癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
Anti-ATM (C-terminal region) Antibody
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, FC, ICC, IP |
|---|---|
| Primary Accession | Q13315 |
| Host | Mouse |
| Clonality | Mouse Monoclonal |
| Isotype | IgG2b |
| Clone Names | M361 |
| Calculated MW | 350687 Da |
| Gene ID | 472 |
|---|---|
| Other Names | ataxia telangiectasia mutated, AT1 ATDC TEL1 TELO1 |
| Target/Specificity | Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. Activation of ATM after DNA damage involves Cdk5 mediated phosphorylation of Ser-794 followed by autophosphorylation at Ser-1891. Active ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis and DNA repair. The Cdk5–ATM pathway regulates phosphorylation and function of the ATM targets p53 and H2AX in postmitotic neurons. Other known substrates of ATM include Chk2, Chk1, CtIP, 4E-BP1, BRCA1, RPA3, SMC1, FANCD2, Rad17, Artemis, Nbs1, and the I-2 regulatory subunit of PP1. Thus, activation of Cdk5 by DNA damage may be an important initiator of ATM-dependent regulation of cell cycle checkpoints. |
| Dilution | WB~~1:1000 FC~~1:10~50 ICC~~N/A IP~~N/A |
| Format | Protein A Purified |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Anti-ATM (C-terminal region) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Shipping | Blue Ice |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. Activation of ATM after DNA damage involves Cdk5 mediated phosphorylation of Ser-794 followed by autophosphorylation at Ser-1891. Active ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis and DNA repair. The Cdk5–ATM pathway regulates phosphorylation and function of the ATM targets p53 and H2AX in postmitotic neurons. Other known substrates of ATM include Chk2, Chk1, CtIP, 4E-BP1, BRCA1, RPA3, SMC1, FANCD2, Rad17, Artemis, Nbs1, and the I-2 regulatory subunit of PP1. Thus, activation of Cdk5 by DNA damage may be an important initiator of ATM-dependent regulation of cell cycle checkpoints.
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