G2298
Anti-GATA6 (221-235) antibody produced in rabbit
IgG fraction of antiserum, buffered aqueous solution
Synonyme(s) :
Anti-GATA binding protein 6
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About This Item
Code UNSPSC :
12352203
Produits recommandés
Source biologique
rabbit
Conjugué
unconjugated
Forme d'anticorps
IgG fraction of antiserum
Type de produit anticorps
primary antibodies
Clone
polyclonal
Forme
buffered aqueous solution
Poids mol.
antigen ~60 kDa
Espèces réactives
human
Technique(s)
western blot: 1:500-1:2,000
Numéro d'accès UniProt
Conditions d'expédition
dry ice
Température de stockage
−20°C
Informations sur le gène
human ... GATA6(2627)
Immunogène
synthetic peptide corresponding to amino acids 221-235 of human GATA6
Application
Anti-GATA6 antibody produced in rabbit is suitable for western blotting at a working dilution of 1:500-1:2000.
Yale Center for High Throughput Cell Biology IF-tested antibodies. Each antibody is tested by immunofluorescence against HUVEC cells using the Yale HTCB IF protocol. To learn more about us and Yale Center for High Throughput Cell Biology partnership, visit sigma.com/htcb-if.
Yale Center for High Throughput Cell Biology IF-tested antibodies. Each antibody is tested by immunofluorescence against HUVEC cells using the Yale HTCB IF protocol. To learn more about us and Yale Center for High Throughput Cell Biology partnership, visit sigma.com/htcb-if.
Actions biochimiques/physiologiques
GATA6 (GATA binding protein 6) gene encodes a member of a family of zinc finger transcription factors. During vertebrate development, it plays a key role in the regulation of cellular differentiation and organogenesis. It may play a crucial role in cardiac differentiation. Mutation in this gene causes human cardiac outflow tract defects by disrupting semaphorin-plexin signaling.
Forme physique
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Clause de non-responsabilité
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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E Suzuki et al.
Genomics, 38(3), 283-290 (1996-12-15)
GATA factors constitute a family of transcriptional regulatory proteins expressed with distinct developmental and tissue-specific profiles and thought to regulate cell-restricted programs of gene expression. Here we describe the molecular cloning, chromosomal location, and transcription of the human GATA-6 gene.
Xuechao Jiang et al.
Orphanet journal of rare diseases, 16(1), 334-334 (2021-08-02)
TBX1 (T-box transcription factor 1) is a major candidate gene that likely contributes to the etiology of velo-cardio-facial syndrome/DiGeorge syndrome (VCFS/DGS). Although the haploinsufficiency of TBX1 in both mice and humans results in congenital cardiac malformations, little has been elucidated
I C Huggon et al.
Biochimica et biophysica acta, 1353(2), 98-102 (1997-08-07)
Human GATA-6 has been cloned from foetal heart by a combination of PCR-based methods and cDNA library screening. The 3.8 kbp cDNA has a coding sequence of 1347 bp the 449 aa protein is virtually identical in the two zinc-finger
A Brewer et al.
The Journal of biological chemistry, 274(53), 38004-38016 (1999-12-23)
GATA-6 has been implicated in the regulation of myocardial differentiation during cardiogenesis. To determine how its expression is controlled, we have characterized the human and mouse genes. We have mapped their transcriptional start sites and demonstrate that two alternative promoters
GATA6 mutations cause human cardiac outflow tract defects by disrupting semaphorin-plexin signaling.
Kazuki Kodo et al.
Proceedings of the National Academy of Sciences of the United States of America, 106(33), 13933-13938 (2009-08-12)
Congenital heart diseases (CHD) occur in nearly 1% of all live births and are the major cause of infant mortality and morbidity. Although an improved understanding of the genetic causes of CHD would provide insight into the underlying pathobiology, the
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