# Abnormal STAT3 Signaling and Aberrant O-Glycosylation of IgA1 in IgA Nephropathy

> **NIH NIH K01** · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2021 · $152,704

## Abstract

Project Summary/Abstract
The purpose of this proposal for the K01 Administrative Supplemental Award from the NIDDK is to enhance
the learning and research skills of the applicant in order to transition into an independent investigator. The
justification portion of this proposal outlines the critical timeframes that the COVID-19 restrictions occurred
under, and how this led to ceased production when manuscripts and grant preliminary data was being
generated. The research portion of this proposal is focused on the mechanisms of autoantigen production in
IgA nephropathy (IgAN), and how the applicant will finish critical experiments necessary for a successful R01-
A1 submission.
 The goal of the applicant is to become an independent investigator, and as a current assistant
professor this will require more training and time. This will be accomplished through collaboration with mentors
who have extensive experience in molecular biology research, and execution of experiments listed in the
research strategy. The university has exceptional core programs set up to help young investigators with finding
and writing grants, obtaining proper collaborative expertise, research training programs, and lab management
courses.
 IgAN is an autoimmune disease, which leads to decreased kidney function, with 40-50% of patients
requiring dialysis and/or transplantation. In this autoimmune disease, B cells from the immune system produce
IgA1 that has an aberrant glycosylation (termed Gd-IgA1) that causes the body to recognize IgA1 as a foreign
antigen. The autoantigen, Gd-IgA1, is elevated in IgAN patients and forms the basis for immune-complex
formation, which deposits in the kidney, leading to progressive kidney damage. The aims of this proposal are
to identify mechanisms responsible for elevated Gd-IgA1 production in patient B cells after cytokine exposure.
Identification of specific glycosylation enzymes that are differentially regulated and over activation signal
transducer and activator of transcription 3 (STAT3) by cytokines in IgAN patient B cells has provided us with a
strong starting point. We propose to investigate mechanisms responsible for altered signaling in IgAN patients,
thereby providing a bases for future drug development to reduce autoantigen production.

## Key facts

- **NIH application ID:** 10384158
- **Project number:** 3K01DK106341-05S1
- **Recipient organization:** UNIVERSITY OF ALABAMA AT BIRMINGHAM
- **Principal Investigator:** Colin Robert Reily
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $152,704
- **Award type:** 3
- **Project period:** 2015-08-01 → 2022-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10384158

## Citation

> US National Institutes of Health, RePORTER application 10384158, Abnormal STAT3 Signaling and Aberrant O-Glycosylation of IgA1 in IgA Nephropathy (3K01DK106341-05S1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10384158. Licensed CC0.

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