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biological source
mouse
antibody form
purified antibody
antibody product type
primary antibodies
clone
6F12-H4, monoclonal
species reactivity
mouse, human
technique(s)
ChIP: suitable (ChIP-seq), dot blot: suitable, immunofluorescence: suitable, inhibition assay: suitable (peptide), western blot: suitable
isotype
IgG1κ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
trimethylation (Lys9)
Quality Level
Gene Information
human ... H3C1(8350)
mouse ... H3C1(360198)
Categorías relacionadas
General description
Application
Datos representativos de un lote anterior. La cromatina 3T3 L1 tratada con ultrasonidos fue sometida a inmunoprecipitación de cromatina utilizando anti-trimetilhistona H3 (Lys9) y el kit Magna ChIP G (Nº de ref. 17-611). La inmunoprecipitación exitosa de fragmentos de ADN asociados a la trimetilhistona H3 (Lys9) se verificó mediante qPCR utilizando cebadores que flanquean el promotor p16.
Análisis de inhibición de péptidos:
El ensayo de bloqueo de péptidos demuestra una preferencia clara del anticuerpo por la forma trimetilada frente a la forma dimetilada.
Inmunoprecipitación de la cromatina (CHIP):
Análisis de ChIP de blancos cromosómicos Suv39h conocidos (H3K9me3 en los satélites principales, células ES de ratón).
Análisis mediante inmunotransferencia por puntos:
Análisis mediante inmunotransferencia por puntos que demuestra la especificidad del anti-H3K9me3, clon 6F12-H4, por la Lys9 trimetilada de la histona H3.
Biochem/physiol Actions
Physical form
Analysis Note
Análisis mediante inmunotransferencia Western: Una dilución 0,5 – 5 μg de este lote detectó la trimetil histona H3 (Lys9) en extractos ácidos de HeLa.
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Clase de almacenamiento
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificados de análisis (COA)
Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»
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Contenido relacionado
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).
"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."
Número de artículo de comercio global
| SKU | GTIN |
|---|---|
| 05-1242 | 04053252740237 |
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