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The protein encoded by GTF2I contains five GTF2I-like repeats and each repeat possesses a potential helix-loop-helix (HLH) motif.
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we identified largest-ever effect on Asian rheumatoid arthritis across human non-HLA regions at GTF2I by heterogeneity mapping followed by replication studies, and pinpointed a possible causal variant
the frequency of GTF2I mutation is higher in more indolent TETs and correlated with better prognosis.
GTF2I/Gtf2i, its physiologic role in human disorders was relatively unknown until recently. Novel studies show that it is involved in an array of human diseases including neurocognitive disorders, systemic lupus erythematosus (SLE), and cancer.
the results reported here support a model whereby common genetic variation in GTF2I mediates human sociality and anxiety via effects on oxytocin reactivity.
GTF2I mutations common in thymic epithelial tumors are not present/uncommon in hematological malignancies.
a new BRAF (zeige BRAF Proteine) fusion in pilocytic astrocytoma
A common polymorphism in the Williams syndrome gene GTF2I associated with reduced social anxiety predicts decreased threat-related amygdala reactivity, which mediates an association between genotype and increased warmth in women.
We identified rs117026326 on GTF2I with GWAS significance (P = 1.10 x 10(-15)) and rs13079920 on RBMS3 (zeige RBMS3 Proteine) with suggestive significance (P = 2.90 x 10(-5)) associating with Primary Sjogren's syndrome in women.
The authors found that human adenovirus 5 infection or ectopic E4-ORF3 expression leads to SUMOylation of TFII-I that precedes a rapid decline in TFII-I protein levels.
A novel interaction between TFII-I and Mdm2 (zeige MDM2 Proteine) with a negative effect on TFII-I transcriptional activity has been documented.
The Cre-mediated deletion of exon 3 recapitulates a genetic null phenotype, indicating that the conditional Gtf2i line is a valuable tool for studying TFII-I function during embryonic development
found a highly conserved DNA element, common to a set of genes regulated by TFII-I, and identified and validated novel in vivo neuronal targets of this protein affecting the PI3K and TGFbeta (zeige TGFB1 Proteine) signaling pathways
GTF2IRD2 (zeige GTF2IRD2 Proteine) has evolved as a regulator of GTF2IRD1 and TFII-I; inhibiting their function by direct interaction and sequestration into inactive nuclear zones.
data support the hypothesis that upregulation of TFII-I factors leads to activation of a specific group of developmental genes during mESC differentiation
GTF2I duplication results in separation anxiety in mice and humans
In order to clarify the involvement of GTF2I in neurocognitive function, especially social behavior, we have developed and characterized Gtf2i-deficient mice.
Results suggest that DJ-1 (zeige PARK7 Proteine) together with TFII-I operate in concert to cope with various insults and to sustain pancreatic beta-cell function.
behavioral characterization of heterozygous mice with a deletion of the first 140 amino-acids of TFII-I.
data demonstrate that TFII-I, through a Src (zeige SRC Proteine)-dependent mechanism, reversibly translocates from the cytoplasm to the nucleus, leading to the transcriptional activation of growth-regulated genes
acts as a transcriptional cofactor for the SUMO ubiquitin-protein isopeptide ligase family member Miz1/PIASxbeta /Siz2 (zeige PIAS2 Proteine)
This gene encodes a multifunctional phosphoprotein with roles in transcription and signal transduction. It is deleted in Williams-Beuren syndrome, a multisystem developmental disorder caused by the deletion of contiguous genes at chromosome 7q11.23. Alternative splicing results in multiple transcript variants. Related pseudogenes have been identified on chromosomes 7, 13 and 21.
BTK-associated protein, 135kD
, Bruton tyrosine kinase-associated protein 135
, SRF-Phox1-interacting protein
, Williams-Beuren syndrome chromosome region 6
, general transcription factor II-I
, BTK-associated protein 135
, general transcription factor II, i
, general transcription factor IIi L homeolog
, general transcription factor IIi S homeolog