevance because lipocortin expression has been correlated to
rheumatic diseases such as arthritis and systemic lupus
erythematosus and through its steroid-mediated control of
prostaglandin synthesis, a vital aspect in the inflammatory
response.

## Key facts

- **NIH application ID:** 3158086
- **Project number:** 5R01AR037353-02
- **Recipient organization:** UNIVERSITY OF FLORIDA
- **SAM.gov UEI:** NNFQH1JAPEP3
- **Principal Investigator:** HARRY S NICK
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $117,330
- **Award type:** 5
- **Project period:** 1987-07-01 → 1990-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3158086

## Citation

> US National Institutes of Health, RePORTER application 3158086, MOLECULAR MECHANISMS FOR LIPOCORTIN GENE EXPRESSION (5R01AR037353-02). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3158086. Licensed CC0.

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