07-463
Anti-Trimethyl-Histon-H4(Lys20)-Antikörper
from rabbit, purified by affinity chromatography
Synonym(e):
Histone H4 (trimethyl Lys20), H4K20me3
Größe auswählen
| Packungsgröße | SKU | Verfügbarkeit | Preis |
|---|---|---|---|
| 100 μg | Warenkorb auf Verfügbarkeit prüfen | € 545,00 |
Über diesen Artikel
biological source
rabbit
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
human, mouse, rat
technique(s)
ChIP: suitable, dot blot: suitable, immunoprecipitation (IP): suitable, western blot: suitable
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
trimethylation (Lys20)
Gene Information
human ... H4C1(8359)
mouse ... H4C1(326619)
General description
Immunogen
Application
Histone
Epigenetik & Zellkernfunktion
Dot-Blot-Spezifizitätsanalyse: Nichtmodifizierte und verschiedene modifizierte Histon-Peptide (siehe Tabellen) wurden mit Anti-Trimethyl-Histon H4 (Lys20) (4 µg/ml) untersucht.
Chromatin-Immunpräzipitation: Eine repräsentative Charge immunpräzipitierte Histon H4 mit Chromatin aus HeLa-Zellen.
Immunpräzipitation: Eine repräsentative Charge immunpräzipitierte Trimethyl-Histon H4 (Lys20) aus HeLa-Zelllysat.
Biochem/physiol Actions
Physical form
Preparation Note
Analysis Note
HeLa-Säureextrakt und verschiedene rekombinante Histon-Proteine.
Western-Blot-Analyse: 2 µg/ml dieses Antikörpers wiesen Histon H4 (Lys20) in 10 µg HeLa-Säureextrakt nach.
Other Notes
Disclaimer
1 of 1
Dieser Artikel | |||
|---|---|---|---|
| clone polyclonal | clone monoclonal | clone monoclonal | clone polyclonal |
| biological source rabbit | biological source rabbit | biological source rabbit | biological source rabbit |
| species reactivity human, mouse, rat | species reactivity vertebrates, human | species reactivity human, vertebrates | species reactivity rat, human, mouse |
| antibody form affinity isolated antibody | antibody form culture supernatant | antibody form culture supernatant | antibody form affinity isolated antibody |
| Gene Information human ... H4C1(8359) | Gene Information human ... H4C1(8359) | Gene Information human ... H4C1(8359) | Gene Information human ... H4C1(8359) |
| technique(s) ChIP: suitable, immunoprecipitation (IP): suitable, dot blot: suitable, western blot: suitable | technique(s) ChIP: suitable, dot blot: suitable, western blot: suitable | technique(s) ChIP: suitable, dot blot: suitable, western blot: suitable | technique(s) ChIP: suitable, dot blot: suitable, immunoprecipitation (IP): suitable, western blot: suitable |
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Lagerklasse
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Analysenzertifikate (COA)
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Verwandter Inhalt
Signaling Product Guide: Antibodies, small molecule inhibitors, kits, assays and proteins for signaling research.
"Epigenetics describes heritable changes in gene expression caused by non-genetic mechanisms instead of by alterations in DNA sequence. These changes can be cell- or tissue-specific, and can be passed on to multiple generations. Epigenetic regulation enriches DNAbased information, allowing a cell to vary its response across diverse biological and environmental contexts. Although epigenetic mechanisms are primarily centered in the nucleus, these mechanisms can be induced by environmental signals such as hormones, nutrients, stress, and cellular damage, pointing to the involvement of cytoplasmic and extracellular factors in epigenetic regulation."
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).