Cell Signaling

Dr. Suresh K. Alahari (salaha@lsuhsc.edu)
- Associate Professor
Performs research investigating the role of Nischarin in breast tumor progression. Current studies are identifying proteins that interact with Nischarin in breast cancer cells using proteomics as well as yeast two-hybrid approaches. A detailed understanding of the mechanistic basis of tumor cell migration and invasion can significantly advance the development of new therapeutics that stop tumor growth and metastasis. Click here to learn more about Dr. Alahari's research.

Dr. Arthur L. Haas (ahaas@lsuhsc.edu)
- Professor and Chairman
Ubiquitin conjugation targets proteins for degradation. Ubiquitin conjugation is a fundamental cellular process that has been implicated in gene regulation, DNA repair, stress response, cell cycle progression, various forms of muscle atrophy, and Alzheimers dementia. Dr. Haas has identified a second constitutive system within cells that is parallel but distinct from ubiquitin in which the 15 kDa interferon-like protein ISG15/UCRP is conjugated to a smaller subset of intracellular targets. The conjugation of ISG15 to intracellular targets functions to regulate protein-protein interactions. The Haas laboratory is interested in characterization of the enzymes involved in the respective conjugation reactions; structure-function analysis of these enzymes; and examining the roles of ubiquitin and ISG15 conjugation in cellular regulation. Click here to learn more about Dr. Haas's research.

Dr. Kim Brint Pedersen (kpeder@lsuhsc.edu)
- Assistant Professor
Whole-body fuel metabolism is integrated by signals derived from the nervous system, by hormones, and by the availability of circulating substrates. If defects in this signaling occur, metabolic diseases such as diabetes can arise. As signals of the fed and fasted states, the hormones insulin and glucagon elicit signal transduction cascades giving rise to appropriate biological effects in different cell types. An elevated concentration of glucose is another signal of the fed state that can elicit changes in gene expression, e.g. in pancreatic beta-cells and in hepatocytes. The laboratory does research on glucose regulation of genes involved in intermediary metabolism such as the gene encoding the catalytic subunit of glucose-6-phosphatase.

Dr. Wayne V. Vedeckis (wvedec@lsuhsc.edu)
- Professor
Steroid hormone action; structure, function, and genomic interactions of glucocorticoid receptor proteins; steroid hormone regulation of proto-oncogene expression and cellular proliferation. The glucocorticoid receptor (GR) is a hormone-activated transcription factor that regulates the expression of many genes in various cell types. Glucocorticoid hormone treatment of non-apoptotic cells causes down-regulation of GR expression [Barrett, Vig, and Vedeckis, Biochemistry 35, 9746-9753, (1996)], which may desensitize the cell to hormone to maintain homeostasis. Interestingly, glucocorticoid hormone treatment has the opposite effect on several types of immune cells. Glucocorticoid hormone up-regulates GR expression in immature T-cells, thymocytes, and leukemic T-lymphoblasts which undergo terminal differentiation and apoptosis in response to the hormone [Barrett, Vig, and Vedeckis, Biochemistry 35, 9746-9753, (1996)]. Dr. Vedeckis' research is focused on understanding the differential regulation of the the glucocorticoid receptor in different cell types. To this end, they have isolated, cloned and characterized sequences upstream of the human GR gene [Breslin and Vedeckis, J. Steroid Biochem. Molec. Biol. 67, 369-381, (1998) and references therein] and discovered that there are five different untranslated exon 1 sequences spliced to the GR mRNA protein coding sequences (which begin in exon 2) [Breslin, Geng, and Vedeckis, Mol. Endocrinol 15, 1381-1395, (2001)]. These five primary transcripts arise from the alternative usage of three promoters plus alternative splicing. The discovery of this new GR promoter and exon has significant medical relevance. Click here to learn more about Dr. Vedeckis' research.