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05-224 Anti-p53 Antibody, clone BP53-12

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      Key Specifications Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      HIHC, IP, WBMPurifiedMonoclonal Antibody
      Catalogue Number05-224
      Brand Family Upstate
      Trade Name
      • Upstate
      DescriptionAnti-p53 Antibody, clone BP53-12
      Background InformationThe human wild-type p53 protein is a 393 amino acid nuclear phosphoprotein, present in the nucleus of all normal mammalian cells where it appears to be involved in the regulation of cell proliferation. The normal protein has a very short half-life and is present in only minute amounts in normal tissues and cells. In contrast, mutant p53 protein produced by malignant cells is usually a product of a point mutation in the p53 gene leading to substitution of a single amino acid that significantly prolongs the half-life of the protein. The accumulation of high levels of p53 is a potential novel marker for malignancy.
      Product Information
      • Raji cell lysate
      PresentationProtein G Purified immunoglobulin in Protein G Purified immunoglobulin in of 0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.05% sodium azide before the addition of glycerol to 30%
      Quality LevelMQ100
      ApplicationAnti-p53 Antibody, clone BP53-12 is a high quality Mouse Monoclonal Antibody for the detection of p53 & has been validated in IHC, IP & WB.
      Key Applications
      • Immunohistochemistry
      • Immunoprecipitation
      • Western Blotting
      Biological Information
      ImmunogenRecombinant human wild type p53
      ConcentrationPlease refer to the Certificate of Analysis for the lot-specific concentration.
      SpecificityRecognizes p53.
      Species Reactivity
      • Human
      Antibody TypeMonoclonal Antibody
      Entrez Gene Number
      Entrez Gene SummaryTumor protein p53, a nuclear protein, plays an essential role in the regulation of cell cycle, specifically in the transition from G0 to G1. It is found in very low levels in normal cells, however, in a variety of transformed cell lines, it is expressed in high amounts, and believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing DNA-binding, oligomerization and transcription activation domains. It is postulated to bind as a tetramer to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome.
      Gene Symbol
      • TP53
      • P53
      • TRP53
      • p53
      • LFS1
      Purification MethodProtein A Purfied
      UniProt Number
      UniProt SummaryFUNCTION: SwissProt: P04637 # Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression.
      COFACTOR: Binds 1 zinc ion per subunit.
      SIZE: 393 amino acids; 43653 Da
      SUBUNIT: Interacts with AXIN1. Probably part of a complex consisting of TP53, HIPK2 and AXIN1 (By similarity). Binds DNA as a homotetramer. Interacts with histone acetyltransferases EP300 and methyltransferases HRMT1L2 and CARM1, and recruits them to promoters. In vitro, the interaction of TP53 with cancer- associated/HPV (E6) viral proteins leads to ubiquitination and degradation of TP53 giving a possible model for cell growth regulation. This complex formation requires an additional factor, E6-AP, which stably associates with TP53 in the presence of E6. C- terminus interacts with TAF1, when TAF1 is part of the TFIID complex. Interacts with ING4 and this interaction may be indirect. Found in a complex with CABLES1 and TP73. Interacts with HIPK1, HIPK2, and P53DINP1. Interacts with WWOX. May interacts with HCV core protein. Interacts with USP7 and SYVN1. Interacts with HSP90AB1 (By similarity). Interacts with BANP.
      SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Endoplasmic reticulum. Note=Interaction with BANP promotes nuclear localization.
      DOMAIN: SwissProt: P04637 The nuclear export signal acts as a transcriptional repression domain.
