Affinage

TRIOBP

TRIO and F-actin-binding protein · UniProt Q9H2D6

Length
2365 aa
Mass
261.4 kDa
Annotated
2026-06-10
63 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/8 claims corpus-supported (88%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TRIOBP encodes multiple actin-associated isoforms whose unifying activity is binding, bundling, and stabilizing F-actin to control cytoskeletal architecture across tissues (PMID:11148140, PMID:20510926, PMID:23789641). The stereocilia-specific isoforms TRIOBP-4 and TRIOBP-5 bundle actin filaments into uniquely dense rootlet structures at the base of inner ear hair cell stereocilia; this bundling, mapped to the R1 repeat motif, confers the mechanical rigidity and durability that stereocilia require, and its loss in knockout mice abolishes rootlet formation and produces profound deafness (PMID:20510926, PMID:23789641, PMID:35737845). Rootlet assembly is organized cooperatively with ANKRD24, which rings the stereocilia insertion point and is mutually interdependent with TRIOBP-5 for correct localization (PMID:35175278). Consistent with this essential structural role, truncating TRIOBP mutations cause autosomal recessive nonsyndromic deafness DFNB28 (PMID:16385458, PMID:16385457). The widely expressed TRIOBP-1/Tara isoform stabilizes F-actin more broadly and acts as a signaling scaffold: it binds the Trio RhoGEF at adherens junctions, where it restrains a Rac1–p38–Tbx3 cascade to maintain E-cadherin transcription (PMID:11148140, PMID:21482718), and it cooperates with Ndel1 to drive filopodia formation and cell migration (PMID:27546710). TRIOBP-1 additionally functions in mitosis, where Plk1 phosphorylates it at Thr-457 to direct centrosomal localization required for faithful chromosome segregation, and where it recruits TRF1 and tankyrase 1 to spindle poles (PMID:22820163, PMID:24692559); its abundance is set by HECT-domain E3 ligase-mediated ubiquitination and degradation (PMID:18194665, PMID:41242366). TRIOBP-1 also binds the hERG potassium channel and limits its surface expression, thereby modulating cardiac action potential repolarization (PMID:29507111). Through the TRIOBP–Trio–β-catenin and RAI14–F-actin–YAP mechanotransduction axes, TRIOBP isoforms promote profibrotic gene programs in lung and kidney (PMID:38157020, PMID:41242366).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2001 High

    Established TRIOBP-1/Tara as a direct F-actin-binding protein that physically partners with the Trio RhoGEF, defining its founding role as a cytoskeletal stabilizer.

    Evidence Yeast two-hybrid, reciprocal Co-IP, in vitro F-actin binding, and Latrunculin B resistance assays in cultured cells

    PMID:11148140

    Open questions at the time
    • Did not define which actin structures are physiologically regulated in vivo
    • Functional consequence of the Trio interaction not yet resolved
  2. 2005 Medium

    Linked TRIOBP to human hearing by showing that truncating mutations in a long isoform cause DFNB28 deafness, with the protein localizing to stereocilia F-actin.

    Evidence Genetic linkage and mutation cosegregation across multiple families plus anti-TRIOBP immunolocalization in inner ear

    PMID:16385457 PMID:16385458

    Open questions at the time
    • Localization not coupled to a functional rescue experiment
    • Molecular mechanism by which loss causes deafness not addressed
  3. 2008 Medium

    Identified HECTD3 as an E3 ligase that ubiquitinates and degrades TRIOBP-1, placing TRIOBP turnover within cell cycle control.

    Evidence In vitro pull-down, Co-IP, ubiquitination assay, and siRNA knockdown with spindle phenotype scoring

    PMID:18194665

    Open questions at the time
    • Single lab
    • Multipolar spindle phenotype not directly attributed to TRIOBP accumulation
  4. 2010 High

    Defined the core mechanistic function of stereocilia TRIOBP: bundling actin into dense rootlets that provide mechanical durability, with knockout abolishing rootlets and causing deafness.

    Evidence In vitro bundling assay with purified TRIOBP-4, immunolocalization, and Triobp-knockout mice with auditory, electrophysiology, and EM analysis

    PMID:20510926

    Open questions at the time
    • Did not map the actin-binding domain
    • Did not identify cofactors organizing rootlet geometry
  5. 2011 High

    Placed TRIOBP-1 in a junctional signaling pathway, showing it restrains a Trio-Rac1-p38-Tbx3 cascade to sustain E-cadherin transcription.

