HPA018142
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
Recommended Products
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)
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:
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
Anastasia Spyropoulou et al.
Neuromolecular medicine, 16(1), 70-82 (2013-08-15)
Posttranslational modifications of histones are considered as critical regulators of gene expression, playing significant role in the pathogenesis and progression of tumors. Trimethylation of histone 3 lysine 9 (H3K9me3), a repressed transcription mark, is mainly regulated by the histone lysine
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
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
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