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HPA008786

Sigma-Aldrich

Anti-TBX5 antibody produced in rabbit

enhanced validation

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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About This Item

UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.41

biological source

rabbit

Quality Level

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:
  • 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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WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

常规特殊物品

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
Ioannis Kokkinopoulos et al.
PloS one, 10(10), e0140831-e0140831 (2015-10-16)
In the early vertebrate embryo, cardiac progenitor/precursor cells (CPs) give rise to cardiac structures. Better understanding their biological character is critical to understand the heart development and to apply CPs for the clinical arena. However, our knowledge remains incomplete. With
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

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