    Evidence shRNA knockdown, pharmacological and mutant rescue, Co-IP, and luciferase reporter in MDCK epithelial cells

    PMID:21482718

    Open questions at the time
    • Whether the actin-binding activity is required for pathway restraint not separated
    • In vivo relevance of the epithelial pathway not tested
  6. 2012 High

    Showed Plk1 phosphorylates TRIOBP-1 at Thr-457 to drive centrosomal localization needed for accurate chromosome segregation, extending its role into mitosis.

    Evidence Co-IP, in vitro kinase assay, T457A phosphosite mutant, and cell cycle analysis in HeLa cells

    PMID:22820163

    Open questions at the time
    • Single lab
    • Downstream centrosomal effectors of phosphorylated TRIOBP not identified
  7. 2014 High

    Established a mitotic scaffolding role in which TRIOBP-1 recruits TRF1 and tankyrase 1 to spindle poles, regulated by Nek2A phosphorylation.

    Evidence Reciprocal Co-IP, domain mapping, siRNA knockdown, and live-cell imaging

    PMID:24692559

    Open questions at the time
    • Functional purpose of telomere protein relocalization to poles unresolved
    • Single lab
  8. 2014 Medium

    Extended TRIOBP-4/-5 cytoskeletal function to cancer cell motility through filopodia formation, and revealed isoform-specific aggregation behavior of TRIOBP-1.

    Evidence siRNA knockdown with GFP rescue and motility assays in pancreatic cancer cells; insolubility and over-expression assays in neuroblastoma cells

    PMID:25130170 PMID:25333879

    Open questions at the time
    • Mechanism linking TRIOBP to filopodial nucleation not defined
    • Physiological significance of TRIOBP-1 aggregation unclear
  9. 2016 Medium

    Identified Ndel1 as a TRIOBP-1 partner whose complex synergistically promotes F-actin assembly and filopodia during cell migration.

    Evidence Co-IP, domain deletion, wound healing and Boyden chamber assays, and confocal microscopy

    PMID:27546710

    Open questions at the time
    • Single study
    • In vivo migration context not tested
  10. 2017 Medium

    Dissected TRIOBP-1 coiled-coil architecture, attributing F-actin depolymerization inhibition, oligomerization, neurite outgrowth effects, and aggregation propensity to the central domain.

    Evidence Domain deletion mutagenesis with depolymerization, insolubility, and neurite outgrowth assays

    PMID:28438837

    Open questions at the time
    • Structural basis of oligomerization not resolved
    • Link between aggregation and physiological function unclear
  11. 2018 High

    Revealed a cardiac role: TRIOBP-1 binds hERG and suppresses its surface expression, modulating repolarizing current and action potential.

    Evidence Y2H, FRET, Co-IP, shRNA, and patch clamp across HEK293, native cardiac tissue, and iPSC-derived cardiomyocytes

    PMID:29507111

    Open questions at the time
    • Whether endogenous TRIOBP-1 levels regulate IKr physiologically not established
    • Trafficking step at which hERG is retained not defined
  12. 2018 Medium

    Positioned TRIOBP-1/-5 as effectors of an Sp1/miR-3178 axis controlling cancer cell migration and invasion.

    Evidence 3'UTR luciferase, ChIP, migration/invasion assays, and overexpression rescue

    PMID:30195749

    Open questions at the time
    • Single lab
    • Direct cytoskeletal mechanism downstream not dissected
  13. 2022 High

    Defined ANKRD24 as the rootlet-organizing partner of TRIOBP-5, with reciprocal interdependence required for proper stereocilia rootlet assembly and hearing.

    Evidence Super-resolution microscopy, reciprocal knockout mislocalization, and exogenous rescue with auditory testing

    PMID:35175278

    Open questions at the time
    • Molecular nature of the ANKRD24-TRIOBP-5 contact not mapped to residues
    • How the ring geometry templates rootlet boundaries unresolved
  14. 2022 High

    Quantified the tissue-mechanical consequence of TRIOBP loss, showing disrupted radial stiffness gradients in the cochlear sensory epithelium.