      PTM: Acetylated. Acetylation of Lys-382 by CREBBP enhances transcriptional activity. Deacetylation of Lys-382 by SIRT1 impairs its ability to induce proapoptotic program and modulate cell senescence. & Phosphorylation on Ser residues mediates transcriptional activation. Phosphorylated by HIPK1 (By similarity). Phosphorylated on Thr-18 by VRK1, which may prevent the interaction with MDM2. Phosphorylated on Thr-55 by TAF1, which promotes MDM2-mediated degradation. Phosphorylated on Ser-46 by HIPK2 upon UV irradiation. Phosphorylation on Ser-46 is required for acetylation by CREBBP. Phosphorylated on Ser-392 following UV but not gamma irradiation. Phosphorylated upon DNA damage, probably by ATM or ATR. Phosphorylated on Ser-15 upon ultraviolet irradiation; which is enhanced by interaction with BANP. & Dephosphorylated by PP2A. SV40 small T antigen inhibits the dephosphorylation by the AC form of PP2A. & May be O-glycosylated in the C-terminal basic region. Studied in EB-1 cell line. & Ubiquitinated by SYVN1, which leads to proteasomal degradation.
      DISEASE: SwissProt: P04637 # TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. & Defects in TP53 are involved in esophageal squamous cell carcinoma (ESCC) [MIM:133239]. ESCC is a tumor of the esophagus. & Defects in TP53 are a cause of Li-Fraumeni syndrome (LFS) [MIM:151623]. LFS is an autosomal dominant familial cancer syndrome that in its classic form is defined by the existence of both a proband with a sarcoma and two other first-degree relatives with a cancer by age 45 years. In these families the affected relatives develop a diverse set of malignancies at unusually early ages. The spectrum of cancers in LFS includes breast carcinomas, soft-tissue sarcomas, brain tumors, osteosarcoma, leukemia and adreno-cortical carcinoma. Other possible component tumors of LFS are melanoma, gonadal cell tumors and carcinomas of the lung, pancreas and prostate. & Defects in TP53 may be associated with nasopharyngeal carcinoma [MIM:161550]; also known as nasopharyngeal cancer. & Defects in TP53 are found in Barrett metaplasia; also known as Barrett esophagus. It is a condition in which the normally stratified squamous epithelium of the lower esophagus is replaced by a metaplastic columnar epithelium. The condition develops as a complication in approximately 10% of patients with chronic gastroesophageal reflux disease and predisposes to the development of esophageal adenocarcinoma. & Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:275355]. & Defects in TP53 are involved in oral squamous cell carcinoma (OSCC). Cigarette smoke is a prime mutagenic agent in cancer of the aerodigestive tract. & Defects in TP53 are a cause of lung cancer [MIM:211980]. & Defects in TP53 are a cause of choroid plexus papilloma [MIM:260500]. Choroid plexus papilloma is a slow-growing benign tumor of the choroid plexus that often invades the leptomeninges. In children it is usually in a lateral ventricle but in adults it is more often in the fourth ventricle. Hydrocephalus is common, either from obstruction or from tumor secretion of cerebrospinal fluid. If it undergoes malignant transformation it is called a choroid plexus carcinoma. Primary choroid plexus tumors are rare and usually occur in early childhood. & Defects in TP53 are a cause of one form of hereditary adrenocortical carcinoma (ADCC) [MIM:202300]. ADCC is a rare childhood tumor, representing about 0.4% of childhood tumors, with a high incidence of associated tumors. ADCC occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome [MIM:130650] and is a component tumor in Li-Fraumeni syndrome [MIM:151623].
      SIMILARITY: Belongs to the p53 family.
      Molecular Weight53 kDa
      Physicochemical Information
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Quality Assuranceroutinely evaluated on RIPA lysate of human Raji cells
      Usage Statement
      • Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
      Storage and Shipping Information
      Storage ConditionsMaintain for 2 years at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
      Packaging Information
      Material Size200 µL
      Transport Information
      Supplemental Information


