Associate Provost for Research Boston University Medical Campus
NIDDK - National Institute of Diabetes & Digestive & Kidney Diseases	Research Resources

Abstract

Abstract: DESCRIPTION (provided by applicant): Goals: The overall goals of this application are to examine the role of a the 13-catenin-Lef signaling pathway in contributing to the alterations in gene expression associated with acute renal injury and to elucidate the role of this pathway in modulating events associated with recovery of renal function. Specific aims Each specific aims will test one of three interrelated hypotheses: Specific aim 1: To test the hypothesis that ATP depletion-repletion activates the Beta-catenin Lef pathway in cultured proximal tubular cells. Specific aim 2: To examine our hypothesis that ATP depletion-repletion results in beta-catenin-Lef mediated activation of gene expression. Specific aim 3: To test our hypothesis that the Beta-catenin-lef-1 pathway alone or in association with NF-kappB inhibits apoptosis induced by ATP depletion-repletion. Long-term goals: To elucidate the mechanisms involved in the process of recovery and repair from acute renal failure (ARF). Significance: Elucidation of the mechanisms involved in recovery and repair may lead to insight that facilitate the development of therapeutic interventions that promote recovery from ARF.

Thesaurus Terms:
acute renal failure, adenosine triphosphate, cadherin, cellular pathology, renal ischemia /hypoxia, renal tubule
apoptosis, basement membrane, cell cell interaction, gene expression, lithium, nuclear factor kappa beta, phosphorylation, regeneration, transcription factor
tissue /cell culture, transfection

Institution:	BOSTON MEDICAL CENTER
	ONE BOSTON MEDICAL CENTER PLACE
	BOSTON, MA 02118
Fiscal Year:	2005
Department:
Project Start:	01-JUL-1998
Project End:	31-MAY-2007
ICD:	NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
IRG:	GMB