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Validated All-in-One™ qPCR Primer for GTF2I(NM_001518.4) Search again
Product ID:
HQP008506
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BAP135, BTKAP1, DIWS, GTFII-I, IB291, SPIN, TFII-I, WBS, WBSCR6
Gene Description:
general transcription factor IIi
Target Gene Accession:
NM_001518.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- G-kinase I beta interacted specifically with TFII-I, an unusual transcriptional regulator that associates with multiple proteins to modulate both basal and signal-induced transcription
- GTF2IRD1 and GTF2I have roles in causing deficits on visual spatial functioning
- Comparison of these five families with reports of other individuals with partial deletions of the WS region most strongly implicates GTF2I in the mental retardation of WS.
- TFII-I is required for optimal induction of Grp78 by ER stress
- These results demonstrate that USF1/USF2 and TFII-I interact cooperatively at the upstream RBEIII element and are necessary for the induction of latent HIV-1 in response to T-cell activation signals.
- human VEGFR-2 promoter is functionally counter-regulated by TFII-I and TFII-IRD1.
- cGMP-dependent protein kinase Ibeta binds to TFII-I and IRAG through a common interaction motif
- TFII-I is recruited to the cyclin D1 promoter and transcriptionally activates this gene.
- TFII-I directly interacts with Bright through amino acids in Bright's protein interaction domain
- The data suggest that TFII-I and USF regulate chromatin structure accessibility and recruitment of transcription complexes in the beta-globin gene locus.
- observations suggest a model in which TFII-I suppresses agonist-induced calcium entry by competing with TRPC3 for binding to phospholipase C-gamma
- TFII-I, PARP1, and SFPQ proteins, each previously implicated in gene regulation, form a complex controlling transcription of DYX1C1. Allelic differences in the promoter or 5'UTR of DYX1C1 may affect factor binding and thus regulation of the gene.
- Bioinformatics and microarray results were combined to identify TFII-I downstream targets in the vertebrate genome.
- These results demonstrate an essential role of TFII-I bound at an upstream LTR element for viral replication.
- alpha(2)-macroglobulin induced increase in GRP78 synthesis is caused by transcriptional upregulation of TFII-I
- analyzed promoter regions of TFII-I genes and described their additional exons, as well as tested tissue specificity of both previously reported and novel alternatively spliced isoforms