# Role of Muc1 in the b-catenin Response to Acute Kidney Injury

> **NIH NIH K01** · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · 2021 · $54,000

## Abstract

Project summary/abstract
Dr. Al-bataineh’s career goals for the award period are to develop a research project and professional
expertise that will enable him to develop scientific independence from his mentor and to establish his own
career path to independent translational research in acute kidney injury. Dr. Al-bataineh will further his
laboratory research and training by developing his proficiency in (i) validated animal models of renal injury
including the two-kidney hanging-weight mouse model of ischemia-reperfusion injury (IRI), and mouse model
of AKI-CKD progression, (ii) advanced approaches of kidney microscopy including multiphoton microscopy,
three-dimensional imaging, and quantitative microscopic analyses, and (iii) technical expertise in molecular
biology techniques such as ChIPseq and promoter-luciferase reporter assays. Dr. Al-bataineh plans to make
the transition to an independent, tenure track position within 2-3 years of his mentored research training during
this award. His long-term career goal is to become a fully independent academic investigator in the broad fields
of renal physiology and kidney disease, performing research that provides insight into fundamental
physiological problems that impact clinical issues, with a particular focus on AKI pathology, prevention, and
treatment. -catenin signaling is a complex cellular response that is activated in renal tubules during kidney
injury. While moderate ischemia results in transient induction of -catenin levels that associated with kidney
protection, severe ischemia leads to sustained activation of the -catenin pathway and development of kidney
fibrosis, implicating severity of injury as a key determinant of long term outcome. Emerging evidence supports
a role for the transmembrane glycoprotein mucin 1 (MUC1 in humans, Muc1 in animals) in regulating -catenin
activity. In tumor cells, (i) MUC1 directly binds to -catenin in the cytoplasm and nucleus, (ii) MUC1 blocks
glycogen synthase kinase 3 (GSK3)-mediated degradation of -catenin, and (iii) MUC1 overexpression
correlates with increased levels of nuclear -catenin and its transcriptional activity. We previously reported that
Muc1, found on the apical surface of normal kidney epithelia, plays a protective role in a mouse model of
ischemia-reperfusion injury (IRI) by comparing kidney function and morphology in Muc1 KO mice and congenic
control mice (AJP-Renal 2015; PMID: 25925251). Our recent studies showed that Muc1 induction and
targeting to the nucleus after moderate ischemia was associated with increased -catenin levels and signaling
(AJP-Renal 2016; PMID: 26739894). We also observed that sustained upregulation of Muc1 was also
associated with prolonged induction of -catenin in mouse kidney homogenates at 7 d after severe ischemia.
Based on these findings and on previous reports related to the acute and chronic effects of -catenin after
kidney injury, we hypothesize that Muc1 protects against the early stages of A...

## Key facts

- **NIH application ID:** 10323751
- **Project number:** 3K01DK109038-05S1
- **Recipient organization:** UNIVERSITY OF PITTSBURGH AT PITTSBURGH
- **Principal Investigator:** Mohammad Al-bataineh
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $54,000
- **Award type:** 3
- **Project period:** 2016-09-15 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10323751

## Citation

> US National Institutes of Health, RePORTER application 10323751, Role of Muc1 in the b-catenin Response to Acute Kidney Injury (3K01DK109038-05S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10323751. Licensed CC0.

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