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About This Item
biological source
rabbit
Quality Level
antibody form
serum
antibody product type
primary antibodies
clone
polyclonal
species reactivity
Saccharomyces cerevisiae, yeast, human
manufacturer/tradename
Upstate®
technique(s)
ChIP: suitable (ChIP-seq)
dot blot: suitable
multiplexing: suitable
western blot: suitable
isotype
IgG
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
acetylation (Lys14)
Gene Information
human ... H3C1(8350)
General description
Immunogen
Application
An independent laboratory has shown this antibody preferentially immunoprecipitates chromatin from wild type yeast and not from yeast strains containing a Lysine substitution to Alanine at residue 14.
Beadlyte Histone-Peptide Specificity Assay:
1:1000-1:5000 dilutions of a previous lot were incubated with histone H3 peptides containing various modifications conjugated to Luminex microspheres. No cross-reactivity with peptides containing acetyl-lysine 9 or acetyl-lysine 27 was detected.
Epigenetics & Nuclear Function
Histones
Biochem/physiol Actions
Physical form
Preparation Note
For maximum recovery of product, centrifuge the vial prior to removing the cap.
Analysis Note
C6 cell lysate, NIH 3T3 cell lysate, human breast carcinoma and human lung carcinoma.
Western Blot Analysis:
A 1:1000-1:5000 dilution of this lot detected acetyl-Histone H3 (Lys14) in acid extracts from sodium butyrate treated HeLa cells (Catalog # 17-305).
Other Notes
Legal Information
Disclaimer
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
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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Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).
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