
Thermo Fisher Scientific Phospho-ATM (Ser1987) Polyclonal Antibody
ATM 단백질의 Ser1987 인산화 상태를 특이적으로 인식하는 Rabbit Polyclonal 항체. Western blot에서 검증됨. 인간, 마우스, 랫트 시료에 반응. 세포 내 DNA 손상 반응 및 ATM 신호전달 연구에 적합.
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Applications
Western Blot (WB)
- Tested Dilution: 1:1,000–1:3,000
Product Specifications
| 항목 | 내용 |
|---|---|
| Species Reactivity | Human, Mouse, Rat |
| Host / Isotype | Rabbit / IgG |
| Class | Polyclonal |
| Type | Antibody |
| Immunogen | A synthesized peptide derived from human ATM (Accession Q13315), corresponding to amino acid residues around phosphorylated Ser1987 |
| Conjugate | Unconjugated |
| Form | Liquid |
| Concentration | 1 mg/mL |
| Purification | Sequential chromatography |
| Storage Buffer | PBS, pH 7.4, with 50% glycerol |
| Contains | 0.02% sodium azide |
| Storage Conditions | -20°C |
| Shipping Conditions | Wet ice |
| RRID | AB_2817515 |
Product Specific Information
Antibody detects endogenous levels of ATM only when phosphorylated at Ser1987.
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 within the phosphoinositide 3-kinase (PI3K) superfamily.
ATM phosphorylates proteins rather than lipids and targets multiple downstream regulators of the cell cycle, including P53, Mdm2, BRCA1, and SMC1.
ATM is essential for repairing double-stranded DNA breaks caused by ionizing radiation and other mutagens.
The C-terminal region of ATM shows homology to catalytic domains of PI3 kinases.
Upon exposure to ionizing radiation, ATM becomes autophosphorylated and activated, initiating kinase cascades that regulate cell cycle, apoptosis, and DNA damage repair.
ATM also participates in apoptosis signaling through interactions 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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