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PLA0011

Sigma-Aldrich

Rabbit anti-DNMT1 Antibody, Affinity Purified

Powered by Bethyl Laboratories, Inc.

Synonym(s):

ADCADN, AIM, CXXC-type zinc finger protein 9, CXXC9, DNA MTase HsaI, DNA methyltransferase HsaI, DNMT, Dnmt1, HSN1E, MCMT, m.HsaI

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

100

antibody form

affinity purified immunoglobulin

antibody product type

primary antibodies

grade

Powered by Bethyl Laboratories, Inc.

species reactivity

human

technique(s)

immunoprecipitation (IP): 2-4 μg/mg
western blot: 1:2000-1:10,000

accession no.

NP_001370.1

UniProt accession no.

P26358

shipped in

wet ice

storage temp.

2-8°C

target post-translational modification

unmodified

Gene Information

rabbit ... DNMT1(1786)

Immunogen

The epitope recognized by PLA0011 maps to a region between residue 700 and 750 of human DNA-Methyltranserase 1 using the numbering given in entry NP_001370.1 (GeneID 1786).

Physical form

Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% sodium azide

Other Notes

DNA methyltransferase 1 (DNMT1) catalyzes the methylation of the 5′-cytosine in the dinucleotide sequence, CpG. DNMT1 is thought to be responsible for the regulation of methylation patterns that are important in development and influence gene expression in a time- and tissue-specific manner.

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

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

新产品

Certificates of Analysis (COA)

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Clara Dees et al.
The Journal of clinical investigation, 130(5), 2347-2363 (2020-01-29)
Fibroblasts are key effector cells in tissue remodeling. They remain persistently activated in fibrotic diseases, resulting in progressive deposition of extracellular matrix. Although fibroblast activation may be initiated by external factors, prolonged activation can induce an "autonomous," self-maintaining profibrotic phenotype

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