ABIN1 as a modulator of innate immune signaling via toll-like receptors (TLRS)

Active Project Grant Awarded Last action

Award ID
F32AI200292
Recipient
Awarding agency
Obligated
$76,780

Award facts

Assistance listing
93.855 Allergy and Infectious Diseases Research
Completion date 0% complete
Place of performance
Salt Lake City, UT 84112, USA

Award details come from USAspending.gov.

Description

As the agency reported it.

Abstract
Toll-like receptors (TLR) play a key role in the innate immune system through the direct recognition of pathogen components. TLR signaling leads to inflammation, and this response is carefully balanced to protect against pathogens while protecting the host organism from excess inflammation. Excess TLR signaling can lead to exaggerated inflammation, driving inflammatory disease and even leading to autoimmune disorders such as systemic lupus erythematosus (SLE). The protein ABIN1 is an anti-inflammatory protein in the TLR signaling pathway that has been genetically linked with SLE. The kinase TBK1 has been shown to phosphorylate ABIN1, causing transient ABIN1 degradation through autophagy and leading to increased inflammatory signaling. Interestingly, we and others have observed that ABIN1 inhibits TBK1 activity. However, the molecular mechanisms underlying ABIN1'S anti-inflammatory activity remain unclear. We hypothesize that ABIN1 and TBK1 represent a new signaling circuit that balances inflammatory signaling in TLR-stimulated inflammation. To explore this hypothesis, I will define how ABIN1 modulates TBK1 activity through post- translational modifications and characterize how these modifications affect TBK1 kinase activity and ABIN1 autophagy. Next, I will explore if ABIN1 regulates selective autophagy of TLR signaling components, using a highly selective and sensitive form of proximity-dependent labeling and quantitative proteomics to identify ABIN1 interactions in macrophages. Under the training provided in this fellowship, I will gain techniques and knowledge associated with innate immunology, while preparing for a future career as an independent academic researcher. The resources provided in the haecker lab and the university of utah will provide me with ample opportunity to develop my scientific writing, presentation, and mentoring skills, while conducting impactful research focused on the molecular regulation of TLR biology. This work will provide new insight into how molecular events regulate TLR biology, identifying new therapeutic targets for autoimmune diseases like SLE and inflammatory disorders.

Quick answers

Who received award F32AI200292?

F32AI200292 was awarded to University Of Utah by National Institute of Allergy and Infectious Diseases (National Institutes of Health) on December 1, 2026.

How much is award F32AI200292 worth?

$76,780 has been obligated on F32AI200292.

On GovTribe

See this award's full record

  • Every transaction and subaward
  • The recipient's other awards and teaming partners
  • Similar grant awards
  • Ask GovTribe AI about this award
Try for free Login