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GTF2I encodes a multifunctional phosphoprotein with roles in transcription and signal transduction.
We identified rs117026326 on GTF2I with GWAS significance (P = 1.10 x 10(-15)) and rs13079920 on RBMS3 (show RBMS3 Antibodies) 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 (show ASZ1 Antibodies) 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 Antibodies) 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 Antibodies) 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 Antibodies) and Polzeta to promote Translesion synthesis
The GTF2I rs117026326 polymorphism is associated with anti-SSA (show TRIM21 Antibodies)-positive primary Sjogren's syndrome.
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