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Informazioni su questo articolo
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Origine biologica
rabbit
Livello qualitativo
Forma dell’anticorpo
affinity isolated antibody
Tipo di anticorpo
primary antibodies
Clone
polyclonal
Purificato mediante
affinity chromatography
Reattività contro le specie
human, mouse, rat
tecniche
ChIP: suitable
dot blot: suitable
immunoprecipitation (IP): suitable
western blot: suitable
N° accesso NCBI
N° accesso UniProt
Condizioni di spedizione
wet ice
modifica post-traduzionali bersaglio
trimethylation (Lys20)
Informazioni sul gene
human ... H4C1(8359)
mouse ... H4C1(326619)
1 of 4
Questo articolo | 04-079 | 04-079-S | 07-463-S |
|---|---|---|---|
| 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 |
| clone polyclonal | clone monoclonal | clone monoclonal | clone polyclonal |
| antibody form affinity isolated antibody | antibody form culture supernatant | antibody form culture supernatant | antibody form affinity isolated antibody |
| UniProt accession no. | UniProt accession no. | UniProt accession no. | UniProt accession no. |
| shipped in wet ice | shipped in wet ice | shipped in wet ice | shipped in wet ice |
Descrizione generale
Immunogeno
Applicazioni
Epigenetica & funzione nucleare
Analisi di specificità mediante Dot Blot: peptidi istonici non modificati e con varie modificazioni (vedere le tabelle) sono stati identificati mediante l′anticorpo anti-trimetil-istone H4 (Lys20) (4 µg/mL).
Analisi di immunoprecipitazione della cromatina: un lotto rappresentativo ha causato l′immunoprecipitazione dell′istone H4 utilizzando cromatina ottenuta da cellule HeLa.
Analisi di immunoprecipitazione: un lotto rappresentativo ha causato l′immunoprecipitazione del trimetil-istone H4 (Lys20) da lisato di cellule HeLa.
Istoni
Azioni biochim/fisiol
Stato fisico
Nota sulla preparazione
Risultati analitici
Estratto acido di cellule HeLa e varie proteine istoniche ricombinanti.
Saggio di Western blotting: questo anticorpo alla concentrazione di 2 µg/mL ha permesso di rivelare il trimetil-istone H4 (Lys20) in 10 µg di estratto acido di cellule HeLa.
Altre note
Esclusione di responsabilità
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Codice della classe di stoccaggio
12 - Non Combustible Liquids
Classe di pericolosità dell'acqua (WGK)
WGK 1
Punto d’infiammabilità (°F)
Not applicable
Punto d’infiammabilità (°C)
Not applicable
Certificati d'analisi (COA)
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Signaling Product Guide: Antibodies, small molecule inhibitors, kits, assays and proteins for signaling research.
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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