Official websites use .gov

A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS

A lock ( 🔒 ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

Need Help

Molecular Mechanisms of ABL Kinase 2 in the Pathogenesis of Alcohol-Associated Liver Disease

Award Number: R01AA032952
ORGANIZATION: NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 01/31/2031

Group Awards By:

View Award Description

Molecular Mechanisms of ABL Kinase 2 in the Pathogenesis of Alcohol-Associated Liver Disease - Abstract Alcohol-associated liver disease (ALD) is one of the primary causes of chronic liver disease worldwide and cirrhosis-associated deaths in the United States. Current treatments for ALD are not satisfactory. Novel therapeutic strategies are desperately needed. Understanding molecular mechanisms of ALD pathogenesis will provide a groundwork for developing novel treatment strategies for ALD. Abelson-like (ABL) is a non-receptor tyrosine kinase, which includes ABL1 and ABL2, and can be phosphorylated and activated by growth factors, cytokines, DNA damage, oxidative stress, and other signals. ABL activation can target multiple downstream signaling pathways to mediate many cellular functions. Recently, we found that ABL kinases are activated in mouse livers upon ethanol treatment and activated in human alcoholic steatohepatitis (ASH) samples compared to normal livers. Importantly, we found that deletion of Abl2 but not Abl1 attenuated ethanol-induced steatosis, hepatic injury, and inflammation in an ASH model. Further, treatment with ABL kinase inhibitors attenuated alcohol-induced lipid droplet formation and liver injury. Collectively, our data provide a strong premise that ABL2 contributes to the pathogenesis of ALD and that its inhibition may be a promising novel strategy to treat this disease. However, many questions remain to be answered. For example, what are the key downstream targets that mediate the function of ABL2 in ALD? Does ALB2 play a role in EtOH-induced liver fibrosis? What’s the role of ABL2 in alcohol-driven liver tumorigenesis? The overall goal of this proposal is to understand these critical questions, which will provide novel insight into the molecular mechanisms of ALD. Three specific aims are proposed. Aim1 will determine the molecular mechanisms by which ABL2 promotes alcohol-induced steatosis. Aim 2 will define the role of ABL kinases in alcohol-induced fibrosis. Aim 3 will evaluate the role of ABL2 in alcohol-driven liver tumorigenesis. This work has the potential to establish a new therapeutic strategy for treating alcohol-induced liver injury and cancer.


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 = $470,066 )
2026	2026	LOYOLA UNIVERSITY OF CHICAGO	2160 S 1ST AVE	MAYWOOD	IL	60153	COOK	USA	Alcohol Research Programs	000	1	5/5/2026	NEW	$470,066
														Subtotal = $470,066

Grand Total All Awards = $470,066

Top

All Categories

About

Search

Reports

Data Submission

Award Information

Molecular Mechanisms of ABL Kinase 2 in the Pathogenesis of Alcohol-Associated Liver Disease

Award Number: R01AA032952

ORGANIZATION: NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 01/31/2031

Federal Websites

Department of Health & Human Services

HHS Operating Divisions

HHS Staff Divisions

Download A Document Viewer