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Merck

PC461

PhosphoDetect Anti-p53 (pSer¹⁵) (Ab-6) Rabbit pAb

liquid, Calbiochem®, from rabbit

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About This Item

UNSPSC Code:
12352203
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Product Name

PhosphoDetect Anti-p53 (pSer¹⁵) (Ab-6) Rabbit pAb, liquid, Calbiochem®, from rabbit

biological source

rabbit

antibody product type

primary antibodies

form

liquid

does not contain

preservative

species reactivity

human

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
avoid repeated freeze/thaw cycles

isotype

IgG

shipped in

wet ice

storage temp.

−20°C

Quality Level

Analysis Note

Positive Control
MCF7 cells or prostate carcinoma tissue

Application


Immunoblotting (1:5000-1:10,000)
Paraffin Sections (1:1000-1:3000, heat pre-treatment required)

Disclaimer

Toxicity: Standard Handling (A)

General description

Rabbit polyclonal antibody supplied as undiluted serum. Recognizes the ~53 kDa p53 phoshorylated at Ser15.
This PhosphoDetect Anti-p53 (pSer¹⁵) (Ab-6) Rabbit pAb is validated for use in Immunoblotting, Paraffin Sections for the detection of p53 (pSer¹⁵) (Ab-6).
This product has been discontinued.


Recognizes the ~53 kDa p53 protein phosphorylated at Ser15. Does not recognizes unphosphorylated p53.

Immunogen

Human
a synthetic phosphopeptide [VEPPLpSQETFS(C)] corresponding to amino acids 10-20 surrounding the Ser¹⁵ phosphorylation site of human p53

Other Notes

Does not recognizes unphosphorylated p53. Antibody should be titrated for optimal results in individual systems.
Levine, A.J. 1997. Cell88, 323.
Meek, D.W. 1997. Pathol. Biol. Paris45, 804.
Miller, S.D., et al. 1997. Mol. Cell. Biol.17, 2194.
Pellegata, N.S., et al. 1996. Proc. Natl. Acad. Sci. USA93, 15209.
Sturzbecher, H.-W., et al. 1996. EMBO J.15, 1992.
Argarwal, M.L., et al. 1995. Proc. Natl. Acad. Sci. USA92, 8493.
Götz, C. and Montenarh, M. 1995. Int. J. Oncology6, 1129.
Reed, M. et al. 1995. Proc. Natl. Acad. Sci. USA92, 9455.
Waldman, T., et al. 1995. Cancer Res.55, 5187.
Cho, Y., et al. 1994. Science265, 346.
Clarke, A.R., et al. 1994. Oncogene9, 1767.
El-Deiry, W.S., et al. 1994. Cancer Res.54, 1169.
Greenblatt, M.S., et al. 1994. Cancer Res.54, 4855.
Lane, D.P. 1992. Nature358, 15.

Physical form

Undiluted serum.

Preparation Note

Following initial thaw, aliquot and freeze (-20°C).

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class

10-13 - German Storage Class 10 to 13


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Gary G Chiang et al.
Methods in molecular biology (Clifton, N.J.), 281, 125-141 (2004-06-29)
Members of the phosphoinositide-3-kinase-related kinase (PIKK) family, which includes mTOR, ATM, ATR, and hSMG-1, play important roles in regulating the cellular response to environmental stimuli. Despite the similarity of their catalytic domain to that of phosphoinositide-3-kinase, these extremely large (>250
Tanya E Johnson et al.
Cell reports, 24(6), 1471-1483 (2018-08-09)
Ataxia-telangiectasia mutated (ATM) is a serine/threonine kinase that coordinates the response to DNA double-strand breaks and oxidative stress. NKX3.1, a prostate-specific transcription factor, was recently shown to directly stimulate ATM kinase activity through its highly conserved homeodomain. Here, we show
Ji-Hoon Lee et al.
The Journal of biological chemistry, 288(18), 12840-12851 (2013-03-26)
The Ataxia Telangiectasia-Mutated (ATM) protein kinase is recruited to sites of double-strand DNA breaks by the Mre11/Rad50/Nbs1 (MRN) complex, which also facilitates ATM monomerization and activation. MRN exists in at least two distinct conformational states, dependent on ATP binding and
Cai Bowen et al.
Cell reports, 4(3), 516-529 (2013-07-31)
The prostate tumor suppressor NKX3.1 augments response to DNA damage and enhances survival after DNA damage. Within minutes of DNA damage, NKX3.1 undergoes phosphorylation at tyrosine 222, which is required for a functional interaction with ataxia telangiectasia mutated (ATM) kinase.
Zhi Guo et al.
Cell cycle (Georgetown, Tex.), 9(24), 4805-4811 (2010-12-15)
The Ataxia-Telangiectasia mutated (ATM) kinase is regarded as the major regulator of the cellular response to DNA double strand breaks (DSBs). In response to DSBs, ATM dimers dissociate into active monomers in a process promoted by the Mre11-Rad50-Nbs1 (MRN) complex.

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