p53 (pS46) staining on human colon carcinoma. The colon carcinoma tissue was fixed in formalin and processed. Following antigen retrieval with BD Retrievagen A buffer (Cat. no. 550524), the sections were either left untreated (left panel) or treated with a phosphatase to eliminate all phosphorylation (right panel). The tissue sections were stained with purified Mouse anti-p53 (pS46) with Hematoxylin counterstaining. Original magnification: 20X.
p53 (pS46) staining on human colon carcinoma. The colon carcinoma tissue was fixed in formalin and processed. Following antigen retrieval with BD Retrievagen A buffer (Cat. no. 550524), the sections were either left untreated (left panel) or treated with a phosphatase to eliminate all phosphorylation (right panel). The tissue sections were stained with purified Mouse anti-p53 (pS46) with Hematoxylin counterstaining. Original magnification: 20X.
Preparation And Storage
Product Notices
- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- Please refer to www.bdbiosciences.com/us/s/resources for technical protocols.
- Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
The p53 protein is critical to regulation of normal cell growth and is a suppressor of tumor cell proliferation. Inactivation of p53 by a number of mechanisms, such as missense mutations or interaction with oncogenic viral or cellular proteins, can result in tumor progression. Mutations and/or allelic loss of the p53 gene are associated with a wide variety of human tumors. Known to have a role in transcriptional regulation, p53 suppresses various promoters containing TATA elements in an apparently sequence-independent fashion. p53 also binds to DNA in a sequence-specific manner via recognition of a 20-bp consensus-binding site. This interaction stimulates the expression of genes downstream of the p53 binding site. A number of genes that contain p53-binding sites have been identified, including MDM2, GADD45, and muscle creatine kinase. MDM2 mediates feedback inhibition of p53, which is prevented by phosphorylations of p53 amino-terminal serines and threonines. UV radiation-induced phosphorylation of Serine 46 (S46) is mediated by homeodomain-interacting protein kinase-2 (HIPK2) and is involved in the promotion of apoptosis. Other stress stimuli mediate S46 phosphorylation in p53 via as yet unidentified kinase(s).
The I117-1091 mAb recognizes p53 phosphorylated at S46.
Development References (5)
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Bode AM, Dong Z. Post-translational modification of p53 in tumorigenesis. Nat Rev Cancer. 2004; 4:793-805. (Biology).
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D'Orazi G, Cecchinelli B, Bruno T, et al. Homeodomain-interacting protein kinase-2 phosphorylates p53 at Ser 46 and mediates apoptosis. Nat Cell Biol. 2002; 4:11-19. (Biology).
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Di Stefano V, Blandino G, Sacchi A, Soddu S, D'Orazi G. HIPK2 neutralizes MDM2 inhibition rescuing p53 transcription activity and apoptotic function. Oncogene. 2004; 23(30):5185-5192. (Biology).
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Hofmann TG, Moller A, Sirma H, et al. Regulation of p53 activity by its interaction with homeodomain-interacting protein kinase-2. Nat Cell Biol. 2002; 4:1-10. (Biology). View Reference
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Saito S, Goodarzi AA, Higashimoto Y, et al. ATM mediates phosphorylation at multiple p53 sites, including Ser46, in response to ionizing radiation. J Biol Chem. 2002; 277(15):12491-12494. (Biology).
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