    Evidence AFM nanoscale stiffness mapping and FIB/SEM in Triobp knockout mice

    PMID:35737845

    Open questions at the time
    • Direct link from stiffness changes to mechanotransduction deficits not established
  15. 2022 Medium

    Narrowed TRIOBP-1 aggregation determinants to short N-terminal and central segments and associated insoluble TRIOBP-1 with psychiatric disease brains.

    Evidence Truncation mutagenesis with high-stringency insolubility assays and post-mortem brain fractionation

    PMID:36232351

    Open questions at the time
    • Causality between aggregation and disease not established
    • Single lab
  16. 2023 Medium

    Connected TRIOBP-Trio signaling to fibrosis by showing the interaction modulates beta-catenin nucleocytoplasmic translocation in pulmonary epithelial-mesenchymal crosstalk.

    Evidence siRNA knockdown, Co-IP, beta-catenin translocation assay, and in vivo fibrosis model

    PMID:38157020

    Open questions at the time
    • Whether actin bundling is required for beta-catenin regulation not separated
    • Single lab
  17. 2025 Medium

    Defined a RAI14-TRIOBP-YAP mechanotransduction axis in renal fibrosis, where RAI14 stabilizes TRIOBP against HECTD1 ubiquitination to enhance cytoskeletal tension and YAP activation.

    Evidence Co-IP, ubiquitination assay, F-actin and YAP translocation assays, and RAI14 knockout mice with multi-omics

    PMID:41242366

    Open questions at the time
    • HECTD1 ubiquitination site on TRIOBP not mapped
    • Single lab
  18. 2025 Medium

    Established TRIOBP as a downstream effector of a SYISL/miR-23a ceRNA axis driving fibroblast-to-myofibroblast transition.

    Evidence RNA pulldown, 3'UTR luciferase, miRNA mimic/inhibitor epistasis, and in vivo AAV-shRNA delivery

    PMID:40419807

    Open questions at the time
    • Single lab
    • Cytoskeletal mechanism downstream of TRIOBP in myofibroblasts not dissected

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TRIOBP isoform-specific activities (rootlet bundling vs. signaling scaffold vs. channel regulation) are partitioned and coordinated within a single tissue, and whether aggregation has a physiological role, remain open.
  • No unified structural model relating actin-binding repeats and coiled-coil domains to each isoform function
  • Causal role of TRIOBP-1 aggregation in psychiatric disease unestablished
  • In vivo significance of cardiac and centrosomal roles not tested in animal models

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 4 GO:0060090 molecular adaptor activity 3
Localization
GO:0005856 cytoskeleton 3 GO:0005815 microtubule organizing center 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1640170 Cell Cycle 3 R-HSA-1643685 Disease 2
Partners
ANKRD24HECTD3KCNH2NDEL1PLK1TNKSTRF1TRIO
Complex memberships
stereocilia rootlet

