# Structural basis of BBSome-mediated ciliary exit

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2021 · $688,587

## Abstract

PROJECT SUMMARY
Primary cilia organize signaling pathways such as vision, olfaction and Hedgehog signaling. Proper functioning
of these pathways is critically dependent on the movements of molecules into, inside and out of cilia, yet our
understanding of the basic mechanisms governing trafficking through cilia remains fragmentary. Past work
from the lab identified and characterized the BBSome, a protein complex that ferries signaling receptors out of
cilia and clears photoreceptor outer segments of unwanted proteins. The relevance of the BBSome to human
health and disease is evidence by the fact that BBSome dysfunction causes Bardet-Biedl Syndrome (BBS), a
hereditary disease characterized by obesity, retinal degeneration, polydactyly and kidney malformations.
The major goal of this proposal is to determine the structure and function of the molecular cogs and levers
within the BBSome that enable selective removal of proteins from cilia. The proposed studies will cast new light
on ciliary trafficking and lay the basis of future therapeutic interventions.

## Key facts

- **NIH application ID:** 10161785
- **Project number:** 5R01EY031462-02
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Maxence V Nachury
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $688,587
- **Award type:** 5
- **Project period:** 2020-06-01 → 2024-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10161785

## Citation

> US National Institutes of Health, RePORTER application 10161785, Structural basis of BBSome-mediated ciliary exit (5R01EY031462-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10161785. Licensed CC0.

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