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GTF2I encodes a multifunctional phosphoprotein with roles in transcription and signal transduction. Additionally we are shipping GTF2I Antibodies (118) and many more products for this protein.
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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 (show GTF2IRD1 Proteins) 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)
TFII-I has a role in regulating immunoglobulin promoter activity
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 (show GTF2IRD1 Proteins) 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.
Findings implicate the GTF2I gene in the neurogenetic basis of social communication and social anxiety, both in Williams syndrome and among individuals in healthy populations
TFII-I bridges Proliferating Cell Nuclear Antigen (show PCNA Proteins) and Polzeta to promote Translesion synthesis
The GTF2I rs117026326 polymorphism is associated with anti-SSA (show TRIM21 Proteins)-positive primary Sjogren's syndrome.
A proportion of this transcriptional dysregulation is caused by dosage imbalances in GTF2I, which encodes a key transcription factor at 7q11.23 that is associated with the LSD1 (show KDM1A Proteins) repressive chromatin complex and silences its dosage-sensitive targets.
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