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 TRIOBP-1/Tara directly binds F-actin in vitro and associates with the Trio guanine nucleotide exchange factor (via yeast two-hybrid and mammalian co-immunoprecipitation). Overexpression of Tara stabilizes F-actin structures, enhances stress fibers and cortical actin, and increases cell spreading, while Tara-expressing cells show relative resistance to Latrunculin B-induced F-actin destabilization. Yeast two-hybrid, co-immunoprecipitation, in vitro F-actin binding assay, Latrunculin B treatment, fluorescence microscopy Journal of cell science High 11148140
2005 Mutations in a novel long isoform of TRIOBP (218 kDa) cause DFNB28 hereditary deafness. The long isoform has a restricted expression profile including cochlea, retina, and fetal brain. Antibody staining shows TRIOBP protein expression in sensory cells of the inner ear and colocalization with F-actin along the length of stereocilia. Genetic linkage/mutation analysis, RT-PCR expression profiling, immunofluorescence with anti-TRIOBP antibody American journal of human genetics Medium 16385458
2005 Six distinct TRIOBP mutant alleles (four nonsense, two frameshift) in exon 6 cosegregate with autosomal recessive nonsyndromic deafness across seven families, establishing TRIOBP as the DFNB28 gene. Genetic linkage analysis, mutation screening, cosegregation analysis American journal of human genetics Medium 16385457
2008 HECTD3, a HECT-domain E3 ubiquitin ligase, directly binds TRIOBP-1/Tara in vitro and forms a complex in vivo. HECTD3 overexpression enhances ubiquitination of Tara and promotes its degradation; siRNA depletion of HECTD3 decreases Tara degradation. HECTD3 depletion also leads to multipolar spindle formation, suggesting that HECTD3-mediated ubiquitination and degradation of Tara facilitates cell cycle progression. In vitro pull-down, co-immunoprecipitation, ubiquitination assay, siRNA knockdown, confocal microscopy Biochemical and biophysical research communications Medium 18194665
2010 TRIOBP isoform 4 (TRIOBP-4) bundles actin filaments into uniquely dense bundles in vitro resembling stereocilia rootlets. TRIOBP localizes specifically to rootlets of inner ear hair cell stereocilia. Triobp-knockout mice (Triobp(Δex8/Δex8)) are profoundly deaf; their stereocilia develop normally but fail to form rootlets and are easier to deflect and damage. Thus TRIOBP F-actin bundling provides mechanical durability and rigidity to stereocilia. In vitro F-actin bundling assay with purified TRIOBP-4, immunolocalization, knockout mouse model with auditory and electrophysiology testing, electron microscopy Cell High 20510926
2011 Tara is enriched at E-cadherin-based adherens junctions. Tara knockdown in MDCK cells activates Rac1 through the Trio RhoGEF (which binds E-cadherin), leading to increased p38 phosphorylation and phosphorylation of Tbx3, a transcriptional E-cadherin repressor, thereby decreasing E-cadherin transcription. E-cadherin loss is rescued by ITX3 (Trio RhoGEF inhibitor), SB203580 (p38 inhibitor), or dephosphomimetic Tbx3. Tara also modulates circumferential actin-belt density and epithelial cyst morphology. shRNA knockdown, co-immunoprecipitation, pharmacological inhibition, phosphomimetic/dephosphomimetic mutant rescue, confocal microscopy, luciferase reporter The Journal of cell biology High 21482718
2012 Polo-like kinase 1 (Plk1) interacts with and phosphorylates Tara at Thr-457 in vivo and in vitro. This Plk1-dependent phosphorylation is required for centrosomal localization of Tara. A non-phosphorylatable Tara mutant (T457A) causes aberrant mitotic delay in HeLa cells, demonstrating that Plk1-mediated phosphorylation of Tara at Thr-457 is required for faithful chromosome segregation. Co-immunoprecipitation, in vitro kinase assay, phosphosite mutagenesis, confocal microscopy, cell cycle analysis Experimental cell research High 22820163