      Anti-p53 Antibody, clone BP53-12 SDS


      Safety Data Sheet (SDS) 

      Anti-p53 Antibody, clone BP53-12 Certificates of Analysis

      TitleLot Number
      Anti-p53, clone BP53-12 3170820
      Anti-p53, clone BP53-12 (mouse monoclonal IgG2a) - 2326369 2326369
      Anti-p53, clone BP53-12 (mouse monoclonal IgG2a) - 2387515 2387515
      Anti-p53, clone BP53-12 - NG1701811 NG1701811
      Anti-p53, clone BP53-12 (mouse monoclonal IgG2a) 2931079
      Anti-p53, clone BP53-12 (mouse monoclonal IgG2a) - 2168321 2168321
      Anti-p53, clone BP53-12 - 0701049645 0701049645
      Anti-p53, clone BP53-12 - 0702051786 0702051786
      Anti-p53, clone BP53-12 - 15366 15366
      Anti-p53, clone BP53-12 - 18088 18088


      Reference overviewApplicationPub Med ID
      Phytometabolite Dehydroleucodine Induces Cell Cycle Arrest, Apoptosis, and DNA Damage in Human Astrocytoma Cells through p73/p53 Regulation.
      Bailon-Moscoso, N; González-Arévalo, G; Velásquez-Rojas, G; Malagon, O; Vidari, G; Zentella-Dehesa, A; Ratovitski, EA; Ostrosky-Wegman, P
      PloS one  10  e0136527  2015

      Show Abstract
      Western Blotting26309132 26309132
      The induction of the p53 tumor suppressor protein bridges the apoptotic and autophagic signaling pathways to regulate cell death in prostate cancer cells.
      Ringer, L; Sirajuddin, P; Tricoli, L; Waye, S; Choudhry, MU; Parasido, E; Sivakumar, A; Heckler, M; Naeem, A; Abdelgawad, I; Liu, X; Feldman, AS; Lee, RJ; Wu, CL; Yenugonda, V; Kallakury, B; Dritschilo, A; Lynch, J; Schlegel, R; Rodriguez, O; Pestell, RG; Avantaggiati, ML; Albanese, C
      Oncotarget  5  10678-91  2014

      Show Abstract
      25296977 25296977
      Differential effect of hypoxia on etoposide-induced DNA damage response and p53 regulation in different cell types.
      Sermeus, Audrey, et al.
      J. Cell. Physiol., (2013)  2013

      Show Abstract
      23702906 23702906
      HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells.
      Peixoto, P, et al.
      Cell death and differentiation, (2012)  2012

      Show Abstract
      22301920 22301920
      The inhibition of autophagy sensitises colon cancer cells with wild-type p53 but not mutant p53 to topotecan treatment.
      Li, DD; Sun, T; Wu, XQ; Chen, SP; Deng, R; Jiang, S; Feng, GK; Pan, JX; Zhang, XS; Zeng, YX; Zhu, XF
      PloS one  7  e45058  2012

      Show Abstract
      Western Blotting23024792 23024792
      MG132 inhibition of proteasome blocks apoptosis induced by severe DNA damage.
      Zhang, L; Hu, JJ; Gong, F
      Cell cycle (Georgetown, Tex.)  10  3515-8  2011

      Show Abstract
      22031102 22031102
      Expression of a homeostatic regulator, Wip1 (wild-type p53-induced phosphatase), is temporally induced by c-Jun and p53 in response to UV irradiation.
      Song, JY; Han, HS; Sabapathy, K; Lee, BM; Yu, E; Choi, J
      The Journal of biological chemistry  285  9067-76  2010

      Show Abstract Full Text Article
      20093361 20093361
      Translocation of p53 to mitochondria is regulated by its lipid binding property to anionic phospholipids and it participates in cell death control.
      Ching-Hao Li,Yu-Wen Cheng,Po-Ling Liao,Jaw-Jou Kang
      Neoplasia (New York, N.Y.)  12  2010

      Show Abstract Full Text Article
      20126473 20126473
      The estrogen receptor alpha pathway induces oncogenic Wip1 phosphatase gene expression.
      Hye-Sook Han, Eunsil Yu, Ji-Young Song, Ji-Young Park, Se Jin Jang, Jene Choi, Hye-Sook Han, Eunsil Yu, Ji-Young Song, Ji-Young Park, Se Jin Jang, Jene Choi, Hye-Sook Han, Eunsil Yu, Ji-Young Song, Ji-Young Park, Se Jin Jang, Jene Choi
      Molecular cancer research : MCR  7  713-23  2009

      Show Abstract
      19435816 19435816
      Hypoxia induces protection against etoposide-induced apoptosis: molecular profiling of changes in gene expression and transcription factor activity.
      Sermeus, A; Cosse, JP; Crespin, M; Mainfroid, V; de Longueville, F; Ninane, N; Raes, M; Remacle, J; Michiels, C
      Molecular cancer  7  27  2008

      Show Abstract
      18366759 18366759


      What is the concentration of this antibody?We are not able to quantitate cultured supernatants.

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      Life Science Research > Antibodies and Assays > Primary Antibodies