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Thermo Fisher Scientific ATM Monoclonal Antibody (5C5)
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Thermo Fisher Scientific ATM Monoclonal Antibody (5C5)

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Human ATM 단백질을 인식하는 Mouse IgG1 단클론 항체로, WB 및 ELISA에 적합. 비결합형 액상 형태이며, 단기 4°C, 장기 -20°C 보관 권장. DNA 손상 반응 및 세포주기 조절 연구에 유용.

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마지막 업데이트 2025. 08. 05. 오후 03:43
Thermo Fisher Scientific MA515816 ATM Monoclonal Antibody (5C5) 100 ul pk판매 단위 pk ·
재고 확인 필요
742,900원VAT 포함 817,190원

Thermo Fisher Scientific · Thermo Fisher Scientific ATM Monoclonal Antibody (5C5)

Applications

Western Blot (WB)

  • Tested Dilution: 1:500–1:2,000

ELISA

  • Tested Dilution: 1:10,000

Product Specifications

항목 내용
Species Reactivity Human
Host / Isotype Mouse / IgG1
Class Monoclonal
Type Antibody
Clone 5C5
Immunogen Purified recombinant fragment of human ATM expressed in E. coli
Conjugate Unconjugated
Form Liquid
Concentration Not determined
Storage Buffer Ascites
Contains 0.03% sodium azide
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_11155793

Product Specific Information

MA5-15816 targets ATM in indirect ELISA and WB applications, showing reactivity with human samples.
The immunogen is a purified recombinant fragment of human ATM expressed in E. coli.
MA5-15816 detects ATM, which has a predicted molecular weight of approximately 351 kDa.


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. ATM phosphorylates proteins rather than lipids and has downstream targets that act as cell-cycle regulators, 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 extensive homology to catalytic domains of PI3 kinases.
Studies show ATM becomes autophosphorylated and upregulated upon exposure to ionizing radiation. AT cells are hypersensitive to ionizing radiation, impaired in mediating DNA synthesis inhibition, and display delays in p53 induction.
DNA damage caused by ionizing radiation activates ATM kinase, leading to a cascade of kinase reactions regulating cell cycle, apoptosis, and DNA damage 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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