2013 The R1 repeat motif is the major actin-binding domain of TRIOBP-4. Deletion of both R1 and R2 motifs completely abolishes actin-binding and bundling activities and impairs localization to cellular actin structures. Deletion of R2 alone retains F-actin bundling and actin colocalization. R1-deleted TRIOBP-4 (consisting mainly of R2) forms only thin F-actin bundles in vitro and fails to colocalize with actin filaments in cells. Actin cosedimentation assay, in vitro F-actin bundling assay, electron microscopy, fluorescence microscopy, deletion mutagenesis Biochemistry High 23789641
2014 TAP68 (TRIOBP-1) interacts with TRF1 in mitotic cells. TAP68 co-localizes with TRF1 to telomeres during interphase. After nuclear envelope breakdown, TAP68 translocates to spindle poles and recruits TRF1. Nek2A-dependent phosphorylation of TAP68 at Thr-221 coincides with its dissociation from telomeres. The first coiled-coil domain of TAP68 is responsible for binding and recruiting TRF1 and tankyrase 1 to the centrosome. siRNA depletion of TAP68 blocks centrosomal localization of TRF1 and tankyrase 1 and perturbs chromosome segregation. Co-immunoprecipitation, siRNA knockdown, domain deletion mapping, immunofluorescence microscopy, live cell imaging The Journal of biological chemistry High 24692559
2014 TRIOBP-4 and TRIOBP-5 are upregulated in pancreatic carcinoma cells. Knockdown of TRIOBP-4/-5 leads to loss of filopodia and decreased cell motility; re-expression of GFP-TRIOBP-4 or -5 restores filopodial formation in TRIOBP-4/-5-deficient PANC-1 cells, demonstrating a role in promoting cell motility via regulation of filopodia actin structures. siRNA knockdown, GFP-tagged rescue expression, confocal microscopy, wound healing/motility assay Cancer letters Medium 25130170
2014 TRIOBP-1 has a high aggregation propensity when over-expressed in neuroblastoma cells, whereas the TRIOBP-4 isoform does not. Endogenous TRIOBP-1 can spontaneously aggregate, doing so more in post-mitotic cell cultures. Aggregated TRIOBP-1 affects cell morphology in Neuroscreen-1 cells. Over-expression in neuroblastoma/NS-1 cells, insolubility assay, immunofluorescence microscopy PloS one Medium 25333879
2016 Ndel1 interacts physically with Tara (TRIOBP-1). Ndel1- or Tara-deficient cells are defective in cell migration. Tara overexpression accumulates Ndel1 at the cell periphery, co-localizing with F-actin; this redistribution requires the Ndel1-interacting domain of Tara. Co-expression of Ndel1 and Tara causes synergistic increases in F-actin levels and filopodia formation, indicating that the Ndel1-Tara complex regulates actin remodeling during cell movement. Co-immunoprecipitation, domain deletion analysis, wound healing assay, Boyden chamber assay, confocal microscopy, siRNA knockdown Scientific reports Medium 27546710
2017 TRIOBP-1 possesses two distinct coiled-coil domains (central and C-terminal). The central domain inhibits F-actin depolymerization, mediates oligomerization of TRIOBP-1, and affects neurite outgrowth along with the N-terminal PH domain. The aggregation propensity of TRIOBP-1 arises from its central domain, with an 8-25 amino acid linker region (around residues 324-348) between the first two coiled coils being essential for aggregate formation. Domain deletion mutagenesis, F-actin depolymerization assay, insolubility assay in neuroblastoma cells, neurite outgrowth assay The Journal of biological chemistry Medium 28438837
2018 TRIOBP-1 interacts directly with the hERG cardiac potassium channel protein (identified by yeast two-hybrid and confirmed by FRET and co-immunoprecipitation in HEK293 cells and native cardiac tissue). TRIOBP-1 overexpression reduces hERG surface expression and current density (IKr); shRNA knockdown of TRIOBP-1 increases hERG protein levels. In human stem cell-derived cardiomyocytes, TRIOBP-1 overexpression causes intracellular co-sequestration of hERG, reduces native IKr, and disrupts action potential repolarization. Yeast two-hybrid, FRET, co-immunoprecipitation, shRNA knockdown, whole-cell patch clamp, immunolabeling, human iPSC-derived cardiomyocytes Journal of cell science High 29507111
