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Key Documents

M7443

Sigma-Aldrich

Anti-MeCP2 antibody, Mouse monoclonal

clone Men-8, purified from hybridoma cell culture

Synonyme(s) :

Anti-AUTSX3, Anti-MRX16, Anti-MRX79, Anti-MRXS13, Anti-MRXSL, Anti-PPMX, Anti-RS, Anti-RTS, Anti-RTT

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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

purified from hybridoma cell culture

Type de produit anticorps

primary antibodies

Clone

Men-8, monoclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~75 kDa

Espèces réactives

mouse, human, rat, monkey

Conditionnement

antibody small pack of 25 μL

Technique(s)

immunocytochemistry: suitable
indirect ELISA: suitable
microarray: suitable
western blot: 1-2 μg/test using nuclear extract of cultured human acute T cell leukemia Jurkat cells or MCF7 cells

Isotype

IgG1

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... MECP2(4204)
mouse ... Mecp2(17257)
rat ... Mecp2(29386)

Catégories apparentées

Description générale

Methyl-CpG binding protein 2 (MeCP2) possesses a methyl-CpG-binding domain (MBD) and a transcriptional repression domain.
Monoclonal Anti-MeCP2 (mouse IgG1 isotype) is derived from the Men-8 hybridoma produced by the fusion of mouse myeloma cells (NS1) and splenocytes from BALB/c mice immunized with a synthetic peptide corresponding to the N-terminus of human MeCP2.

Immunogène

synthetic peptide corresponding to the N-terminus (amino acids 15-30) of human MeCP2.

Application

Monoclonal Anti-MeCP2 antibody has been used:
  • in western blotting
  • in immunoblotting
  • in flow cytometry
  • in immunohistofluorescence
  • in immunocytochemistry

Actions biochimiques/physiologiques

MeCP2 (methyl-CpG binding protein 2) silences transcription by recruiting the histone deacetylase (HDAC) repressive machinery via recruitment of the Sin 3A corepressor, thus removing acetyl groups from histones and consequently, silencing genes.
Methyl-CpG binding protein 2 (MeCP2) has been shown be crucial for brain development. It part of the methyl-CpG-binding proteins, which are involved in repression of gene expression by binding to methylated DNA. Mutations in the gene encoding MeCP2 have been associated with Rett syndrome (RTT).

Forme physique

Solution in 0.01 M phosphate buffered saline 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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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Radically truncated MeCP2 rescues Rett syndrome-like neurological defects
Tillotson R, et al.
Nature, 550(7676), 398-398 (2017)
Paul D Ross et al.
Human molecular genetics, 25(20), 4389-4404 (2017-02-09)
Rett syndrome (RTT) is a severe genetic disorder resulting from mutations in the X-linked MECP2 gene. MeCP2 protein is highly expressed in the nervous system and deficiency in the mouse central nervous system alone recapitulates many features of the disorder.
Rett syndrome mutations abolish the interaction of MeCP2 with the NCoR/SMRT co-repressor
Lyst M J, et al.
Nature Neuroscience, 16(7), 898-898 (2013)
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice
Lawson-Yuen A, et al.
Brain Research, 1180, 1-6 (2007)
A codon-optimized Mecp2 transgene corrects breathing deficits and improves survival in a mouse model of Rett syndrome
Matagne V, et al.
Neurobiology of Disease, 99, 1-11 (2017)

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