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Mouse Anti-GTF2I Recombinant Antibody (CBYJT-1332) (CBMAB-T0348-YJ)

Provided herein is a Mouse monoclonal antibody, which binds to GTF2I (General Transcription Factor IIi). The antibody can be used for immunoassay techniques, such as WB, IP, IF.
See all GTF2I antibodies

Summary

Host Animal
Mouse
Specificity
Human, Rat, Mouse
Clone
CBYJT-1332
Antibody Isotype
IgG
Application
WB, IP, IF

Basic Information

Immunogen
Amino acids 650-857 of TFII-I of TFII-I of human origin
Specificity
Human, Rat, Mouse
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Buffer
PBS, pH 7.4
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
aa 650-857

Target

Full Name
GTF2I
Introduction
GTF2I interacts with the basal transcription machinery by coordinating the formation of a multiprotein complex at the C-FOS promoter, and linking specific signal responsive activator complexes. GTF2I promotes the formation of stable high-order complexes of SRF and PHOX1 and interacts cooperatively with PHOX1 to promote serum-inducible transcription of a reporter gene deriven by the C-FOS serum response element (SRE). GTF2I acts as a coregulator for USF1 by binding independently two promoter elements, a pyrimidine-rich initiator (Inr) and an upstream E-box. It is required for the formation of functional ARID3A DNA-binding complexes and for activation of immunoglobulin heavy-chain transcription upon B-lymphocyte activation.
Entrez Gene ID
Human2969
Mouse14886
Rat353256
UniProt ID
HumanP78347
MouseQ9ESZ8
RatQ5U2Y1
Alternative Names
General Transcription Factor IIi; Bruton Tyrosine Kinase-Associated Protein 135; SRF-Phox1-Interacting Protein; GTFII-I; WBSCR6; BAP135; TFII-I; SPIN; Williams-Beuren Syndrome Chromosomal Region 6 Protein; Williams-Beuren Syndrome Chromosome Region 6
Function
Interacts with the basal transcription machinery by coordinating the formation of a multiprotein complex at the C-FOS promoter, and linking specific signal responsive activator complexes. Promotes the formation of stable high-order complexes of SRF and PHOX1 and interacts cooperatively with PHOX1 to promote serum-inducible transcription of a reporter gene deriven by the C-FOS serum response element (SRE). Acts as a coregulator for USF1 by binding independently two promoter elements, a pyrimidine-rich initiator (Inr) and an upstream E-box. Required for the formation of functional ARID3A DNA-binding complexes and for activation of immunoglobulin heavy-chain transcription upon B-lymphocyte activation.
Biological Process
Negative regulation of angiogenesis Source: MGI
Positive regulation of DNA repair by transcription from RNA polymerase II promoter Source: ARUK-UCL
Cellular Location
Cytoplasm; Nucleus. Colocalizes with BTK in the cytoplasm.
Involvement in disease
GTF2I is located in the Williams-Beuren syndrome (WBS) critical region. WBS results from a hemizygous deletion of several genes on chromosome 7q11.23, thought to arise as a consequence of unequal crossing over between highly homologous low-copy repeat sequences flanking the deleted region. Haploinsufficiency of GTF2I may be the cause of certain cardiovascular and musculo-skeletal abnormalities observed in the disease.
PTM
Transiently phosphorylated on tyrosine residues by BTK in response to B-cell receptor stimulation. Phosphorylation on Tyr-248 and Tyr-398, and perhaps, on Tyr-503 contributes to BTK-mediated transcriptional activation.
Sumoylated.

Pan, Y., Iejima, D., Nakayama, M., Suga, A., Noda, T., Kaur, I., ... & Iwata, T. (2021). Binding of Gtf2i-β/δ transcription factors to the ARMS2 gene leads to increased circulating HTRA1 in AMD patients and in vitro. Journal of Biological Chemistry, 296.

Lee, J., Rho, J. H., Roehrl, M. H., & Wang, J. Y. (2021). Dermatan sulfate is a potential regulator of IgH via interactions with pre-BCR, GTF2I, and BiP ER complex in pre-B lymphoblasts. Frontiers in immunology, 12, 680212.

Liu, C., Yan, S., Chen, H., Wu, Z., Li, L., Cheng, L., ... & Li, Y. (2021). Association of GTF2I, NFKB1, and TYK2 regional polymorphisms with systemic sclerosis in a Chinese Han population. Frontiers in Immunology, 12, 640083.

Shimoyama, S., Nakagawa, I., Jiang, J. J., Matsumoto, I., Chiorini, J. A., Hasegawa, Y., ... & Murakami, M. (2021). Sjögren’s syndrome-associated SNPs increase GTF2I expression in salivary gland cells to enhance inflammation development. International immunology, 33(8), 423-434.

Cavallo, F., Troglio, F., Fagà, G., Fancelli, D., Shyti, R., Trattaro, S., ... & Testa, G. (2020). High-throughput screening identifies histone deacetylase inhibitors that modulate GTF2I expression in 7q11. 23 microduplication autism spectrum disorder patient-derived cortical neurons. Molecular autism, 11(1), 1-18.

Kim, I. K., Rao, G., Zhao, X., Fan, R., Avantaggiati, M. L., Wang, Y., ... & Giaccone, G. (2020). Mutant GTF2I induces cell transformation and metabolic alterations in thymic epithelial cells. Cell Death & Differentiation, 27(7), 2263-2279.

Higuchi, R., Goto, T., Hirotsu, Y., Yokoyama, Y., Nakagomi, T., Otake, S., ... & Omata, M. (2020). Primary driver mutations in GTF2I specific to the development of thymomas. Cancers, 12(8), 2032.

Barak, B., Zhang, Z., Liu, Y., Nir, A., Trangle, S. S., Ennis, M., ... & Feng, G. (2019). Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drug. Nature neuroscience, 22(5), 700-708.

Kopp, N., McCullough, K., Maloney, S. E., & Dougherty, J. D. (2019). Gtf2i and Gtf2ird1 mutation do not account for the full phenotypic effect of the Williams syndrome critical region in mouse models. Human molecular genetics, 28(20), 3443-3465.

Chailangkarn, T., Noree, C., & Muotri, A. R. (2018). The contribution of GTF2I haploinsufficiency to Williams syndrome. Molecular and cellular probes, 40, 45-51.

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For research use only. Not intended for any clinical use.

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