NIH-funded research R01 grant

Rhes‑SUMO pathway's role in Huntington's disease

Official title: Rhes-SUMO Pathway in Huntington Disease

Funded at Florida Atlantic University · NIH-11299742 · Data updated 2026-11-12

This work looks at whether the Rhes‑SUMO protein system increases toxic huntingtin and helps it spread in the brain, which may explain early striatal damage in people with Huntington's disease.

Quick facts

Grant typeR01 grant
Study typeNIH-funded research
Funding institutionFlorida Atlantic University
NIH-funded
Lab location1 site (Boca Raton, United States)
Project startSeptember 21, 2022
Project endAugust 31, 2028
Funding year2024
Award (this year)$119,008
NIH project number7R01NS128225-04
Project IDNIH-11299742 on NIH RePORTER

Who could benefit from this research

Could help

People who carry the HTT gene mutation — either diagnosed with Huntington's disease or pre-symptomatic carriers — are the patients most relevant to this research.

Less likely to help

People without the HTT mutation or those looking for immediate clinical treatments are unlikely to benefit directly because this is laboratory and animal-focused work.

What this research studies

Researchers are focusing on two molecules — Rhes and SUMO1 — that seem to change levels and spread of mutant huntingtin protein in the brain. They will use cell models and a genetically accurate mouse model of HD to track how Rhes and SUMO1 affect huntingtin movement between neurons and its buildup. The team will test whether reducing SUMO signaling or removing SUMO1 lowers toxic huntingtin and improves brain structure and behavior in the animal model. Results are intended to point to targets that could be used to slow striatal damage and limit spread of the disease.

Why it matters

Potential benefit: If successful, this work could point to new ways to lower toxic huntingtin or block its spread, potentially leading to therapies that slow or prevent Huntington's progression.

How similar studies have gone: Previous preclinical studies have shown Rhes interacts with mutant huntingtin and that reducing SUMO1 can improve outcomes in HD mouse models, so there is encouraging lab-based evidence but no proven human therapies yet.

Where this research is happening

  • Florida Atlantic University
    Boca Raton, United States
    Active

Researchers

  • Principal investigator: Subramaniam, Srinivasa — Florida Atlantic University
  • Study coordinator: Subramaniam, Srinivasa

Related research

Other NIH-funded projects on the same topics.

About this research

  1. This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
  2. Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
  3. For full project details, budget, and progress reports, visit the official NIH RePORTER page.
Last reviewed 2026-11-14 by the Find a Trial editorial team. Information on this page is for educational purposes and is not medical advice. Always consult qualified healthcare professionals about clinical trial participation.