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M7443

Sigma-Aldrich

Anti-MeCP2 antibody, Mouse monoclonal

clone Men-8, purified from hybridoma cell culture

Synonym(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

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified from hybridoma cell culture

antibody product type

primary antibodies

clone

Men-8, monoclonal

form

buffered aqueous solution

mol wt

antigen ~75 kDa

species reactivity

mouse, human, rat, monkey

packaging

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

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

General description

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.

Application

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

Biochem/physiol Actions

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).

Physical form

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

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

12 - Non Combustible Liquids

WGK

nwg

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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Radically truncated MeCP2 rescues Rett syndrome-like neurological defects
Tillotson R, et al.
Nature, 550(7676), 398-398 (2017)
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)
Smitha Sripathy et al.
Proceedings of the National Academy of Sciences of the United States of America, 114(7), 1619-1624 (2017-02-02)
Rett syndrome (RS) is a debilitating neurological disorder affecting mostly girls with heterozygous mutations in the gene encoding the methyl-CpG-binding protein MeCP2 on the X chromosome. Because restoration of MeCP2 expression in a mouse model reverses neurologic deficits in adult

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