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HPA018142

Sigma-Aldrich

Anti-SETDB1 antibody produced in rabbit

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

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About This Item

MDL number:
UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

human

technique(s)

immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:200-1:500

immunogen sequence

KLRFLIFFDDGYASYVTQSELYPICRPLKKTWEDIEDISCRDFIEEYVTAYPNRPMVLLKSGQLIKTEWEGTWWKSRVEEVDGSLVRILFLDDKRCEWIYRGSTRLEPMFSMKTSSASALEKKQGQLRTRPNMGAVRSKGPVVQYTQD

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... SETDB1(9869)

General description

The gene SET domain bifurcated-1 (SETDB1) is located in human chromosome 1 (1q21). The encoded protein contains a DNA methyl binding domain and catalytic SET domain at the N- and C-terminus respectively. In non­-small lung cancer cells SETDB1 is present mainly in the nucleus, with additional cytoplasmic expression. Similarly, mouse embryos showed SETDB1 signal in the nucleus.

Immunogen

Histone-lysine N-methyltransferase SETDB1 recombinant protein epitope signature tag (PrEST)

Application

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunohistochemistry (1 paper)

Biochem/physiol Actions

SET domain bifurcated-1 (SETDB1) is responsible for methylation of histone 3 lysine-9 in euchromatic region, resulting in a repressed transcription mark. During DNA replication, it is recruited by Methyl-CpG-binding domain protein-1 (MBD1) and forms a replication coupled complex with chromatin assemble factor CAF-1 to methylate lysine-9 at the newly deposited histone 3. The gene is up-regulated in glioma tissues, melanomas, non-small and small lung cancers. SETDB1 undergoes gene amplification in lung tumorigenesis. Higher expression causes stimulation of WNT-β-catenin pathway and down-regulation of P53 expression, resulting in enhanced non-small cell lung cancer growth. Role of SETDB1 in cancer is also suggested by its association with the promyelocytic nuclear leukemia-nuclear bodies and increased expression in broncoepithelial cells. SETDB1 is involved in proviral silencing during embryogenesis when DNA methylation is dynamically reprogrammed.

Features and Benefits

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Linkage

Corresponding Antigen APREST73723

Physical form

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

Legal Information

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

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

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

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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Shuai Han et al.
Journal of experimental & clinical cancer research : CR, 39(1), 218-218 (2020-10-17)
Glioblastoma is a common disease of the central nervous system (CNS), with high morbidity and mortality. In the infiltrate in the tumor microenvironment, tumor-associated macrophages (TAMs) are abundant, which are important factors in glioblastoma progression. However, the exact details of
Maria Kostaki et al.
Experimental dermatology, 23(5), 332-338 (2014-03-29)
Epigenetic mechanisms participate in melanoma development and progression. The effect of histone modifications and their catalysing enzymes over euchromatic promoter DNA methylation in melanoma remains unclear. This study investigated the potential association of p16(INK) (4A) promoter methylation with histone methyltransferase
M Rodriguez-Paredes et al.
Oncogene, 33(21), 2807-2813 (2013-06-19)
Disruption of the histone modification patterns is one of the most common features of human tumors. However, few genetic alterations in the histone modifier genes have been described in tumorigenesis. Herein we show that the histone methyltransferase SETDB1 undergoes gene
Wenlin Yang et al.
International journal of molecular medicine, 53(4) (2024-03-01)
SET domain bifurcated 1 (SETDB1), a pivotal histone lysine methyltransferase, is transported to the cytoplasm via a chromosome region maintenance 1 (CMR1)‑dependent pathway, contributing to non‑histone methylation. However, the function and underlying mechanism of cytoplasmic SETDB1 in breast cancer remain
Hideo Watanabe et al.
Cancer cell international, 8, 15-15 (2008-11-05)
Alterations in the processing of the genetic information in carcinogenesis result from stable genetic mutations or epigenetic modifications. It is becoming clear that nucleosomal histones are central to proper gene expression and that aberrant DNA methylation of genes and histone

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