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GTF2I encodes a multifunctional phosphoprotein with roles in transcription and signal transduction. Additionally we are shipping GTF2I Antibodies (125) and many more products for this protein.
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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 (show TGFB1 Proteins) signaling pathways
GTF2IRD2 (show GTF2IRD2 Proteins) 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 (show PARK7 Proteins) 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 (show SRC Proteins)-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 (show PIAS2 Proteins)
GTF2I mutations common in thymic epithelial tumors are not present/uncommon in hematological malignancies.
a new BRAF (show BRAF Proteins) 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 (show RBMS3 Proteins) 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 (show MDM2 Proteins) with a negative effect on TFII-I transcriptional activity has been documented.
Copy-number variation in the general transcription factor gene, GTF2I is associated with gene-dose-dependent anxiety in mouse models and in both Williams syndrome and Dup7.
show that SUMOylation is critical for TFII-I to promote cell proliferation and colony formation. Our findings contribute to understanding the role of SUMOylation in liver cancer development
Study demonstrates a significant association between SLE in Chinese Han population and the GTF2I rs117026326 T allele/GTF2IRD1 rs4717901 C allele.
Rather than contributing positively to promoter activity, a putative initiator element at the transcription start site acts as a target for negative regulation imposed on the L4P promoter of human adenovirus Type 5 by cellular TFII-I.
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 135
, Bruton tyrosine kinase-associated protein 135
, general transcription factor II-I
, BTK-associated protein, 135kD
, SRF-Phox1-interacting protein
, Williams-Beuren syndrome chromosome region 6
, general transcription factor II, i