2018 Sp1 transcriptionally suppresses miR-3178, and miR-3178 directly targets the 3' UTR of TRIOBP-1 and TRIOBP-5, reducing their expression. Overexpression of TRIOBP-1 rescues the inhibitory effect of miR-3178 on cell migration and invasion, establishing TRIOBP-1 as a downstream effector of the Sp1/miR-3178 axis in cancer cell metastasis. Luciferase reporter assay (3'UTR), ChIP, migration/invasion assays, overexpression rescue Molecular therapy. Nucleic acids Medium 30195749
2022 ANKRD24 concentrates at the stereocilia insertion point forming a ring at the junction between lower and upper rootlets, where it surrounds and binds TRIOBP-5 which bundles rootlet F-actin. TRIOBP-5 is mislocalized in Ankrd24KO/KO hair cells, and ANKRD24 no longer localizes with rootlets in mice lacking TRIOBP-5; exogenous DsRed-TRIOBP-5 restores endogenous ANKRD24 to rootlets, demonstrating mutual interdependence. Ankrd24KO/KO mice show progressive hearing loss and increased susceptibility to overstimulation. Super-resolution microscopy, knockout mouse models, exogenous rescue expression, immunolocalization, auditory function testing The Journal of cell biology High 35175278
2022 TRIOBP deficiency (knockout of isoforms 4 and 5 or isoform 5 alone) significantly disrupts the magnitude and orientation of bidirectional radial stiffness gradients in the cochlear sensory epithelium and causes ultrastructural changes in supporting cell phalangeal microfilaments and hair cell cuticular plate F-actin bundles, as measured by nanoscale AFM mapping. Atomic force microscopy (AFM) stiffness mapping, focused ion beam/scanning electron microscopy, Triobp knockout mouse models Proceedings of the National Academy of Sciences of the United States of America High 35737845
2022 TRIOBP-1 aggregation in neuroblastoma cells can be narrowed to an 8 amino acid region (333-340) as the primary aggregation-critical segment, and a second region at the extreme N-terminus (first 59 amino acids, optionally expressed) can independently induce aggregation; the 597 aa form lacking these 59 aa has reduced aggregation propensity. Insoluble TRIOBP-1 is more prevalent in brains from both schizophrenia and major depressive disorder patients compared to controls. Truncation mutagenesis, insolubility assay (high-stringency), expression in neuroblastoma cells, post-mortem brain fractionation International journal of molecular sciences Medium 36232351
2023 TRIOBP interacts with TRIO RhoGEF and promotes abnormal epithelial-mesenchymal crosstalk in pulmonary fibrosis. TRIOBP knockdown inhibits epithelial cell proliferation and attenuates fibroblast activation. The TRIOBP-TRIO interaction modulates nucleocytoplasmic translocation of β-catenin. The miR-29b–TRIOBP–TRIO–β-catenin axis regulates lung regeneration and fibrosis. siRNA knockdown, co-immunoprecipitation, β-catenin nuclear translocation assay, in vivo fibrosis model Cellular and molecular life sciences : CMLS Medium 38157020
2025 In renal fibrosis, retinoic acid (RA) upregulates RAI14, which binds and stabilizes TRIOBP by preventing its HECTD1-mediated ubiquitination and degradation. Stabilized TRIOBP enhances F-actin assembly and cytoskeletal tension, leading to YAP nuclear translocation and activation of profibrotic gene programs. Genetic ablation of RAI14 significantly attenuates renal fibrosis in vivo. Co-immunoprecipitation, ubiquitination assay, siRNA/genetic knockdown, F-actin assembly assay, YAP nuclear translocation assay, in vivo knockout mouse, spatial metabolomics, single-cell transcriptomics Cellular signalling Medium 41242366
2025 SYISL lncRNA acts as a competing endogenous RNA (ceRNA) that directly binds miR-23a, thereby derepressing TRIOBP expression via its 3'UTR. Knockdown of TRIOBP amplifies anti-fibrotic effects of miR-23a mimics and abolishes pro-fibrotic activity of miR-23a inhibitors, establishing TRIOBP as a downstream effector of the SYISL/miR-23a axis in fibroblast-to-myofibroblast transition. RNA pulldown/luciferase reporter (3'UTR), siRNA knockdown, miRNA mimic/inhibitor assay, in vivo AAV-shRNA delivery Cellular and molecular life sciences : CMLS Medium 40419807

