製品名
抗トリメチル-ヒストンH3(Lys9)抗体 クローン6F12-H4, clone 6F12-H4, from mouse
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)
関連するカテゴリー
Analysis Note
ウェスタンブロッティング: 希釈倍率0.5–5 μgで使用、HeLa酸抽出物中のトリメチルヒストンH3(Lys9)を検出できます。
Application
前ロットの代表的なデータ。超音波処理した3T3L1クロマチンを、抗トリメチルヒストンH3(Lys9)抗体およびMagna ChIP G(カタログ番号:17-611)キットを用いたクロマチン免疫沈降に供しました。トリメチルヒストンH3(Lys9)関連DNA断片の免疫沈降の成功は、p16プロモーターに隣接するプライマーを用いたqPCRによって検証しました。
ペプチド阻害分析:
ペプチド阻害アッセイは、トリメチル型とジメチル型の抗体で異なる選好性を示します。
クロマチン免疫沈降(ChIP):
既知の染色体Suv39h標的(主要サテライトのH3K9me3、マウスES細胞)のChIP解析。
ドットブロッティング:
ヒストンH3のトリメチルLys9に対する抗H3K9me3抗体 クローン6F12-H4の特異性を示すドットブロッティング:
Biochem/physiol Actions
General description
Physical form
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保管分類
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
試験成績書(COA)
製品のロット番号・バッチ番号を入力して、試験成績書(COA) を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。
関連コンテンツ
"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).
グローバルトレードアイテム番号
| カタログ番号 | GTIN |
|---|---|
| 05-1242 | 04053252740237 |
ライフサイエンス、有機合成、材料科学、クロマトグラフィー、分析など、あらゆる分野の研究に経験のあるメンバーがおります。.
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