# Mechanism behind blindness linked to excess glutamylation

> **NIH NIH F31** · WEST VIRGINIA UNIVERSITY · 2022 · $46,752

## Abstract

Abstract
Post-translational modification of proteins play an important role in increasing the complexity and functional
diversity of limited set of proteins expressed in the cell. One such interesting and highly significant chemical
modification is glutamylation. Protein glutamylation is a post-translational modification (PTM) that adds glutamate
to one of the glutamic residues in the C terminus of the protein. Protein Glutamylation is dynamic and controlled
by repertoire of enzymes, tubulin tyrosine ligase-Like (TTLLs) that add glutamyl group, and by another family of
enzymes called cytosolic carboxypeptidase (CCPs or AGBLs) that cleaves the glutamate.
Mutation in one member of deglutamylase family, AGBL5 is linked to inherited blindness in humans. While
glutamylation is thought to aid in trafficking of proteins, the mechanism behind the blindness linked to excess
glutamylation in not known. This proposal aims to investigate the consequences of excess glutamylation in the
rod and cone photoreceptors with a mouse model that lacks AGBL5.
This fellowship will help reach my long-term goal of understanding mechanisms behind diseases that afflict
humans. The findings from this study will advance our understanding of the mechanism underlying the genetic
blindness and human health.

## Key facts

- **NIH application ID:** 10485943
- **Project number:** 5F31EY031964-02
- **Recipient organization:** WEST VIRGINIA UNIVERSITY
- **Principal Investigator:** Rawaa Aljammal
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $46,752
- **Award type:** 5
- **Project period:** 2021-08-10 → 2023-08-09

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10485943

## Citation

> US National Institutes of Health, RePORTER application 10485943, Mechanism behind blindness linked to excess glutamylation (5F31EY031964-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10485943. Licensed CC0.

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