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Render Timestamp: 2024-11-21T14:06:37.827Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-20 06:15:35.461
Product last modified at: 2024-11-19T21:30:11.004Z
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PDP - Template Name: Monoclonal Antibody (Alexa Fluor Conjugate)
PDP - Template ID: *******c8ce56b

p53 (1C12) Mouse mAb (Alexa Fluor® 488 Conjugate) #2015

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    Supporting Data

    REACTIVITY H M R Hm Mk
    SENSITIVITY Endogenous
    MW (kDa)
    Source/Isotype Mouse IgG1
    Application Key:
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Hm-Hamster 
    • Mk-Monkey 

    Product Information

    Product Description

    This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 488 fluorescent dye and tested in-house for direct flow cytometry and immunofluorescent analysis in human and mouse cells. The antibody is expected to exhibit the same species cross-reactivity as the unconjugated p53 (1C12) Mouse mAb #2524.

    Product Usage Information

    Application Dilution
    Flow Cytometry (Fixed/Permeabilized) 1:50

    Storage

    Supplied in PBS (pH 7.2), less than 0.1% sodium azide and 2 mg/ml BSA. Store at 4°C. Do not aliquot the antibody. Protect from light. Do not freeze.

    Protocol

    Specificity / Sensitivity

    p53 (1C12) Mouse mAb (Alexa Fluor® 488 Conjugate) detects endogenous levels of total p53 protein.

    Species Reactivity:

    Human, Mouse, Rat, Hamster, Monkey

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Rabbit

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser20 of human p53. The antibody was conjugated to Alexa Fluor® 488 under optimal conditions with an F/P ratio of 2-6.

    Background

    The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). p53 is phosphorylated at multiple sites in vivo and by several different protein kinases in vitro (2,3). DNA damage induces phosphorylation of p53 at Ser15 and Ser20 and leads to a reduced interaction between p53 and its negative regulator, the oncoprotein MDM2 (4). MDM2 inhibits p53 accumulation by targeting it for ubiquitination and proteasomal degradation (5,6). p53 can be phosphorylated by ATM, ATR, and DNA-PK at Ser15 and Ser37. Phosphorylation impairs the ability of MDM2 to bind p53, promoting both the accumulation and activation of p53 in response to DNA damage (4,7). Chk2 and Chk1 can phosphorylate p53 at Ser20, enhancing its tetramerization, stability, and activity (8,9). p53 is phosphorylated at Ser392 in vivo (10,11) and by CAK in vitro (11). Phosphorylation of p53 at Ser392 is increased in human tumors (12) and has been reported to influence the growth suppressor function, DNA binding, and transcriptional activation of p53 (10,13,14). p53 is phosphorylated at Ser6 and Ser9 by CK1δ and CK1ε both in vitro and in vivo (13,15). Phosphorylation of p53 at Ser46 regulates the ability of p53 to induce apoptosis (16). Acetylation of p53 is mediated by p300 and CBP acetyltransferases. Inhibition of deacetylation suppressing MDM2 from recruiting HDAC1 complex by p19 (ARF) stabilizes p53. Acetylation appears to play a positive role in the accumulation of p53 protein in stress response (17). Following DNA damage, human p53 becomes acetylated at Lys382 (Lys379 in mouse) in vivo to enhance p53-DNA binding (18). Deacetylation of p53 occurs through interaction with the SIRT1 protein, a deacetylase that may be involved in cellular aging and the DNA damage response (19).
    1. Levine, A.J. (1997) Cell 88, 323-31.
    2. Meek, D.W. (1994) Semin Cancer Biol 5, 203-10.
    3. Milczarek, G.J. et al. (1997) Life Sci 60, 1-11.
    4. Shieh, S.Y. et al. (1997) Cell 91, 325-34.
    5. Chehab, N.H. et al. (1999) Proc Natl Acad Sci U S A 96, 13777-82.
    6. Honda, R. et al. (1997) FEBS Lett 420, 25-7.
    7. Tibbetts, R.S. et al. (1999) Genes Dev 13, 152-7.
    8. Shieh, S.Y. et al. (1999) EMBO J 18, 1815-23.
    9. Hirao, A. et al. (2000) Science 287, 1824-7.
    10. Hao, M. et al. (1996) J Biol Chem 271, 29380-5.
    11. Lu, H. et al. (1997) Mol Cell Biol 17, 5923-34.
    12. Ullrich, S.J. et al. (1993) Proc Natl Acad Sci U S A 90, 5954-8.
    13. Kohn, K.W. (1999) Mol Biol Cell 10, 2703-34.
    14. Lohrum, M. and Scheidtmann, K.H. (1996) Oncogene 13, 2527-39.
    15. Knippschild, U. et al. (1997) Oncogene 15, 1727-36.
    16. Oda, K. et al. (2000) Cell 102, 849-62.
    17. Ito, A. et al. (2001) EMBO J 20, 1331-40.
    18. Sakaguchi, K. et al. (1998) Genes Dev 12, 2831-41.
    19. Solomon, J.M. et al. (2006) Mol Cell Biol 26, 28-38.
    For Research Use Only. Not For Use In Diagnostic Procedures.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    This product is provided under an intellectual property license from Life Technologies Corporation. The transfer of this product is conditioned on the buyer using the purchased product solely in research conducted by the buyer, excluding contract research or any fee for service research, and the buyer must not (1) use this product or its components for (a) diagnostic, therapeutic or prophylactic purposes; (b) testing, analysis or screening services, or information in return for compensation on a per-test basis; or (c) manufacturing or quality assurance or quality control, and/or (2) sell or transfer this product or its components for resale, whether or not resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad, CA 92008 USA or [email protected].
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