
Thermo Fisher Scientific Phospho-ATM (Ser1981) Monoclonal Antibody (M366)
Phospho-ATM (Ser1981) 단일클론 항체로 인간, 생쥐, 랫트 시료에서 ATM 단백질의 인산화 형태 검출에 적합. WB, ICC/IF, IP 응용 가능. Protein A로 정제된 액상 형태로 안정적이며, DNA 손상 반응 연구에 유용.
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Applications
| Application | Tested Dilution |
|---|---|
| Western Blot (WB) | 1:1,000 |
| Immunocytochemistry (ICC/IF) | 1:200 |
| Immunoprecipitation (IP) | 1:100 |
Product Specifications
| 항목 | 내용 |
|---|---|
| Species Reactivity | Human, Mouse, Rat |
| Host / Isotype | Mouse / IgG1 |
| Class | Monoclonal |
| Type | Antibody |
| Clone | M366 |
| Immunogen | Clone M366 was generated from a phospho-peptide that included amino acids surrounding Serine 1981 in human ATM. This sequence has high homology to the conserved site in rat and mouse ATM. |
| Conjugate | Unconjugated |
| Form | Liquid |
| Concentration | 0.44 mg/mL |
| Purification | Protein A |
| Storage Buffer | PBS with 1 mg/mL BSA, 50% glycerol |
| Contains | 0.05% sodium azide |
| Storage Conditions | -20°C, Avoid Freeze/Thaw Cycles |
| Shipping Conditions | Wet ice |
| RRID | AB_2942600 |
Product Specific Information
This antibody detects a 370 kDa protein corresponding to the molecular mass of ATM on SDS-PAGE immunoblots of calyculin A treated human A431 and Jurkat cells, but is not observed in control cells.
Target Information
Ataxia-telangiectasia Mutated (ATM) is a protein belonging to the PI3/PI4 kinase family. Ataxia-telangiectasia is a rare autosomal recessive disorder characterized by progressive neurologic degeneration, immunologic deficiency, and increased risk of lymphoid cancer. The ATM gene encodes a protein of the phosphoinositide 3-kinase (PI3K) superfamily that phosphorylates proteins instead of lipids. ATM has downstream targets including P53, Mdm2, BRCA1, and SMC1, which act as cell-cycle regulators. It is essential for repairing double-stranded DNA breaks caused by ionizing radiation and other mutagens. The C-terminal region of ATM shares homology with catalytic domains of PI3 kinases. ATM becomes autophosphorylated and upregulated upon exposure to ionizing radiation. AT cells are hypersensitive to radiation, show impaired DNA synthesis inhibition, and delayed p53 induction. DNA damage activates ATM-kinase, triggering kinase cascades that regulate cell cycle, apoptosis, and DNA repair. Studies have linked ATM to apoptosis along with Nbs1 and Chk2 in the E2F1 pathway.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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