anti-ATM, mAb (9A2)

CHF 322.00
In stock
YIF-LF-MA0254100 µlCHF 322.00
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Product Details
Synonyms ATM; EC=2.7.11.1; A-T Mutated; Serine-Protein Kinase ATM; Ataxia Telangiectasia Mutated
Product Type Monoclonal Antibody
Properties
Clone 9A2
Isotype Mouse IgG2b κ
Immunogen/Antigen Recombinant human His-ATM (aa 2841-3056) protein purified from E. coli.
Application

ELISA
Western Blot (1:2,000)
Immunoprecipitation (1 μl)

Crossreactivity Human
Purity Detail Ammonium sulfate precipitation.
Formulation Liquid. HEPES with 0.15M NaCl, 0.01% BSA, 0.03% sodium azide, and 50% glycerol.
Other Product Data

Click here for Original Manufacturer Product Datasheet
Our product description may differ slightly from the original manufacturers product datasheet.

Declaration Manufactured by AbFrontier
Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Use/Stability Stable for at least 1 year after receipt when stored at -20°C.
Documents
MSDS Inquire
Product Specification Sheet
Datasheet Download PDF

Ataxia telangiectasia mutated (ATM) is a serine/threonine-specific protein kinase that is activated by DNA double-strand breaks. It phosphorylates several key proteins that initiate activation of the DNA damage checkpoint, leading to cell cycle arrest, DNA repair or apoptosis. Several of these targets are p53, CHK2, BRCA1, and H2AX. ATM triggers the G1/S checkpoint; ATR (Ataxia telangiectasia and Rad3-related) prevents G1/S stasis. In this single point in the cell cycle, it would appear that ATM and ATR function in opposition to one another. Ataxia telangiectasia (AT) is a rare neurodegenerative, autosomal recessive disorder characterized by chromosome instability, radiosensitivity, immunodeficiency and a predisposition for cancer. The ATR (ATM and Rad3-related) kinase and its downstream effector kinase, Chk1, are central regulators of the replication checkpoint. Loss of these checkpoint proteins causes replication fork collapse and chromosomal rearrangements. ATR are thought to be master controllers of cell cycle checkpoint signaling pathways that are required for cell response to DNA damage and for genome stability. Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Plays a role in replication-dependent histone mRNA degradation. Binds DNA ends.

Product References

1) Paulsen RD and Cimprich KA. (2007), DNA Repair (Amst) 6 (7):953-966. (General)
2) Hurley PJ and Bunz F. (2007), Cell Cycle. 6(4):414-417. (General)
3) Kurz EU and Lees-Miller SP, (2005), DNA Repair (Amst) 3 (8-9):889-900. (General)

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