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anti-Human TRIOBP Antikörper:
anti-Mouse (Murine) TRIOBP Antikörper:
anti-Rat (Rattus) TRIOBP Antikörper:
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Human Polyclonal TRIOBP Primary Antibody für IHC, IHC (p) - ABIN4362545
Bradshaw, Bader, Prikulis, Lueking, Müllner, Korth: Aggregation of the protein TRIOBP-1 and its potential relevance to schizophrenia. in PLoS ONE 2014
Case Reports: novel TRIOBP mutations associated with moderate, stable hereditary hearing impairment.
Based on whole exome analysis, we identified two TRIOBP pathogenic variants (c.802_805delCAGG, p.Gln268Leufs*610 and c.5014G>T, p.Gly1672*, the first of which was novel) causative of nonsyndromic, peri (zeige PLIN1 Antikörper)- to postlingual, moderate-to-severe hearing loss in three siblings from a Polish family.
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 (zeige ISG20 Antikörper). 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 (zeige ILDR1 Antikörper) and rs9493672 in EYA4 (zeige EYA4 Antikörper) (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 (zeige TERF1 Antikörper)-tankyrase 1 (zeige TNKS Antikörper) localization to the centrosome and in mitotic regulation
the centrosomal localization of Tara depended on the Thr (zeige TRH Antikörper)-457 phosphorylation and the kinase activity of Plk1 (zeige PLK1 Antikörper).
Data show that 4-oxo-4-HPR (zeige HPR Antikörper) inhibited tubulin (zeige TUBB Antikörper) polymerization and modulated gene expression of spindle aberration associated genes Kif 1C, Kif 2A, Eg5 (zeige KIF11 Antikörper), Tara, tankyrase-1 (zeige TNKS Antikörper), centractin (zeige ACTR1A Antikörper), and TOGp (zeige CKAP5 Antikörper).
Mutations in TRIOBP, which encodes a putative cytoskeletal-organizing protein, are associated with nonsyndromic recessive deafness.
missense mutations in the Pejvakin (PJVK (zeige DFNB59 Antikörper) or DFNB59 (zeige DFNB59 Antikörper)) gene were first identified in patients with audiological hallmarks of auditory neuropathy spectrum disorder, whereas all other PJVK (zeige DFNB59 Antikörper) alleles cause hearing loss of cochlear origin. These findings suggest that complex pathogenetic mechanisms underlie human deafness DFNB59 (zeige DFNB59 Antikörper).
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 (zeige TRIO Antikörper) RhoGEF (zeige ARHGEF28 Antikörper), which binds to E-cadherin (zeige CDH1 Antikörper) and subsequently increases the phosphorylation of p38 (zeige CRK Antikörper) and Tbx3 (zeige TBX3 Antikörper), a transcriptional E-cadherin (zeige CDH1 Antikörper) 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