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Validated All-in-One™ qPCR Primer for TBX5(NM_000192.3) Search again
Product ID:
HQP017930
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HOS
Gene Description:
T-box transcription factor 5
Target Gene Accession:
NM_000192.3(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:
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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 is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box.
Gene References into function
- large TBX5 deletion in a family with Holt-Oram syndrome
- These results reveal TBX5 as a new regulator of apoptosis and cell growth, suggesting a possible mechanism for Holt-Oram syndrome, and a potential reagent for controlling tumor growth.
- functional analysis of missense mutations associated with Holt-Oram syndrome
- results implicate GATA4 as a genetic cause of human cardiac septal defects, perhaps through its interaction with TBX5
- Causes of phenotypic diversity in cardiac embryogenesis in TBX5 mutations.
- TBX5 nuclear localization is mediated by dual cooperative intramolecular signals
- Studies enhance understanding of the structure-function relationship of TBX5 and suggest that truncation mutations of TBX5 could cause Holt-Oram syndrome (HOS) through the loss of its transactivating domain and/or the nuclear localization signal.
- Eight novel TBX5 mutations found in patients with non-Holt-Oram syndrome complex cardiac malformations.
- NKX2.5 inhibits myocyte differentiation and myotube formation, and up-regulates Gata4 and Tbx5 expression
- Novel mutations within the TBX5 gene are associated with Holt-Oram syndrome.
- This study confirms TBX5 genetic testing should be reserved for patients who fulfill the strict phenotypic criteria for Holt-Oram syndrome.
- Tbx18 interacts with Gata4 and Nkx2-5 and competes Tbx5-mediated activation of the cardiac Natriuretic peptide precursor type a-promoter. Tbx18 down-regulates Tbx6-activated Delta-like 1 expression in the somitic mesoderm in vivo
- Tbx5-dependent pathway for the transcriptional control of diastolic function, with potential implications for the pathogenesis of heart failure
- we describe a large atypical Holt-Oram syndrome family with mild skeletal deformations and paroxysmal atrial fibrillation, but few have congenital heart disease. Sequencing of TBX5 revealed a novel mutation, c.373G>A, resulting in p.Gly125Arg.
- The residues 267-448 at the C-terminus of TBX5 are highly homologous to the C-terminus domain of yeast DNA-directed RNA polymerase II largest subunit.
- Fluorescence in situ hybridization did not show major deletions or duplications at chromosome 22q11 as well as the TBX5/TBX3 region at 12q24.1.
- The mutation c.1333delC does not locate within functional domains, but impairs the activation of the downstream target