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Primary Antibodies > DNA Damage and Repair Antibodies

ATM Protein Kinase S1981 Antibody

Rabbit Polyclonal

Code

600-401-398

Size

100 µg

Price

$334.00

Availability

Ships next business day.

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Polyclonal rabbit anti ATM antibody detects ATM in HeLa Nuclear lysates run on 4-8% gel and transferred for 1 hr at 100V to 0.45 um nitrocelllose
Membrane was Blocked in 5% Blotto 1 Hour 4oC. HRP Goat anti Rabbit 611-103-122 Lot#21231 was used for detection 1:20,000 in MB-070 1 Hour 4oC

Shipping & Handling Fees Apply.

Shipping:

$85.00 to United States

Handling:

$45.00

Synonyms: Ataxia telangiectasia mutated

Datasheet
References
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ATM Protein Kinase S1981 Antibody Properties

Description

Anti-ATM Protein Kinase S1981 (RABBIT) Antibody - 600-401-398

Host

Rabbit

Target Species

Human

Known Cross Reactivity

Human, Mouse

Clonality

Polyclonal

Application

ELISA : 1:10,000 - 1:50,000
Western Blot : 1:500- 1:2,000
Other Dilution: User Optimized

Physical State

Liquid (sterile filtered)

Shipping condition

Dry Ice

Format

IgG

Label

Unconjugated

Concentration

1.1 mg/mL by UV absorbance at 280 nm

Buffer

0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2

Preservative

0.01% (w/v) Sodium Azide

Stabilizer

None

GeneName

ATM

ATM Protein Kinase S1981 Antibody Description

Background

ATM, the gene mutated in the hereditary disease ataxia-telangiectasia, codes for a protein kinase that acts as a master regulator of cellular responses to DNA double-strand breaks. ATM is normally inactive and the question of how it is activated in the event of DNA damage (due to ionizing radiation for instance) is central to understanding its function. ATM protein is now shown to be present in undamaged cells as an inactive dimer. Low doses of ionizing radiation, which induce only a few DNA breaks, activate at least half of the total ATM protein present, possibly in response to changes in chromatin structure. The ATM gene encodes a 370-kDa protein that belongs to the phosphoinositide 3-kinase (PI(3)K) superfamily, but which phosphorylates proteins rather than lipids. The 350-amino-acid kinase domain at the carboxy terminus of this large protein is the only segment of ATM with an assigned function. Exposure of cells to IR triggers ATM kinase activity, and this function is required for arrests in G1, S and G2 phases of the cell cycle. Several substrates of the ATM kinase participate in these IR-induced cell-cycle arrests. These include p53, Mdm2 and Chk2 in the G1 checkpoint; Nbs1, Brca1, FancD2 and SMC1 in the transient IR-induced S-phase arrest; and Brca1 and hRad17 in the G2/M checkpoint. See Bakkenist, C. J. & Kastan, M. B. Nature 421, 499-506 (2003) for a complete presentation of this antibody's specificity and utility.

Immunogen

This antibody was affinity purified from whole rabbit serum prepared by repeated immunizations with a synthetic peptide S-L-A-F-E-E-G-S-Q-S-T-T-I-S-S corresponding to aa 1974-1988 of human ATM conjugated to KLH using maleimide.

Immunogen Type

Peptide

Storage Condition

Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use.

Application Note

Affinity purified rabbit anti-ATM has been tested by ELISA, immunofluorescence microscopy, western blotting and biological assays against both the native and recombinant forms of the protein.

Purity/Specifity

This affinity-purified antibody is directed against human ATM and is useful in determining its presence in various assays. This polyclonal anti-ATM antibody detects native and over-expressed proteins found in various tissues and extracts. Reactivity is observed against human ATM and cross reactivity with ATM from other mammalian sources has not been tested.

Disclaimer Note-General

This product is for research use only and is not intended for therapeutic or diagnostic applications. Please contact a technical service representative for more information. All products of animal origin manufactured by Rockland Immunochemicals are derived from starting materials of North American origin. Collection was performed in United States Department of Agriculture (USDA) inspected facilities and all materials have been inspected and certified to be free of disease and suitable for exportation. All properties listed are typical characteristics and are not specifications. All suggestions and data are offered in good faith but without guarantee as conditions and methods of use of our products are beyond our control. All claims must be made within 30 days following the date of delivery. The prospective user must determine the suitability of our materials before adopting them on a commercial scale. Suggested uses of our products are not recommendations to use our products in violation of any patent or as a license under any patent of Rockland Immunochemicals, Inc. If you require a commercial license to use this material and do not have one, then return this material, unopened to: Rockland Inc., P.O. BOX 326, Gilbertsville, Pennsylvania, USA.

General Reference

Bakkenist, C. J. & Kastan, M. B. (2003). DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation. Nature 421, 499-506. Kitagawa R, Bakkenist CJ, McKinnon PJ, Kastan MB. (2004) Phosphorylation of SMC1 is a critical downstream event in the ATM-NBS1-BRCA1 pathway. Genes Dev. 18(12):1423-38. Falck, J. Coates, J. and Jackson, S.P. (2005) Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage. Nature 434: 605-611. Bartkova J, Horejsi Z, Koed K, Kramer A, Tort F, Zieger K, Guldberg P, Sehested M, Nesland JM, Lukas C, Orntoft T, Lukas J, Bartek J. (2005) DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis. Nature 434; 864-870. Bartkova J, Bakkenist CJ, Rajpert-De Meyts E, Skakkebaek NE, Sehested M, Lukas J, Kastan MB, Bartek J. (2005) ATM Activation in Normal Human Tissues and Testicular Cancer. Cell Cycle 4;(6) [Epub ahead of print]. Shi Y, Dodson GE, Mukhopadhyay PS, Shanware NP, Trinh AT, Tibbetts RS. (2007) Identification of carboxyl-terminal MCM3 phosphorylation sites using polyreactive phosphospecific antibodies. J Biol Chem. 282(12):9236-43. Batchelor, E., Mock, C.S., Bhan, I., Loewer, A., Lahav, G. (2008) Recurrent Initiation: A Mechanism for Triggering p53 Pulses in Response to DNA Damage. Mol Cell. 30(3): 277-89.

Specific Reference

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