Informacje o tej pozycji
Przejdź do
biological source
rabbit
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
mouse, human
technique(s)
dot blot: suitable, immunocytochemistry: suitable, inhibition assay: suitable (peptide), western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
trimethylation (Lys27)
Gene Information
human ... HIST1H3F(8968)
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Ta pozycja | |||
|---|---|---|---|
| Quality Level 100 | Quality Level 100 | Quality Level 100 | Quality Level 100 |
| antibody form affinity isolated antibody | antibody form affinity isolated antibody | antibody form affinity isolated antibody | antibody form affinity isolated antibody |
| biological source rabbit | biological source rabbit | biological source rabbit | biological source rabbit |
| technique(s) dot blot: suitable, inhibition assay: suitable (peptide), immunocytochemistry: suitable, western blot: suitable | technique(s) dot blot: suitable, immunoprecipitation (IP): suitable, western blot: suitable | technique(s) dot blot: suitable, western blot: suitable | technique(s) dot blot: suitable, immunoprecipitation (IP): suitable, western blot: suitable |
| UniProt accession no. | UniProt accession no. | UniProt accession no. | UniProt accession no. |
| clone polyclonal | clone polyclonal | clone polyclonal | clone polyclonal |
General description
Immunogen
Application
Peptide Inhibition Assay: This antibody peptide blocked on HeLa cell extracts.
Epigenetics & Nuclear Function
Histones
Biochem/physiol Actions
Physical form
Preparation Note
Analysis Note
HeLa acid extract and recombinant Histone H3
Western Blot Analysis: 0.1 µg/ml of this antibody detected histone H3 in 10 µg of HeLa acid extract .
Other Notes
Disclaimer
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Klasa składowania
12 - Non Combustible Liquids
wgk
WGK 1
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Powiązane treści
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).
Numer pozycji handlu globalnego
| SKU | NUMER GTIN |
|---|---|
| ABE44 | 04053252675270 |
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