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

Acid-Sensing Ion Channel 1a Regulates Synapse-Glioblastoma Integration

Award Number: R01NS143931
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/15/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2031

Group Awards By:

View Award Description

Acid-Sensing Ion Channel 1a Regulates Synapse-Glioblastoma Integration - PROJECT SUMMARY Glioblastoma (GBM) is one of the most common and deadly brain cancers with a poor prognosis. Recent Cancer Neuroscience findings have revealed bona fide neuron-GBM synapses and their critical roles in driving GBM growth and migration; however, the mechanisms by which the neuron-GBM synapses are modulated remain to be understood. Our preliminary findings suggest a proton (H+) signaling pathway actively mediates neuron-GBM synaptic communications via the Acid-sensing Ion Channel 1a (ASIC1a). Using electrophysiology and genetically engineered mice of ASIC1a, we demonstrate that acid activation of neurons enhances neuron- GBM synaptic communications, and the synaptic response is dependent on the expression of ASIC1a in the brain. Importantly, genetically ablating ASIC1a in glutamatergic neurons reduces GBM burden in vivo and increases mouse survival. Based on preliminary data, our central hypothesis is that GBM TME-induced H+ activates glutamatergic neuronal ASIC1a, strengthens neuron-GBM synaptic transmission, and accelerates GBM progression. The Pan (neuronal activity-dependent gliomagenesis) and Du (H+/ASIC signaling in synaptic transmission) laboratories will work together to address this hypothesis using genetically engineered mice of Asic1a, electrophysiology, advanced microscopy, and various murine and human GBM models. We will address the hypothesis by determining the role of GBM TME-induced extracellular acidification in shaping ASIC1a-dependent neuron-GBM synapse (Aim 1), the effects of the neuron-GBM synapse on GBM cellular functions (Aim 2), and whether glutamatergic neuronal ASIC1a contributes to GBM pathophysiology (Aim 3). Successful completion of these studies will provide important insights into how H+/ASIC1a singling contributes to neuron-GBM synaptic communications and GBM progression and provide new possibilities for treating GBM and related neurological disorders in patients.


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 = $633,653 )
2026	2026	THE UNIVERISTY OF TEXAS M.D. ANDERSON CANCER CENTER	1515 HOLCOMBE BLVD	HOUSTON	TX	77030	HARRIS	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	7/8/2026	NEW	$633,653
														Subtotal = $633,653

Grand Total All Awards = $633,653

Top

All Categories

About

Search

Reports

Data Submission

Award Information

Acid-Sensing Ion Channel 1a Regulates Synapse-Glioblastoma Integration

Award Number: R01NS143931

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 07/15/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2031

Federal Websites

Department of Health & Human Services

HHS Operating Divisions

HHS Staff Divisions

Download A Document Viewer