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Control Mechanisms of Human Voltage Gated Proton Channels, hHv1

Award Number: R35GM151963
ORGANIZATION: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 02/01/2024
PERIOD OF PERFORMANCE END DATE: 01/31/2029

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Control Mechanisms of Human Voltage Gated Proton Channels, hHv1 - Project Summary/Abstract The voltage gated proton channel (HV1) exists in many human tissues and plays numerous roles vital to human health. For example, it contributes to bacterial killing by white blood cells, sperm maturation and mobility, histamine release by basophils, B lymphocyte signaling, and airway fluid regulation. Abnormal HV1 function has been implicated in breast cancer metastasis, brain damage in ischemic stroke, and exacerbation of chronic lymphocytic leukemia. As its gene was not reported until 2006, HV1 is a newcomer to the voltage gated ion channel family. Its structure is unique in resembling a crucial component of all voltage-gated ion channels, namely the voltage-sensing domain that detects membrane potential and transduces this into channel opening or closing. Its newcomer status, unique structure, and essential roles in human health and disease make understanding HV1 function and dysfunction highly significant. The DeCoursey lab has been deeply involved in the study of HV1, from discovering its existence in mammalian and human cells, to identifying its role in a number of human cells and tissues, to finally dissecting the molecule itself to identify which parts perform the major functions. Over the next five years we intend to expand our knowledge of this important molecule at multiple levels, building on our recent progress. Structure-function knowledge is crucial both for understanding mechanisms and for drug design. Much has been learned about structure-function relationships from mutations to the human channel. We believe that it will be more productive in the future to explore structure-function relationships in the highly variable naturally-occurring HV1 in diverse species. An exciting new direction will be studying the involvement of cholesterol and membrane lipid “rafts” in the physiological regulation of hHV1 function. Another focus will be to determine the relationship between hHV1 mutations in B lymphocyte malignancies.


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 = $391,050 )
2026	2026	RUSH UNIVERSITY MEDICAL CENTER	1653 W CONGRESS PKWY	CHICAGO	IL	60612	COOK	USA	Biomedical Research and Research Training	000	3	1/19/2026	NON-COMPETING CONTINUATION	$391,050
														Subtotal = $391,050

Issue Date FY: 2025 ( Subtotal = $434,500 )
2025	2025	RUSH UNIVERSITY MEDICAL CENTER	1653 W CONGRESS PKWY	CHICAGO	IL	60612	COOK	USA	Biomedical Research and Research Training	002	2	8/5/2025	NON-COMPETING CONTINUATION	$43,450
2025	2025	RUSH UNIVERSITY MEDICAL CENTER	1653 W CONGRESS PKWY	CHICAGO	IL	60612	COOK	USA	Biomedical Research and Research Training	001	2	1/16/2025	NON-COMPETING CONTINUATION	$391,050
2025	2024	RUSH UNIVERSITY MEDICAL CENTER	1653 W CONGRESS PKWY	CHICAGO	IL	60612	COOK	USA	Biomedical Research and Research Training	000	1	11/22/2024	NEW	$0
														Subtotal = $434,500

Issue Date FY: 2024 ( Subtotal = $434,500 )
2024	2024	RUSH UNIVERSITY MEDICAL CENTER	1653 W CONGRESS PKWY	CHICAGO	IL	60612	COOK	USA	Biomedical Research and Research Training	000	1	1/23/2024	NEW	$434,500
														Subtotal = $434,500

Grand Total All Awards = $1,260,050

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Control Mechanisms of Human Voltage Gated Proton Channels, hHv1

Award Number: R35GM151963

ORGANIZATION: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 02/01/2024

PERIOD OF PERFORMANCE END DATE: 01/31/2029

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