
Thermo Fisher Scientific ATM Polyclonal Antibody
ATM 단백질을 인식하는 Rabbit Polyclonal Antibody로, Western blot 및 IHC(P) 실험에 적합합니다. 인간 ATM 단백질의 1980–2338 아미노산 영역을 항원으로 제작되었습니다. DNA 손상 복구 및 세포주기 조절 연구에 활용 가능합니다.
- 카탈로그번호
- PA133016
- 판매단위
- pk
카탈로그
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Applications
| Application | Tested Dilution |
|---|---|
| Western Blot (WB) | 1:500–1:1,000 |
| Immunohistochemistry (Paraffin) (IHC (P)) | 1:50 |
Product Specifications
| 항목 | 내용 |
|---|---|
| Host / Isotype | Rabbit / IgG |
| Class | Polyclonal |
| Type | Antibody |
| Immunogen | Recombinant human ATM fragment (amino acids 1980–2338) |
| Conjugate | Unconjugated |
| Form | Liquid |
| Concentration | Not determined |
| Storage conditions | Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles. |
| Shipping conditions | Wet ice |
| RRID | AB_1956224 |
Product Specific Information
Store product as a concentrated solution. Centrifuge briefly prior to opening the vial.
Target Information
Ataxia-telangiectasia Mutated (ATM) is a protein that belongs to the PI3/PI4 kinase family.
Ataxia-telangiectasia is a rare autosomal recessive disorder characterized by progressive neurologic degeneration, immunologic deficiency, and an increased risk of lymphoid cancer.
The ATM gene encodes a protein that phosphorylates other proteins involved in cell-cycle regulation, including P53, Mdm2, BRCA1, and SMC1.
ATM is responsible 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.
ATM becomes autophosphorylated and upregulated upon exposure to ionizing radiation. AT cells are hypersensitive to radiation, display impaired DNA synthesis inhibition, and delayed p53 induction.
DNA damage activates ATM kinase, triggering a cascade of reactions regulating cell cycle, apoptosis, and DNA damage repair.
ATM is also linked 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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