 |
about | Maps & Directions | contact | admissions | faculty | alumni & development | library | Tech Support Center | dean's office | Policies & Procedures |
 Site Map
|
|
about | Maps & Directions | contact | admissions | faculty | alumni & development | library | Tech Support Center | dean's office | Policies & Procedures |
 |
 |
 |
FAculty directory
M. Alexandra Monroy, PhD
Assistant Professor, Anatomy and Cell Biology Assistant Professor, Surgery Telephone: 215-707-1898 Fax: 215-707-8820 Email: amonroy@temple.edu
Department of Anatomy and Cell BiologyDepartment of Surgery
Dr. Monroy's overall research interest is to understand the signaling mechanisms involved in specific gene regulation.
Regulation of the Prostate Specific Antigen (PSA) Promoter by the cofactor SRCAP.
The expression of PSA is induced by androgens and regulated by the androgen receptor (AR) which is a nuclear receptor. Recently many cofactors implicated in the transcriptional activation by nuclear receptors have been identified and include factors that alter chromatin structure. Local alteration of chromatin structure is necessary to facilitate promoter accessibility. Distinct multiprotein complexes exist that affect local chromatin structure through nucleosome interaction and modulation. The novel protein SRCAP (SNF2-related CBP Activator Protein) was identified by virtue of its interaction with the histone acetyl transferase, CBP (CREB Binding Protein). SRCAP has an ATPase domain and is believed to be involved in chromatin remodeling. It functions as a coactivator for various nuclear receptors including the androgen receptor. The goal of this project is to determine the role that SRCAP plays in PSA gene regulation induced by androgen.
Regulation of macrophage inflammatory marker expression by ligands of peroxisome proliferator-activated receptor- gamma (PPAR gamma ).
PPAR gamma is a ligand-activated transcription factor that belongs to the nuclear receptor superfamily. It is required for adipocyte differentiation, and it regulates the expression of many genes involved in metabolism. However, in macrophages it has been shown to trans-repress the expression of inflammatory genes such as TNFalpha, iNOS and COX-2 which are induced by lipopolysaccharide (LPS). It is believed that PPAR gamma inhibits gene expression in a DNA-binding independent manner. It inhibits signaling pathways such as NF-kappaB and AP-1 which are required for inflammatory gene activation. Recently it was shown that activation of PPAR gamma in macrophages retains corepressor complexes at the iNOS promoter and prevents expression of this gene in response to LPS. Using chromatin immunoprecipitation (ChIP) assays we are examining histone modifications induced by PPAR gamma activation at various promoters. The goal of this project is to determine the mechanisms by which PPAR gamma activation downregulates expression of inflammatory genes in splenic macrophages in a murine trauma model, and in human monocyte cell lines.
|
|