Source papers

Stage 0 corpus · 63 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Trial of Atorvastatin in Rheumatoid Arthritis (TARA): double-blind, randomised placebo-controlled trial. Lancet (London, England) 646 15207950
2013 Exploring nucleo-cytoplasmic large DNA viruses in Tara Oceans microbial metagenomes. The ISME journal 163 23575371
2010 Actin-bundling protein TRIOBP forms resilient rootlets of hair cell stereocilia essential for hearing. Cell 162 20510926
2017 Viral to metazoan marine plankton nucleotide sequences from the Tara Oceans expedition. Scientific data 114 28763055
2005 Mutations in a novel isoform of TRIOBP that encodes a filamentous-actin binding protein are responsible for DFNB28 recessive nonsyndromic hearing loss. American journal of human genetics 91 16385458
2001 Tara, a novel F-actin binding protein, associates with the Trio guanine nucleotide exchange factor and regulates actin cytoskeletal organization. Journal of cell science 87 11148140
2005 Mutations in TRIOBP, which encodes a putative cytoskeletal-organizing protein, are associated with nonsyndromic recessive deafness. American journal of human genetics 82 16385457
2020 Global ocean resistome revealed: Exploring antibiotic resistance gene abundance and distribution in TARA Oceans samples. GigaScience 70 32391909
2011 Feasibility of robot-assisted neck dissections via a transaxillary and retroauricular ("TARA") approach in head and neck cancer: preliminary results. Annals of surgical oncology 65 22045466
2011 Tara up-regulates E-cadherin transcription by binding to the Trio RhoGEF and inhibiting Rac signaling. The Journal of cell biology 57 21482718
2010 The Vibrio cholerae virulence regulatory cascade controls glucose uptake through activation of TarA, a small regulatory RNA. Molecular microbiology 37 21091503
2002 Pressure cell assisted solution characterization of polysaccharides. 2. Locust bean gum and tara gum. Biomacromolecules 36 12099820
2008 The E3 ubiquitin ligase HECTD3 regulates ubiquitination and degradation of Tara. Biochemical and biophysical research communications 28 18194665
2020 Depth-dependent mycoplankton glycoside hydrolase gene activity in the open ocean-evidence from the Tara Oceans eukaryote metatranscriptomes. The ISME journal 26 32494052
2020 Influence of dietary inclusion of tannin extracts from mimosa, chestnut and tara on volatile compounds and flavour in lamb meat. Meat science 25 33091724
2014 Aggregation of the protein TRIOBP-1 and its potential relevance to schizophrenia. PloS one 24 25333879
2014 The actin-bundling protein TRIOBP-4 and -5 promotes the motility of pancreatic cancer cells. Cancer letters 22 25130170
2021 Carbon Dioxide Concentration Mechanisms in Natural Populations of Marine Diatoms: Insights From Tara Oceans. Frontiers in plant science 21 33995455
2018 Sp1 Suppresses miR-3178 to Promote the Metastasis Invasion Cascade via Upregulation of TRIOBP. Molecular therapy. Nucleic acids 21 30195749
2016 Regulation of the actin cytoskeleton by the Ndel1-Tara complex is critical for cell migration. Scientific reports 21 27546710
2017 An unpredicted aggregation-critical region of the actin-polymerizing protein TRIOBP-1/Tara, determined by elucidation of its domain structure. The Journal of biological chemistry 20 28438837
2020 The TRIOBP Isoforms and Their Distinct Roles in Actin Stabilization, Deafness, Mental Illness, and Cancer. Molecules (Basel, Switzerland) 19 33121024
2017 Broadening the phenotype of DFNB28: Mutations in TRIOBP are associated with moderate, stable hereditary hearing impairment. Hearing research 18 28089734
2016 Full-field interferometry for counting and differentiating aquatic biotic nanoparticles: from laboratory to Tara Oceans. Biomedical optics express 18 27699134
2017 Whole exome sequencing identifies TRIOBP pathogenic variants as a cause of post-lingual bilateral moderate-to-severe sensorineural hearing loss. BMC medical genetics 17 29197352
2022 ANKRD24 organizes TRIOBP to reinforce stereocilia insertion points. The Journal of cell biology 16 35175278
2013 R1 motif is the major actin-binding domain of TRIOBP-4. Biochemistry 16 23789641
2022 Insights into the remarkable attenuation of hen egg white lysozyme amyloid fibril formation mediated by biogenic gold nanoparticles stabilized by quercetin-functionalized tara gum. International journal of biological macromolecules 15 36586653
2022 A Tara Gum/Olive Mill Wastewaters Phytochemicals Conjugate as a New Ingredient for the Formulation of an Antioxidant-Enriched Pudding. Foods (Basel, Switzerland) 12 35053891
2012 Phosphorylation of Tara by Plk1 is essential for faithful chromosome segregation in mitosis. Experimental cell research 11 22820163
2023 Performance and meat quality in pigs fed hydrolysable tannins from Tara spinosa. Meat science 10 37839294
2018 Localization and functional consequences of a direct interaction between TRIOBP-1 and hERG proteins in the heart. Journal of cell science 10 29507111
2023 TRIOBP modulates β-catenin signaling by regulation of miR-29b in idiopathic pulmonary fibrosis. Cellular and molecular life sciences : CMLS 9 38157020
