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NOBEL PRIZE 2026

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NIHNATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESR01

Cell specific Partitioning Defective Par1a/b deletion effects on renal repair

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Institution
ALBERT EINSTEIN COLLEGE OF MEDICINE, NY
Principal investigator
Kimberly Jean Reidy
Funding
$382K
Duration
2021–2026
Open portfolio

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Abstract

Abstract We will study the role of serine threonine kinases Partitioning defective (Par) 1a and 1b in adaptive and maladaptive repair following tubular injury. In studies by our laboratory of the developing kidney, dual loss of Par1a and 1b impaired Notch activation: this demonstrated for the first time a link between Par1 and Notch signaling. We hypothesize: Par1a/b kinases are activated in proliferating progenitor cells by kidney injury and regulate Jag1-Notch dependent and independent pro-fibrotic pathways. Using inducible cell specific deletion of both Par1a/b in mice, we will test effect of Par1a/b on Notch activation and progenitor cells following injury. We will investigate the mechanisms underlying the novel Par1-Notch link. Our specific aims are: 1) Show that Par1a/b regulates the response to kidney tubule injury via the Notch pathway; and 2) Demonstrate that Par1a/b in tubular progenitor cells promotes maladaptive repair.

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R01NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESPathobiology of Kidney Disease Study Section[PBKD]maladaptivekidneynotchpartitioningprogenitor cellsprogenitortubularcell specific

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