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TRIOBP-1 aggregation, therefore, appears to occur through one or more specific cellular mechanisms, which therefore have the potential to be of physiological relevance for the biological process underlying the development of chronic mental illness.
We discovered two genome-wide significant SNPs. The first was novel and near ISG20 (show ISG20 ELISA Kits). The second was in TRIOBP, a gene previously associated with prelingual nonsyndromic hearing loss. Motivated by our TRIOBP results, we also looked at exons in known hearing loss genes, and identified two additional SNPs, rs2877561 in ILDR1 (show ILDR1 ELISA Kits) and rs9493672 in EYA4 (show EYA4 ELISA Kits) (at a significance threshold adjusted for number of SNPs in those regions).
TRIOBP-1 aggregates are implicated for the first time as a biological element of the neuropathology of a subset of chronic mental illness
High TRIOBP expression is associated with pancreatic cancer.
TAP68 functions in mediating TRF1 (show TERF1 ELISA Kits)-tankyrase 1 (show TNKS ELISA Kits) localization to the centrosome and in mitotic regulation
the centrosomal localization of Tara depended on the Thr (show TRH ELISA Kits)-457 phosphorylation and the kinase activity of Plk1 (show PLK1 ELISA Kits).
Data show that 4-oxo-4-HPR (show HPR ELISA Kits) inhibited tubulin (show TUBB ELISA Kits) polymerization and modulated gene expression of spindle aberration associated genes Kif 1C, Kif 2A, Eg5 (show KIF11 ELISA Kits), Tara, tankyrase-1 (show TNKS ELISA Kits), centractin (show ACTR1A ELISA Kits), and TOGp (show CKAP5 ELISA Kits).
Mutations in TRIOBP, which encodes a putative cytoskeletal-organizing protein, are associated with nonsyndromic recessive deafness.
Mutations in a novel isoform of TRIOBP that encodes a filamentous-actin binding protein are responsible for DFNB28 recessive nonsyndromic hearing loss.
All these findings suggest that HECTD3 (show HECTD3 ELISA Kits) may facilitate cell cycle progression via regulating ubiquitination and degradation of Tara.
missense mutations in the Pejvakin (PJVK (show DFNB59 ELISA Kits) or DFNB59 (show DFNB59 ELISA Kits)) gene were first identified in patients with audiological hallmarks of auditory neuropathy spectrum disorder, whereas all other PJVK (show DFNB59 ELISA Kits) alleles cause hearing loss of cochlear origin. These findings suggest that complex pathogenetic mechanisms underlie human deafness DFNB59 (show DFNB59 ELISA Kits).
R1 motif is the major actin-binding domain of TRIOBP-4, and the binding of R2 motif with actin filaments is nonspecific.
Tara activates Rac1 through the Trio RhoGEF (show ARHGEF28 ELISA Kits), which binds to E-cadherin (show CDH1 ELISA Kits) and subsequently increases the phosphorylation of p38 (show CRK ELISA Kits) and Tbx3 (show TBX3 ELISA Kits), a transcriptional E-cadherin (show CDH1 ELISA Kits) repressor.
mutant Triobp mice are profoundly deaf; stereocilia of Triobp mice develop normally but fail to form rootlets and are easier to deflect and damage.
This gene encodes a protein with an N-terminal pleckstrin homology domain and a C-terminal coiled-coil region. The protein interacts with trio, which is involved with neural tissue development and controlling actin cytoskeleton organization, cell motility and cell growth. The protein also associates with F-actin and stabilizes F-actin structures. Mutations in this gene have been associated with a form of autosomal recessive nonsyndromic deafness. Multiple alternatively spliced transcript variants that would encode different isoforms have been found for this gene, however some transcripts may be subject to nonsense-mediated decay (NMD).
TRIO and F-actin binding protein
, TRIO and F-actin-binding protein
, protein Tara
, tara-like protein
, trio-associated repeat on actin