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

> **NIH NIH R01** · ALBERT EINSTEIN COLLEGE OF MEDICINE · 2024 · $403,893

## 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.

## Key facts

- **NIH application ID:** 10748365
- **Project number:** 5R01DK131176-03
- **Recipient organization:** ALBERT EINSTEIN COLLEGE OF MEDICINE
- **Principal Investigator:** Kimberly Jean Reidy
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $403,893
- **Award type:** 5
- **Project period:** 2021-12-01 → 2025-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10748365

## Citation

> US National Institutes of Health, RePORTER application 10748365, Cell specific Partitioning Defective Par1a/b deletion effects on renal repair (5R01DK131176-03). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10748365. Licensed CC0.

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