HPA008786
Anti-TBX5 antibody produced in rabbit
Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
Anti-4P11, Anti-HOS, Anti-OTTHUMG00000018096, Anti-QOH-1, Anti-T-box 5, Anti-bA342C24.4
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All Photos(4)
About This Item
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biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
product line
Prestige Antibodies® Powered by Atlas Antibodies
form
buffered aqueous glycerol solution
species reactivity
human
enhanced validation
orthogonal RNAseq
Learn more about Antibody Enhanced Validation
technique(s)
immunohistochemistry: 1:50-1:200
immunogen sequence
MSRMQSKEYPVVPRSTVRQKVASNHSPFSSESRALSTSSNLGSQYQCENGVSGPSQDLLPPPNPYPLPQEHSQIYHCTKRKEEECSTTDHPYKKPYMETSPSEEDSFYRSSYPQQQG
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... TBX5(6910)
General description
TBX5 (T-box 5) is a transcription factor belonging to the evolutionary conserved T-box family of genes. This gene is localized to human chromosome 12q24.1. This protein is expressed in proepicardial organ (PEO)/ septum transversum.
Immunogen
T-box 5 recombinant protein epitope signature tag (PrEST)
Application
Anti-TBX5 antibody produced in rabbit, a Prestige Antibody, is developed and validated by the Human Protein Atlas (HPA) project . Each antibody is tested by immunohistochemistry against hundreds of normal and disease tissues. These images can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. The antibodies are also tested using immunofluorescence and western blotting. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
Biochem/physiol Actions
TBX5 (T-box 5) plays a key role in the morphogenesis of vertebrate cardiac system. It controls cardiac growth and development by acing as an inducer of cardiac cell division arrest. Mutations in this gene result in cardiac abnormalities, such as septation defects and isomeris. Mutations also result in deformation of upper limbs and Holt-Oram syndrome (HOS), which is an autosomal dominant disorder. Mutations in this gene are also associated with arrhythmias and non-synodromic/synodromic congenital heart diseases. Loss of function mutation in this gene also results in familial dilated cardiomyopathy.
Features and Benefits
Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.
Every Prestige Antibody is tested in the following ways:
Every Prestige Antibody is tested in the following ways:
- IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
- Protein array of 364 human recombinant protein fragments.
Linkage
Corresponding Antigen APREST70864
Physical form
Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide.
Legal Information
Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Nata Y S-G Diman et al.
Circulation research, 115(10), 834-844 (2014-09-24)
Holt-Oram syndrome is an autosomal dominant heart-hand syndrome caused by mutations in the TBX5 gene. Overexpression of Tbx5 in the chick proepicardial organ impaired coronary blood vessel formation. However, the potential activity of Tbx5 in the epicardium itself, and the
Irfan S Kathiriya et al.
Developmental cell, 56(3), 292-309 (2020-12-16)
Haploinsufficiency of transcriptional regulators causes human congenital heart disease (CHD); however, the underlying CHD gene regulatory network (GRN) imbalances are unknown. Here, we define transcriptional consequences of reduced dosage of the CHD transcription factor, TBX5, in individual cells during cardiomyocyte
Xian-Ling Zhang et al.
Biochemical and biophysical research communications, 459(1), 166-171 (2015-03-01)
The cardiac T-box transcription factor TBX5 is crucial for proper cardiovascular development, and mutations in TBX5 have been associated with various congenital heart diseases and arrhythmias in humans. However, whether mutated TBX5 contributes to dilated cardiomyopathy (DCM) remains unclear. In
C J Hatcher et al.
Developmental biology, 230(2), 177-188 (2001-02-13)
Mutations in human TBX5, a member of the T-box transcription factor gene family, cause congenital cardiac septation defects and isomerism in autosomal dominant Holt-Oram syndrome. To determine the cellular function of TBX5 in cardiogenesis, we overexpressed wild-type and mutant human
Deborah A McDermott et al.
Pediatric research, 58(5), 981-986 (2005-09-27)
Holt-Oram syndrome (HOS) is an autosomal dominant heart-hand syndrome characterized by congenital heart disease (CHD) and upper limb deformity, and caused by mutations in the TBX5 gene. To date, the sensitivity of TBX5 genetic testing for HOS has been unclear.
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