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Merck

M7443

Sigma-Aldrich

Anti-MeCP2 antibody, Mouse monoclonal

clone Men-8, purified from hybridoma cell culture

Synonym(e):

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

MDL-Nummer:
UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

mouse

Qualitätsniveau

Konjugat

unconjugated

Antikörperform

purified from hybridoma cell culture

Antikörper-Produkttyp

primary antibodies

Klon

Men-8, monoclonal

Form

buffered aqueous solution

Mol-Gew.

antigen ~75 kDa

Speziesreaktivität

mouse, human, rat, monkey

Verpackung

antibody small pack of 25 μL

Methode(n)

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

Isotyp

IgG1

UniProt-Hinterlegungsnummer

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

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

Allgemeine Beschreibung

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.

Immunogen

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

Anwendung

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

Biochem./physiol. Wirkung

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).

Physikalische Form

Solution in 0.01 M phosphate buffered saline containing 15 mM sodium azide.

Haftungsausschluss

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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Lagerklassenschlüssel

12 - Non Combustible Liquids

WGK

nwg

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

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)
Ube3a mRNA and protein expression are not decreased in Mecp2R168X mutant mice
Lawson-Yuen A, et al.
Brain Research, 1180, 1-6 (2007)
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)
Gang Meng et al.
Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 36(4), 3009-3015 (2015-01-24)
Methyl-CpG-binding protein 2 (MeCP2) is essential in human brain development and has been linked to several cancer types and neuro-developmental disorders. This study aims to screen the MeCP2 related differentially expressed genes and discover the therapeutic targets for osteosarcoma. CCK8
Shikun He et al.
Investigative ophthalmology & visual science, 56(9), 5579-5589 (2015-08-26)
The purpose of this study was to evaluate expression of methyl-CpG-binding protein 2 (MeCP2) in epiretinal membranes from patients with proliferative vitreoretinopathy (PVR) and to investigate effects of inhibition of MeCP2 and DNA methylation on transforming growth factor (TGF)-β-induced retinal

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