ATM Antibody (C-term)
Purified Rabbit Polyclonal Antibody (Pab)
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- 背景知识
Application
| IHC-P, WB, E |
|---|---|
| Primary Accession | Q13315 |
| Other Accession | Q62388 |
| Reactivity | Human |
| Predicted | Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Antigen Region | 3027-3056 aa |
| Other Names | Serine-protein kinase ATM, Ataxia telangiectasia mutated, A-T mutated, ATM |
|---|---|
| Target/Specificity | This ATM antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 3027~3056 amino acids from the C-terminal region of human ATM. |
| Dilution | IHC-P~~1:100~500 WB~~1:500 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | ATM Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
ATM is involved in signal transduction, cell cycle control and DNA repair, and may function as a tumor suppressor. It is necessary for activation of ABL1 and SAPK, and phosphorylates p53, NFKBIA, BRCA1, CTIP, NIBRIN (NBS1), TERF1, and RAD9. This protein has potential roles in vesicle and/or protein transport, T-cell development, gonad and neurological function. ATM is also part of the BRCA1-associated genome surveillance complex. ATM is induced by ionizing radiation. Defects in ATM are the cause of ataxia talangiectasia (AT), also known as Louis-Bar syndrome, a rare recessive disorder characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. About 30% of AT patients develop lymphomas and leukemias. Defects in ATM also contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. Defects in ATM also contribute to B-cell non-Hodgkin's lymphomas, and to B-cell chronic lymphocytic leukemia, a disease characterized by accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.
REFERENCES
Suzuki, A., et al., J. Biol. Chem. 278(1):48-53 (2003).
Kishi, S., et al., J. Biol. Chem. 276(31):29282-29291 (2001).
Schaffner, C., et al., Proc. Natl. Acad. Sci. U.S.A. 97(6):2773-2778 (2000).
Gatei, M., et al., Nat. Genet. 25(1):115-119 (2000).
Becker-Catania, S.G., et al., Mol. Genet. Metab. 70(2):122-133 (2000).
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