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Last update 08 May 2025

TAX1BP3

Last update 08 May 2025

Basic Info

Synonyms

Glutaminase-interacting protein 3, Tax interaction protein 1, Tax-interacting protein 1

+ [5]

Introduction

May regulate a number of protein-protein interactions by competing for PDZ domain binding sites. Binds CTNNB1 and may thereby act as an inhibitor of the Wnt signaling pathway. Competes with LIN7A for KCNJ4 binding, and thereby promotes KCNJ4 internalization. May play a role in the Rho signaling pathway. May play a role in activation of CDC42 by the viral protein HPV16 E6.

Drugs associated with TAX1BP3

[89Zr]Zr-DFO-L111

Target

TAX1BP3

Mechanism

TAX1BP3 inhibitors

Active Org.

Washington University in St. Louis

Originator Org.

Washington University in St. Louis

Active Indication

Lung Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2023287941

Patent Mining

Target

TAX1BP3

Mechanism-

Active Org.

Washington University in St. Louis [+1]

Originator Org.

Washington University in St. Louis [+1]

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TAX1BP3

100 Translational Medicine associated with TAX1BP3

0 Patents (Medical) associated with TAX1BP3

147

Literatures (Medical) associated with TAX1BP3

01 Apr 2025·Trends in Plant Science

Microbiota-dependent and -independent autoimmunity in plants

Article

Author: Wang, Daowen ; Cyburt, Olivia ; Patel, Dev ; Fu, Zheng Qing ; Liu, Lijing

In a recent study to identify arabidopsis (Arabidopsis thaliana) genes involved in maintaining normal leaf microbiota, Cheng et al. discovered TIP GROWTH DEFECTIVE1 (TIP1) encoding an S-acyltransferase. The tip1 mutant exhibits abnormal microbiota levels and phenotypes resembling autoimmune mutants. Further study revealed the existence of both microbiota-dependent and -independent autoimmunity in plants.

28 Mar 2025·Circulation Research

Taxing Hearts: TAX1BP3 Loss Stirs Up TRPV4 Channels in Arrhythmogenic Cardiomyopathy

Communications

Author: Ratnavadivel, Sandra ; Jreije, Afaf ; Sheikh, Farah

28 Mar 2025·Circulation Research

TAX1BP3 Causes TRPV4-Mediated Autosomal Recessive Arrhythmogenic Cardiomyopathy

Article

Author: Campbell, M. Jay ; Monaco, Gabrielle G. ; Calkins, Hugh ; Dewars, Enya R. ; Perelli, Robin M. ; James, Cynthia A. ; Behura, Alexander S. ; Kurzlechner, Leonie M. ; Muralidharan, Padmapriya ; Ponek, Anna Q. ; Tang, Paul C. ; Asokan, Tulsi ; Cope, Heidi ; Yang, Qixin ; Rehder, Catherine W. ; Spector, Zebulon Z. ; Shashi, Vandana ; Berkman, Amy ; Sala, Angelina M. ; Sun, Bo ; Breglio, Andrew M. ; Ezekian, Jordan E. ; Moya-Mendez, Mary E. ; Landstrom, Andrew P. ; Sullivan, Molly C. ; Zhang, Zhushan

BACKGROUND:Arrhythmogenic cardiomyopathy (ACM) is one of the leading causes of sudden cardiac death in children, young adults, and athletes and is characterized by the fibro-fatty replacement of the myocardium, predominantly of the right ventricle. Sixty percent of patients with ACM have a known genetic cause, but for the remainder, the pathogenesis is unknown. This lack of mechanistic understanding has slowed the development of disease-modifying therapies, and children with ACM have a high degree of morbidity and mortality.METHODS: Induced pluripotent stem cells (iPSCs) from 3 family members were differentiated into cardiac myocytes (CMs). Calcium imaging was conducted by labeling calcium with CAL-520 and confocal imaging to capture calcium sparks after iPSC-CMs were electrically paced. A cardiac-specific, inducible knockout mouse ( Tax1bp3 −/− ) was made and intracardiac electrophysiology studies conducted to observe arrhythmia inducibility following pacing. RESULTS: We identified a kindred with multiple members affected by ACM cosegregating with biallelic variants in the gene TAX1BP3 , which encodes the protein TAX1BP3 (Tax1-binding protein 3). iPSC-CMs derived from this kindred demonstrated increased intracellular lipid droplets, induction of TRPV4 (transient receptor potential vanilloid type 4) expression, and inducible TRPV4 current. This was associated with depletion of the intracellular sarcoplasmic reticulum Ca 2+ store and increased RyR2 (ryanodine receptor 2)-mediated store Ca 2+ leak and delayed afterdepolarizations, a known mechanism of Ca 2+ -mediated arrhythmogenesis. Similarly, Tax1bp3 cardiac-specific knockout mice had increased Ca 2+ leak and were predisposed to ventricular arrhythmias compared with wild-type mice. Ca 2+ leak in both the iPSC-CMs and mouse ventricular myocytes was rescued by small molecule TRPV4 inhibition. This strategy also effectively reduced Ca 2+ leak in a PKP2 (plakophilin 2) p.His773AlafsX8 iPSC-CM model of ACM. CONCLUSIONS: We conclude that TAX1BP3 is associated with rare autosomal recessive ACM through TRPV4-mediated Ca 2+ leak from RyR2. Further, TRPV4 current inhibition has the potential to be a new therapeutic target for ACM.

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TAX1BP3

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