Key features and details
- Mouse monoclonal [10E5] to p53 (acetyl K120)
- Suitable for: Flow Cyt, IP, WB, ELISA, ICC/IF
- Reacts with: Human
- Isotype: IgG1
Product nameAnti-p53 (acetyl K120) antibody [10E5]
See all p53 primary antibodies
DescriptionMouse monoclonal [10E5] to p53 (acetyl K120)
Stimulation may be required to allow detection of the acetylated protein due to low levels of endogenous expression. Please see images below for recommended treatment conditions and positive controls.
Tested applicationsSuitable for: Flow Cyt, IP, WB, ELISA, ICC/IFmore details
Species reactivityReacts with: Human
Synthetic peptide corresponding to Human p53 (acetyl K120).
Database link: P04637
- WB: Crude lysates of HCT116 cells (treated with siRNA to knockdown the expression of a Tip60 interacting protein UHRF1). ICC/IF: HeLa cells treated with 100 nM Doxorubicin for 24 hour.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid repeated freeze / thaw cycles.
Storage bufferpH: 7.40
Constituents: 50% Glycerol, PBS
Concentration information loading...
PurityIon Exchange Chromatography
Light chain typekappa
Our Abpromise guarantee covers the use of ab78316 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
ab170190 - Mouse monoclonal IgG1, is suitable for use as an isotype control with this antibody.
|IP||Use a concentration of 1 µg/ml.|
|WB||Use a concentration of 1 µg/ml. Predicted molecular weight: 53 kDa.
Stimulation may be required to allow detection of the acetylated protein due to low levels of endogenous expression. Please see images below for recommended treatment conditions and positive controls. It is recommended to immunoprecipitate the total p53 before using ab78316 for WB.
|ELISA||Use at an assay dependent concentration.|
FunctionActs 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. Implicated in Notch signaling cross-over. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.
Tissue specificityUbiquitous. Isoforms are expressed in a wide range of normal tissues but in a tissue-dependent manner. Isoform 2 is expressed in most normal tissues but is not detected in brain, lung, prostate, muscle, fetal brain, spinal cord and fetal liver. Isoform 3 is expressed in most normal tissues but is not detected in lung, spleen, testis, fetal brain, spinal cord and fetal liver. Isoform 7 is expressed in most normal tissues but is not detected in prostate, uterus, skeletal muscle and breast. Isoform 8 is detected only in colon, bone marrow, testis, fetal brain and intestine. Isoform 9 is expressed in most normal tissues but is not detected in brain, heart, lung, fetal liver, salivary gland, breast or intestine.
Involvement in diseaseNote=TP53 is found in increased amounts in a wide variety of transformed cells. TP53 is frequently mutated or inactivated in about 60% of cancers. TP53 defects are found in Barrett metaplasia 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 a cause of esophageal cancer (ESCR) [MIM:133239].
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 a proband affected by a sarcoma before 45 years with a first degree relative affected by any tumor before 45 years and another first degree relative with any tumor before 45 years or a sarcoma at any age. Other clinical definitions for LFS have been proposed (PubMed:8118819 and PubMed:8718514) and called Li-Fraumeni like syndrome (LFL). In these families affected relatives develop a diverse set of malignancies at unusually early ages. Four types of cancers account for 80% of tumors occurring in TP53 germline mutation carriers: breast cancers, soft tissue and bone sarcomas, brain tumors (astrocytomas) and adrenocortical carcinomas. Less frequent tumors include choroid plexus carcinoma or papilloma before the age of 15, rhabdomyosarcoma before the age of 5, leukemia, Wilms tumor, malignant phyllodes tumor, colorectal and gastric cancers.
Defects in TP53 are involved in head and neck squamous cell carcinomas (HNSCC) [MIM:275355]; also known as squamous cell carcinoma of the head and neck.
Defects in TP53 are a cause of lung cancer (LNCR) [MIM:211980].
Defects in TP53 are a cause of choroid plexus papilloma (CPLPA) [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 adrenocortical carcinoma (ADCC) [MIM:202300]. ADCC is a rare childhood tumor of the adrenal cortex. It occurs with increased frequency in patients with the Beckwith-Wiedemann syndrome and is a component tumor in Li-Fraumeni syndrome.
Sequence similaritiesBelongs to the p53 family.
DomainThe nuclear export signal acts as a transcriptional repression domain. The TADI and TADII motifs (residues 17 to 25 and 48 to 56) correspond both to 9aaTAD motifs which are transactivation domains present in a large number of yeast and animal transcription factors.
modificationsAcetylated. 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). Phosphorylation at Ser-9 by HIPK4 increases repression activity on BIRC5 promoter. Phosphorylated on Thr-18 by VRK1. Phosphorylated on Ser-20 by CHEK2 in response to DNA damage, which prevents ubiquitination by 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-PPP2R5C holoenzyme at Thr-55. 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 MDM2 and SYVN1, which leads to proteasomal degradation. Ubiquitinated by RFWD3, which works in cooperation with MDM2 and may catalyze the formation of short polyubiquitin chains on p53/TP53 that are not targeted to the proteasome. Ubiquitinated by MKRN1 at Lys-291 and Lys-292, which leads to proteasomal degradation. Deubiquitinated by USP10, leading to its stabilization. Ubiquitinated by TRIM24, which leads to proteasomal degradation. Ubiquitination by TOPORS induces degradation. Deubiquitination by USP7, leading to stabilization. Isoform 4 is monoubiquitinated in an MDM2-independent manner.