2022 Unbalanced bidirectional radial stiffness gradients within the organ of Corti promoted by TRIOBP. Proceedings of the National Academy of Sciences of the United States of America 9 35737845
2020 Gene Similarity Networks Unveil a Potential Novel Unicellular Group Closely Related to Animals from the Tara Oceans Expedition. Genome biology and evolution 9 32533833
2022 TRIOBP-1 Protein Aggregation Exists in Both Major Depressive Disorder and Schizophrenia, and Can Occur through Two Distinct Regions of the Protein. International journal of molecular sciences 8 36232351
2018 Genetic Linkage Analysis of DFNB4, DFNB28, DFNB93 Loci in Autosomal Recessive Non-syndromic Hearing Loss: Evidence for Digenic Inheritance in GJB2 and GJB3 Mutations. Iranian journal of public health 8 29318123
2014 The 68-kDa telomeric repeat binding factor 1 (TRF1)-associated protein (TAP68) interacts with and recruits TRF1 to the spindle pole during mitosis. The Journal of biological chemistry 8 24692559
2007 Expression, purification, and characterization of Tara, a novel telomere repeat-binding factor 1 (TRF1)-binding protein. Protein expression and purification 8 17629495
2025 LncRNA SYISL promotes fibroblast myofibroblast transition via miR-23a-mediated TRIOBP regulation. Cellular and molecular life sciences : CMLS 6 40419807
2023 Known phyla dominate the Tara Oceans RNA virome. Virus evolution 6 38028147
2015 Autosomal Recessive Nonsyndromic Hearing Loss: A Case Report with a Mutation in TRIOBP Gene. International journal of molecular and cellular medicine 6 27014650
2025 Fabricating an antioxidant and bacteriostatic soy protein isolate film double-crosslinked via dialdehyde cellulose nanofibers and Tara tannins for beef tallow and cooked pork preservation. International journal of biological macromolecules 5 39880262
2023 Is Baikiain in Tara Flour a Causative Agent for the Adverse Events Associated with the Recalled Frozen French Lentil & Leek Crumbles Food Product? - A Working Hypothesis. Chemical research in toxicology 5 37255213
2020 Mesonia oceanica sp. nov., isolated from oceans during the Tara oceans expedition, with a preference for mesopelagic waters. International journal of systematic and evolutionary microbiology 5 32589567
2015 Six new cassane diterpenes from the twigs and leaves of Tara (Caesalpinia spinosa Kuntze). Fitoterapia 5 26244825
2023 Micromonospora parastrephiae sp. nov. and Micromonospora tarensis sp. nov., isolated from the rhizosphere of a Parastrephia quadrangularis plant growing in the Salar de Tara region of the Central Andes in Chile. International journal of systematic and evolutionary microbiology 4 38059605
2020 A novel mutation in TRIOBP gene leading to congenital deafness in a Chinese family. BMC medical genetics 4 32487028
2020 A New Pathogenic Variant in the TRIOBP Associated with Profound Deafness Is Remediable with Cochlear Implantation. Audiology & neuro-otology 4 32877897
2004 [Isolation of Tara protein and its gene cloning]. Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 3 15586403
2024 Comprehensive molecular level characterization of protein- and polyphenol-rich tara (Caesalpinia spinosa) seed germ flour suggests novel hypothesis about possible accidental hazards. Food research international (Ottawa, Ont.) 2 38448102
2024 A sensorineural hearing loss harboring novel compound heterozygous variant in the TRIOBP gene: A case report. Heliyon 2 39296067
2023 SYMPTOM SEVERITY IN SCHIZOPHRENIA PATIENTS WITH NPAS3, DYSBINDIN-1 AND/OR TRIOBP PROTEIN PATHOLOGY IN THEIR BLOOD SERUM: A PANSS-BASED FOLLOW UP STUDY. Psychiatria Danubina 2 37480305
2022 Elucidation of repeat motifs R1- and R2-related TRIOBP variants in autosomal recessive nonsyndromic hearing loss DFNB28 among indigenous South African individuals. Molecular genetics & genomic medicine 2 36029164
2021 Case Report: Novel Compound Heterozygous Variants in TRIOBP Associated With Congenital Deafness in a Chinese Family. Frontiers in genetics 2 34868251
2012 A journey from reductionist to systemic cell biology aboard the schooner Tara. Molecular biology of the cell 2 22745340
1982 Carcinogenesis Bioassay of Tara Gum (CAS No. 39300-88-4) in F344 Rats and B6C3F1 Mice (Feed Study). National Toxicology Program technical report series 2 12778212
2024 Analysis of TRIOBP gene in non-syndromic deafness: A case report. Medicine 1 39533558
2026 Structure-based computational investigation of potential TarA inhibitors in Staphylococcus aureus. Molecular diversity 0 41739381
2026 Quality improvement of minced pork during glassy-state frozen storage with high glass transition temperature induced by tara gum. Food research international (Ottawa, Ont.) 0 41763797
2025 Renal tubular-derived retinoic acid drives renal fibrosis via a RAI14-TRIOBP-YAP mechanotransduction axis. Cellular signalling 0 41242366
2021 [Identification of novel pathogenic variants of TRIOBP gene in a pedigree affected with non-syndromic deafness]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 33974254
2016 [Porphyria cutanea tara]. Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete 0 26743054

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