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Validated All-in-One™ qPCR Primer for TBX2(NM_005994.3) Search again
Product ID:
HQP017929
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
VETD
Gene Description:
T-box transcription factor 2
Target Gene Accession:
NM_005994.3(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:
Summary
This gene is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box.
Gene References into function
- identification of a variant T-site as the essential TBX2/TBX3-binding element in the human p14(ARF) promoter
- upregulation of Tbx2 gene in response to tension downregulates CX43 in cranial sutures
- In human melanoma cells, expression of dnTbx2 leads to severely reduced growth and induction of senescence-associated heterochromatin foci.
- Results are consistent with Tbx2 playing a role in cell cycle progression and organization of subnuclear compartments.
- Tbx2 in fibroblasts reduces expression of the COL1A2 gene
- the ability of Tbx2 to repress the p21 gene is enhanced in response to a stress-induced senescence pathway, which leads to a better understanding of the regulation of the anti-senescence function of Tbx2.
- identify a Sp1 element and a reverse CCAAT box to be essential for basal Tbx2 promoter activity
- Tbx2 and Tbx3 may play a dual role during the radial to vertical growth phase transition by both inhibiting senescence via repression of p21(CIP1) expression, and enhancing melanoma invasiveness by decreasing E-cadherin levels.