Monomethylated at Lys-372 by SETD7, leading to stabilization and increased transcriptional activation. Monomethylated at Lys-370 by SMYD2, leading to decreased DNA-binding activity and subsequent transcriptional regulation activity. Lys-372 monomethylation prevents interaction with SMYD2 and subsequent monomethylation at Lys-370. Dimethylated at Lys-373 by EHMT1 and EHMT2. Monomethylated at Lys-382 by SETD8, promoting interaction with L3MBTL1 and leading to repress transcriptional activity. Demethylation of dimethylated Lys-370 by KDM1A prevents interaction with TP53BP1 and represses TP53-mediated transcriptional activation.
Sumoylated by SUMO1.
Cellular localizationCytoplasm; Cytoplasm. Nucleus. Nucleus > PML body. Endoplasmic reticulum. Interaction with BANP promotes nuclear localization. Recruited into PML bodies together with CHEK2; Nucleus. Cytoplasm. Localized in both nucleus and cytoplasm in most cells. In some cells, forms foci in the nucleus that are different from nucleoli; Nucleus. Cytoplasm. Localized in the nucleus in most cells but found in the cytoplasm in some cells; Nucleus. Cytoplasm. Localized mainly in the nucleus with minor staining in the cytoplasm; Nucleus. Cytoplasm. Predominantly nuclear but localizes to the cytoplasm when expressed with isoform 4 and Nucleus. Cytoplasm. Predominantly nuclear but translocates to the cytoplasm following cell stress.
- Information by UniProt
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Samples are crude lysates of HCT116 cells: Left lanes are control. Right lanes are cells treated with siRNA to knockdown the expression of a Tip60 interacting protein UHRF1, which results in an increase in acetylation of p53 at Lys120. Total p53 was immunoprecipitated with anti-p53 monoclonal antibody from the crude extracts and analyzed by western blotting with another anti-p53 antibody (upper panel) and ab78316, at 1µg/ml (middle panel). The lower panel shows total p53.
Overlay histogram showing HeLa cells stained with ab78316 (red line). The cells were fixed with 80% methanol (5 min) and then permeabilized with 0.1% PBS-Tween for 20 min. The cells were then incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific protein-protein interactions followed by the antibody (ab78316, 1/100 dilution) for 30 min at 22ºC. The secondary antibody used was DyLight® 488 goat anti-mouse IgG (H+L) (ab96879) at 1/500 dilution for 30 min at 22ºC. Isotype control antibody (black line) was mouse IgG1 [ICIGG1] (ab91353, 2µg/1x106 cells) used under the same conditions. Acquisition of >5,000 events was performed.
Immunocytochemistry/Immunofluorescence analysis of HeLa cells treated with 100 nM Doxorubicin for 24 hour labelling p53 (acetyl K120) with ab78316 at a dilution of 1/1000. Cells were fixed with 4% paraformaldehyde and permeabilized with 0.25% Triton X-100 in PBS for 10 minutes. DAPI was used to stain the nucleus.
Crude whole cell extracts were prepared from H129 cells (p53 negative cell line) expressing only Myc-p53 (first lane), and both Myc-p53 and His-Tip60 (Second lane). In the upper panel, the cell extracts were immuno-blotted with anti-Myc, anti-His-tag or anti-α-tublin antibodies. In the lower panel, the extracts were immuno-precipitated with ab78316 and the precipitates were immuno-blotted with anti-Myc antibody. Acetylation of p53 at K120 is dependent on Tip60 and promoted by over-expression of His-Tip60.
ab78316 has been referenced in 10 publications.
- Choi YJ et al. Tubastatin A inhibits HDAC and Sirtuin activity rather than being a HDAC6-specific inhibitor in mouse oocytes. Aging (Albany NY) 11:1759-1777 (2019). PubMed: 30913540
- Li J et al. Molecular Mechanism for Selective Cytotoxicity towards Cancer Cells of Diselenide-Containing Paclitaxel Nanoparticles. Int J Biol Sci 15:1755-1770 (2019). PubMed: 31360117
- Yuan F et al. A New Regulatory Mechanism Between P53 And YAP Crosstalk By SIRT1 Mediated Deacetylation To Regulate Cell Cycle And Apoptosis In A549 Cell Lines. Cancer Manag Res 11:8619-8633 (2019). PubMed: 31576168
- Bitler BG et al. ARID1A-mutated ovarian cancers depend on HDAC6 activity. Nat Cell Biol 19:962-973 (2017). PubMed: 28737768
- Zheng S et al. Inhibiting p53 Acetylation Reduces Cancer Chemotoxicity. Cancer Res 77:4342-4354 (2017). PubMed: 28655792
- Largeot A et al. Expression of the MOZ-TIF2 oncoprotein in mice represses senescence. Exp Hematol 44:231-7.e4 (2016). PubMed: 26854485
- Liu N et al. ING5 is a Tip60 cofactor that acetylates p53 in response to DNA damage. Cancer Res 73:3749-60 (2013). PubMed: 23576563
- Gogna R et al. p53's choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation. EMBO Mol Med 5:1662-83 (2013). PubMed: 24096875
- Wen Z et al. Orphan nuclear receptor PNR/NR2E3 stimulates p53 functions by enhancing p53 acetylation. Mol Cell Biol 32:26-35 (2012). WB . PubMed: 22025681
- Mittal S et al. The Ccr4a (CNOT6) and Ccr4b (CNOT6L) deadenylase subunits of the human Ccr4-Not complex contribute to the prevention of cell death and senescence. Mol Biol Cell 22:748-58 (2011). PubMed: 21233283