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Mechanisms of endosomal dysfunction in alcohol-related steatosis and liver injury

Award Number: F32AA032419
ORGANIZATION: NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 10/22/2026
PERIOD OF PERFORMANCE END DATE: 10/21/2027

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Mechanisms of endosomal dysfunction in alcohol-related steatosis and liver injury - Project Summary/Abstract My professional career goal is to conduct independent research in life sciences defining complex biological systems, including and specifically alcohol-associated liver disease (ALD). ALD is a progressive disease that can lead to irreversible and fatal liver damage in the form of inflammation, fibrosis, cirrhosis, and cancer. Unfortunately, therapeutic treatments for ALD are limited. This is in part due to the lack of understanding of ALD progression at the cellular level. The onset of ALD is represented by a reversible steatotic liver stage where lipid droplets (LDs) excessively accumulate within hepatocytes, the highly metabolizing cell type of the liver. This observation suggests chronic alcohol consumption prevents the breakdown of LDs. Previous studies have shown alcohol disrupts endocytic vesicle trafficking proteins, including Rab5, and LD catabolism; however, these cellular mechanisms of perturbation are poorly understood. Therefore, this proposal aims to elucidate the molecular mechanisms in which alcohol affects Rab5 and endocytic trafficking during ALD progression. Preliminary studies show alcohol disrupts Rab5 subcellular localization without affecting Rab5 activity. Altogether, the central hypothesis is alcohol disrupts Rab5 prenylation, a post-translational modification, to drive its altered localization. This will be tested by two specific aims. Aim 1 will define the impact of alcohol on Rab5 subcellular localization and remodeling of the endosome proteome. Aim 2 will determine the impact of alcohol on global changes in protein prenylation (prenyl-proteome) including Rab5. To accomplish these aims, I will acquire training in confocal microscopy and mass spectrometry. This new training will broaden my current skillsets regarding yeast cell culture and genetics, small molecule trafficking and signaling, the use and design of fluorescent biosensors, and inter-organelle communication. My strong advisory team, including my sponsor and co-sponsor Dr. Micah Schott and Dr. Carol Casey, respectively, one collaborator, and five other faculty have significant expertise in the proposed topics and the desired training objectives. The microscopy and mass spectrometry core facilities, and research environment at UNMC will enhance this research and training. Together, I will have the expertise and training needed to successfully accomplish these aims. The results gained from the proposed research will provide a mechanistic understanding of disrupted endocytic trafficking by alcohol in ALD.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $76,780 )
2026	2026	BOARD OF REGENTS OF THE UNIVERSITY OF NEBRASKA	4215 EMILE ST	OMAHA	NE	68105	DOUGLAS	USA	Alcohol Research Programs	000	1	4/28/2026	NEW	$76,780
														Subtotal = $76,780

Grand Total All Awards = $76,780

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Mechanisms of endosomal dysfunction in alcohol-related steatosis and liver injury

Award Number: F32AA032419

ORGANIZATION: NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 10/22/2026

PERIOD OF PERFORMANCE END DATE: 10/21/2027

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