TRIOBP

Last update 08 May 2025

Basic Info

Synonyms

DFNB28, HRIHFB2122, KIAA1662

+ [7]

Introduction

Plays a pivotal role in the formation of stereocilia rootlets. Plays a pivotal role in the formation of stereocilia rootlets. Regulates actin cytoskeletal organization, cell spreading and cell contraction by directly binding and stabilizing filamentous F-actin and prevents its depolymerization (PubMed:18194665, PubMed:28438837). May also serve as a linker protein to recruit proteins required for F-actin formation and turnover (PubMed:18194665). Essential for correct mitotic progression (PubMed:22820163, PubMed:24692559).

100 Clinical Results associated with TRIOBP

100 Translational Medicine associated with TRIOBP

0 Patents (Medical) associated with TRIOBP

115

Literatures (Medical) associated with TRIOBP

01 Apr 2025·Cell Chemical Biology

Molecular mechanism of PP2A/B55α phosphatase inhibition by IER5

Article

Author: Wang, Shumei ; Aster, Jon C ; Rawson, Shaun ; Pan, Li ; Yang, Annie ; Padi, Sathish K R ; Blacklow, Stephen C ; Cao, Ruili ; Jones, Daniel T D

PP2A serine/threonine phosphatases are heterotrimeric complexes that execute many essential physiologic functions. These activities are modulated by additional regulatory proteins, such as ARPP19, FAM122A, and IER5. Here, we report the cryoelectron microscopy (cryo-EM) structure of a complex of PP2A/B55α with the N-terminal structured region of IER5 (IER5-N50), which occludes a surface on B55α used for substrate recruitment, and show that IER5-N50 inhibits PP2A/B55α catalyzed dephosphorylation of pTau in biochemical assays. Mutations of full-length IER5 that disrupt its PP2A/B55α interface interfere with co-immunoprecipitation of PP2A/B55α. IER5 antagonism of B55α in keratinocytes is required for expression of KRT1, a differentiation marker. Mini-IER5 composed of IER5-N50 and a nuclear localization sequence restores this activity in IER5 knockout cells. Using structural bioinformatics, we identify homology of IER5-N50 with SERTA (SEI-1, RBT-1, and TARA) domain containing proteins. These studies define the molecular basis of PP2A/B55α nuclear inhibition by IER5 and suggest a roadmap for selective pharmacologic modulation of PP2A/B55α complexes.

01 Feb 2025·Clinical Genetics

A Frameshift Variant in ANKRD24 Implicates Its Role in Human Non‐Syndromic Hearing Loss

Article

Author: Shokouhian, Ebrahim ; Edizadeh, Masoud ; Najmabadi, Hossein ; Mohseni, Marzieh ; Zare Ashrafi, Farzane ; Kazemi, Negar ; Kahrizi, Kimia ; Rezvani Rezvandeh, Raziye ; Booth, Kevin T. A.

ABSTRACTHearing loss (HL) is the most prevalent sensorineural disorders, affecting about one in 1000 newborns. Over half of the cases are attributed to genetic factors; however, due to the extensive clinical and genetic heterogeneity, many cases remain without a conclusive genetic diagnosis. The advent of next‐generation sequencing methodologies in recent years has greatly helped unravel the genetic etiology of HL by identifying numerous genes and causative variants. Despite this, much remains to be uncovered about the genetic basis of sensorineural hearing loss (SNHL). Here, we report an Iranian consanguineous family with postlingual, moderate‐to‐severe autosomal recessive SNHL. After first excluding plausible variants in known deafness‐causing genes using whole exome sequencing, we reanalyzed the data, using a gene/variant prioritization pipeline established for novel gene discovery for HL. This approach identified a novel homozygous frameshift variant c.1934_1937del; (p.Thr645Lysfs*52) in ANKRD24, which segregated with the HL phenotype in the family. Recently, ANKRD24 has been shown to be a pivotal constituent of the stereocilia rootlet in cochlea hair cells and interacts with TRIOBP, a protein already implicated in human deafness. Our data implicate for the first time, ANKRD24 in human nonsyndromic HL (NSHL) and expands the genetic spectrum of HL.

01 Dec 2024·Cellular and Molecular Life Sciences

TRIOBP modulates β-catenin signaling by regulation of miR-29b in idiopathic pulmonary fibrosis

Article

Author: Zhao, Wenyu ; Wang, Ningdan ; Rosas, Ivan ; Wang, Yaxuan ; Li, Zhongzheng ; Xia, Cong ; Ding, Linke ; Ma, Shuaichen ; Cheng, Lianhui ; Wang, Lan ; Yang, Juntang ; Li, Yajun ; Yu, Guoying ; Liu, Huibing

AbstractIdiopathic pulmonary fibrosis (IPF) is a fatal and devastating lung disease of unknown etiology, described as the result of multiple cycles of epithelial cell injury and fibroblast activation. Despite this impressive increase in understanding, a therapy that reverses this form of fibrosis remains elusive. In our previous study, we found that miR-29b has a therapeutic effect on pulmonary fibrosis. However, its anti-fibrotic mechanism is not yet clear. Recently, our study identified that F-Actin Binding Protein (TRIOBP) is one of the target genes of miR-29b and found that deficiency of TRIOBP increases resistance to lung fibrosis in vivo. TRIOBP knockdown inhibited the proliferation of epithelial cells and attenuated the activation of fibroblasts. In addition, deficiency of Trio Rho Guanine Nucleotide Exchange Factor (TRIO) in epithelial cells and fibroblasts decreases susceptibility to lung fibrosis. TRIOBP interacting with TRIO promoted abnormal epithelial–mesenchymal crosstalk and modulated the nucleocytoplasmic translocation of β-catenin. We concluded that the miR-29b‒TRIOBP–TRIO–β-catenin axis might be a key anti-fibrotic axis in IPF to regulate lung regeneration and fibrosis, which may provide a promising treatment strategy for lung fibrosis.Graphical Abstract

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TRIOBP

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