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Key Documents

07-1375

Sigma-Aldrich

抗磷酸化雄激素受体(Ser81)抗体

Upstate®, from rabbit

别名:

Anti-AIS, Anti-AR8, Anti-DHTR, Anti-HUMARA, Anti-HYSP1, Anti-KD, Anti-NR3C4, Anti-SBMA, Anti-SMAX1, Anti-TFM

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About This Item

分類程式碼代碼:
12352203
eCl@ss:
32160702
NACRES:
NA.41

生物源

rabbit

品質等級

抗體表格

affinity isolated antibody

抗體產品種類

primary antibodies

無性繁殖

polyclonal

純化經由

affinity chromatography

物種活性

human

物種活性(以同源性預測)

dog (expected based only 1 amino acid difference), horse (expected based only 1 amino acid difference), primate (expected based only 1 amino acid difference), bovine (expected based only 1 amino acid difference)

製造商/商標名

Upstate®

技術

western blot: suitable

NCBI登錄號

UniProt登錄號

運輸包裝

wet ice

目標翻譯後修改

phosphorylation (pSer81)

基因資訊

bovine ... Ar(280675)
dog ... Ar(403588)
human ... AR(367)

一般說明

X连锁雄激素受体(二氢睾酮受体;核受体亚家族3 C组成员4)是NR3配体依赖性转录因子家族的成员,其特征在于C末端的配体结合结构域、中央DNA结合结构域和N末端转录激活结构域。 雄激素受体被类固醇激素如睾酮和二氢睾酮激活。活化的雄激素受体从细胞质转移到细胞核,它们形成结合DNA的同型二聚体。雄激素受体与许多衔接子样蛋白结合,并作为复合物起作用,该复合物可以诱导或抑制转录,这取决于其相关蛋白是可能通过修饰染色质影响转录的共激活因子还是共抑制因子。共激活因子参与组蛋白乙酰化和转录激活,而共抑制因子参与组蛋白去乙酰化和转录抑制。雄激素受体对于确定性别和雄性特征很重要。缺陷的雄激素受体可能在Reifenstein综合征,肯尼迪病以及前列腺癌中起作用。

特異性

仅在Ser81磷酸化后检测雄激素受体(AR)

免疫原

对应于人雄激素受体Ser81及其周围氨基酸的KLH结合合成肽。

應用

抗磷酸雄激素受体(Ser81)抗体是一种针对磷酸雄激素受体(Ser81)的抗体,用于WB。
研究子类别
转录因子
研究类别
信号传导

表观遗传学&核功能

品質

通过蛋白质印迹对R1881(甲雌三烯醇酮)处理的LNCap裂解液进行了常规评估

標靶描述

110 kDa

外觀

纯化的兔多克隆抗体,溶于含有0.1 M Tris-甘氨酸(pH 7.4)、150 mM NaCl和0.05%叠氮化钠的缓冲液中。

儲存和穩定性

自收到之日起在2-8°C可稳定保存1年。
处理建议:收到后,在取下瓶盖之前,将小瓶离心并轻轻混合溶液。避免反复冻融,其可能会破坏IgG并影响产品性能。

分析報告

对照
R1881(甲三烯醇酮)处理的LNCap裂解液

法律資訊

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

免責聲明

除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。

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儲存類別代碼

12 - Non Combustible Liquids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Nooshin Mirkheshti et al.
Oncotarget, 7(38), 62240-62254 (2016-08-25)
Androgen receptor (AR) and PI3K/AKT/mTORC1 are major survival signals that drive prostate cancer to a lethal disease. Reciprocal activation of these oncogenic pathways from negative cross talks contributes to low/limited success of pathway-selective inhibitors in curbing prostate cancer progression. We
J M Willder et al.
British journal of cancer, 108(1), 139-148 (2013-01-17)
Prostate cancer cell growth is dependent upon androgen receptor (AR) activation, which is regulated by specific kinases. The aim of the current study is to establish if AR phosphorylation by Cdk1 or ERK1/2 is of prognostic significance. Scansite 2.0 was
Shidong Lv et al.
The Journal of clinical investigation, 131(4) (2020-12-18)
Nuclear localization of the androgen receptor (AR) is necessary for its activation as a transcription factor. Defining the mechanisms regulating AR nuclear localization in androgen-sensitive cells and how these mechanisms are dysregulated in castration-resistant prostate cancer (CRPC) cells is fundamentally
Dagmara McGuinness et al.
Methods in molecular biology (Clifton, N.J.), 1443, 105-117 (2016-06-02)
The detection of phosphorylation status of proteins has become a critical component of the analysis of activity, localization, and turnover studies of most proteins, particularly for those involved in signaling. The androgen receptor is no exception to this rule with
André Richters et al.
Cell chemical biology, 28(2), 134-147 (2020-10-22)
Castration-resistant prostate cancers (CRPCs) lose sensitivity to androgen-deprivation therapies but frequently remain dependent on oncogenic transcription driven by the androgen receptor (AR) and its splice variants. To discover modulators of AR-variant activity, we used a lysate-based small-molecule microarray assay and

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