S8316
Monoclonal Anti-SUV39H1 Histone Methyltransferase antibody produced in mouse
~2 mg/mL, clone 44.1, purified immunoglobulin, buffered aqueous solution
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About This Item
Recommended Products
biological source
mouse
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
44.1, monoclonal
form
buffered aqueous solution
species reactivity
mouse, human
concentration
~2 mg/mL
technique(s)
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
indirect ELISA: suitable
microarray: suitable
western blot: 2-4 μg/mL using extract of HeLa nuclear cells
isotype
IgG1
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... SUV39H1(6839)
mouse ... Suv39h1(20937)
General description
Monoclonal Anti-SUV39H1 Histone Methyltransferase (mouse IgG1 isotype) is derived from the 44.1 hybridoma produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with the recombinant fusion protein MBP-SUV39H1.
Specificity
Monoclonal Anti-SUV39H1 Histone Methyltransferase recognizes an epitope in the N-terminal (195 amino acids) of human and mouse SUV39H1 Histone Methyltransferase.
Immunogen
recombinant fusion protein MBP-SUV39H1
Application
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)
Western Blotting (1 paper)
Monoclonal Anti-SUV39H1 Histone Methyltransferase antibody is suitable for use in ELISA, immunoblotting (~47 kDa), immunoprecipitation, and immunoncytochemistry applications.
For immunoblotting, a working concentration of 2-4 mg/mL is recommended using an extract of HeLa nuclear cells.
For immunoblotting, a working concentration of 2-4 mg/mL is recommended using an extract of HeLa nuclear cells.
Biochem/physiol Actions
Combined disruption of both mouse SUV39H1 and 2 causes chromosomal instability and increased risk of tumorigenesis, as well as complete spermatogenic failure that is caused by non-homologous chromosome associations.
Post -translational modification of histones, such as phosphorylation, acetylation, and methylation, are crucial for chromatin remodeling. SUV39H1 and Suv39h1 are the human and mouse homologs of Drosophila Su(var)3-9 protein, respectively. These proteins selectively methylate histone H3 at lysine 9 creating a high-affinity binding site for the HP1 proteins (heterochromatin protein 1). HP1 proteins are known to interact with transcription suppressor proteins, suggesting that the interactions with SUV39H1 and methylated histone H3 mediate a silence effect on the transcription of target genes. Over-expression of SUV39H1 in HeLa cells causes a redistribution of endogenous HP1 proteins and growth retardation, suggesting that SUV39H1-mediated modulation of heterochromatin can impair cell cycle progression.
The overall identity between the human and mouse SUV39H1 amino acid sequences is 95%, both lacking an N-terminal 155 amino acid stretch from Drosophila Su(var)3-9. As a consequence, cross-species amino acid identity reaches 42% between the fly and the two mammalian proteins. The SUV39H1 protein consists of three regions: a SET domain, a 110 amino acid domain containing several cysteine conserved residues, and a chromo domain.
The overall identity between the human and mouse SUV39H1 amino acid sequences is 95%, both lacking an N-terminal 155 amino acid stretch from Drosophila Su(var)3-9. As a consequence, cross-species amino acid identity reaches 42% between the fly and the two mammalian proteins. The SUV39H1 protein consists of three regions: a SET domain, a 110 amino acid domain containing several cysteine conserved residues, and a chromo domain.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, 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
10 - Combustible liquids
WGK
WGK 3
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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Find documentation for the products that you have recently purchased in the Document Library.
Loss of the Suv39h histone methyltransferases impairs mammalian heterochromatin and genome stability
Peters AHFM, et al.
Cell, 107(3), 323-337 (2001)
Angela M Carter et al.
Oncogenesis, 10(12), 83-83 (2021-12-05)
Pancreatic neuroendocrine tumors (PanNETs) are a heterogeneous population of neoplasms that arise from hormone-secreting islet cells of the pancreas and have increased markedly in incidence over the past four decades. Non-functional PanNETs, which occur more frequently than hormone-secreting tumors, are
Francesco Casciello et al.
Proceedings of the National Academy of Sciences of the United States of America, 114(27), 7077-7082 (2017-06-21)
G9a is an epigenetic regulator that methylates H3K9, generally causing repression of gene expression, and participates in diverse cellular functions. G9a is genetically deregulated in a variety of tumor types and can silence tumor suppressor genes and, therefore, is important
Jun Okabe et al.
Circulation research, 110(8), 1067-1076 (2012-03-10)
Epigenetic changes are implicated in the persisting vascular effects of hyperglycemia. The precise mechanism whereby chromatin structure and subsequent gene expression are regulated by glucose in vascular endothelial cells remain to be fully defined. We have studied the molecular and
Angela M Carter et al.
Proceedings of the National Academy of Sciences of the United States of America, 117(31), 18401-18411 (2020-07-22)
Disparities in cancer patient responses have prompted widespread searches to identify differences in sensitive vs. nonsensitive populations and form the basis of personalized medicine. This customized approach is dependent upon the development of pathway-specific therapeutics in conjunction with biomarkers that
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