Mouse Monoclonal Anti-p53 Antibody from Abcam

Abcam’s Anti-p53 antibody detects both wild-type and mutant-type conformational forms of p53 under denaturing conditions.

  • Product Name - Anti-p53 antibody [PAb 240]
  • Description - Mouse monoclonal [PAb 240] to p53
  • Host Species - Mouse
  • Tested Applications - Suitable for WB, ICC/IF, and IP.
  • Species Reactivity - It reacts with human, dog, cow, rat, mouse, monkey, Syrian hamster, and Chinese hamster.
  • Immunogen - It is a gel-purified p53-beta-galactosidase fusion protein consisting of murine p53 from aa 14-389 (acquired from pSV53C cDNA clone).
  • Epitope - The epitope has been mapped between amino acids 217 and 212 on human p53 (PMID: 1376364).
  • Positive Control - ICC-IF: A431 cells. WB: A431 cell lysate.


Abcam’s Anti-p53 monoclonal antibody detects both wild-type and mutant-type conformational forms of p53 under denaturing conditions. The PAb 240 clone is capable of detecting an epitope that is structurally concealed in the wild-type conformation of p53.

However, it becomes exposed by denaturation or alternatively in mutant conformations of p53 where point mutations occurring in the TP53 gene modify the protein’s structure (Gannon JV et al., 1990; Stephen CW et al., 1992; and Wang PL et al., 2001).

General Notes

The Anti-p53 antibody has been knockout validated in Western blot (WB). The predicted band was observed in wild-type HCT116 cells that were treated with the DNA damaging agent irinotecan. The band was not observed in TP53-knockout HCT116 cells. Abcam recommends using 3% milk as the blocking agent for WB.

It must be noted that target protein expression may be extremely low without treatment/stimulation (for example, a DNA damaging agent).


Abcam’s Abpromise guarantee covers the usage of ab26 in the tested applications listed in the table below. Recommended starting dilutions have been mentioned; the end-user should determine the ideal concentrations/dilutions.

Application Abreviews Notes
IP ☆☆☆☆☆ A concentration of 10 µg/mL should be used.
ICC/IF ☆☆☆☆☆ A concentration of 0.5–1 µg/mL should be used.
ICC/IF ☆☆☆☆ A concentration of 1–5 µg/mL should be used. It identifies a band of about 53 kDa (expected molecular weight is 53 kDa).
It must be noted that target protein expression is likely to be extremely low without treatment/stimulation (for example, DNA damaging agent). Abcam recommends using 3% milk as the blocking agent for WB.



The antibody functions as a tumor suppressor in several types of tumors and, based on the cell type and physiological circumstances, induces apoptosis or growth arrest. It functions as a trans-activator in the regulation of cell cycle, that is, it negatively controls cell division by exploiting a sequence of genes needed for this process.

One of the activated genes acts as an inhibitor of cyclin-dependent kinases. Apoptosis induction appears to be mediated either by repression of Bcl-2 expression or by stimulation of FAS and BAX antigen expression.

Isoform 2 plays a role in Notch signaling crossover and improves Isoform 1’s transactivation activity from some but not all TP53-inducible promoters. Isoform 4 inhibits transactivation activity and damages growth suppression regulated by Isoform 1. Apoptosis mediated by Isoform 1 is suppressed by Isoform 7.

Tissue Specificity

Tissue specificity is ubiquitous. Although isoforms are expressed in an array of normal tissues, they occur in a tissue-dependent way. While Isoform 2 is expressed in the majority of the normal tissues, it is not identified in the lung, brain, fetal liver, fetal brain, spinal cord, muscle, and prostate. Isoform 3, although expressed in the majority of normal tissues, is not identified in the spinal cord, lung, testis, spleen, fetal liver, and fetal brain.

Similarly, Isoform 7 is also expressed in many normal tissues, but is not identified in the uterus, breast, skeletal muscle, and prostate. Isoform 8 is expressed only in intestine, fetal brain, testis, bone marrow, and colon. Isoform 9 is detected in the majority of the normal tissues but not in the brain, intestine, breast, salivary gland, fetal liver, lung, and heart.

Involvement in Disease

It must be noted that many transformed cells contain increased amounts of TP53. TP53 is often inactivated or mutated in approximately 60% of cancers. Barrett metaplasia is associated with TP53 defects. It is a medical disorder in which a metaplastic columnar epithelium replaces the normally stratified squamous epithelium of the lower esophagus.

The condition progresses as a complication in about 10% of patients suffering from chronic gastroesophageal reflux disease, predisposing them to the development of esophageal adenocarcinoma.

TP53 defects are a cause of esophageal cancer (ESCR) [MIM:133239]. Such defects also lead to Li-Fraumeni syndrome (LFS) [MIM:151623], an autosomal dominant familial cancer syndrome.

LFS, in its classic form, is characterized by the existence of a proband influenced by a sarcoma before 45 years—with a first-degree relative influenced by any tumor type prior to 45 years and another first-degree relative with any tumor type prior to 45 years or a sarcoma at any age.

In addition, other clinical definitions for this disorder have been recommended (PubMed:8718514 and PubMed:8118819) and known as Li-Fraumeni like syndrome (LFL). Affected relatives in these families develop a different set of malignancies at abnormally early ages. There are four types of cancers that are responsible for 80% of tumors manifesting in TP53 germline mutation carriers. These include adrenocortical carcinomas, brain tumors (astrocytomas), bone and soft tissue sarcomas, and breast cancers.

Tumors that occur less frequently include papilloma or choroid plexus carcinoma before the age of 15, gastric and colorectal cancers, malignant phyllodes tumor, Wilms tumor, leukemia, and rhabdomyosarcoma before the age of 5. TP53 defects play a role in head and neck squamous cell carcinomas (HNSCC) [MIM:275355], also called squamous cell carcinoma of the head and neck.

TP53 defects also lead to lung cancer (LNCR) [MIM:211980]. Such defects also cause choroid plexus papilloma (CPLPA) [MIM:260500].

Known to be a slow-growing benign tumor of the choroid plexus, choroid plexus papilloma usually invades the leptomeninges. In adults, it is usually in the fourth ventricle, and in children, it is generally in a lateral ventricle.

Hydrocephalus is quite common, caused either from tumor secretion of cerebrospinal fluid or from obstruction. If this condition goes through malignant transformation, it is referred as choroid plexus carcinoma. Although rare, primary choroid plexus tumors mostly occur in early childhood.

TP53 defects also lead to adrenocortical carcinoma (ADCC) [MIM:202300], a rare childhood tumor of the adrenal cortex. ADCC occurs more frequently in patients suffering from the Beckwith-Wiedemann syndrome. It is a component tumor in Li-Fraumeni syndrome.