Mouse Monoclonal P53 acetyl K120 antibody. Suitable for WB, ICC/IF, Flow Cyt (Intra) and reacts with Human samples. Cited in 15 publications. Immunogen corresponding to Synthetic Peptide within Human TP53 acetyl K120.
pH: 6 - 8.5
Constituents: 50% Glycerol (glycerin, glycerine), 50% PBS
WB | ICC/IF | Flow Cyt (Intra) | |
---|---|---|---|
Human | Tested | Tested | Tested |
Species | Dilution info | Notes |
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Species Human | Dilution info 1 µg/mL | Notes 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. |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 1/1000 | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 1/100 | Notes ab170190 - Mouse monoclonal IgG1, is suitable for use as an isotype control with this antibody. |
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Multifunctional transcription factor that induces cell cycle arrest, DNA repair or apoptosis upon binding to its target DNA sequence (PubMed:11025664, PubMed:12524540, PubMed:12810724, PubMed:15186775, PubMed:15340061, PubMed:17317671, PubMed:17349958, PubMed:19556538, PubMed:20673990, PubMed:20959462, PubMed:22726440, PubMed:24051492, PubMed:24652652, PubMed:35618207, PubMed:36634798, PubMed:38653238, PubMed:9840937). Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type (PubMed:11025664, PubMed:12524540, PubMed:12810724, PubMed:15186775, PubMed:15340061, PubMed:17189187, PubMed:17317671, PubMed:17349958, PubMed:19556538, PubMed:20673990, PubMed:20959462, PubMed:22726440, PubMed:24051492, PubMed:24652652, PubMed:38653238, PubMed:9840937). Negatively regulates cell division by controlling expression of a set of genes required for this process (PubMed:11025664, PubMed:12524540, PubMed:12810724, PubMed:15186775, PubMed:15340061, PubMed:17317671, PubMed:17349958, PubMed:19556538, PubMed:20673990, PubMed:20959462, PubMed:22726440, PubMed:24051492, PubMed:24652652, PubMed:9840937). 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 (PubMed:12524540, PubMed:17189187). Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 (PubMed:12524540). However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP (PubMed:12524540). In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seems to have an effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. 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. Regulates the circadian clock by repressing CLOCK-BMAL1-mediated transcriptional activation of PER2 (PubMed:24051492).
P53, TP53, Cellular tumor antigen p53, Antigen NY-CO-13, Phosphoprotein p53, Tumor suppressor p53
Mouse Monoclonal P53 acetyl K120 antibody. Suitable for WB, ICC/IF, Flow Cyt (Intra) and reacts with Human samples. Cited in 15 publications. Immunogen corresponding to Synthetic Peptide within Human TP53 acetyl K120.
pH: 6 - 8.5
Constituents: 50% Glycerol (glycerin, glycerine), 50% PBS
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.
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The protein p53 also known as TP53 or tumor protein p53 has a molecular weight of approximately 53 kDa. It acts as a transcription factor and plays a major role in cell cycle regulation apoptosis and maintaining genomic stability. This protein mainly expresses in the nucleus of cells and acts as a critical regulator of cellular responses to stress signals including DNA damage. Scientists commonly use p53 antibodies in various assays like western blot and p53 immunofluorescence to detect and study its expression and functional status in cells.
P53 functions to control cell division and apoptosis serving as a guardian of the genome by preventing mutation accumulation. It does not form part of a larger complex under normal conditions but interacts with various other molecules to execute its functions. p53 can activate or suppress the transcription of numerous genes involved in cell cycle arrest DNA repair and programmed cell death allowing it to halt the progression of damaged cells and trigger repair mechanisms or eliminate those that cannot be repaired.
P53 acts within several key biological pathways such as the p53 signaling pathway and the intrinsic apoptotic pathway. Its activity involves interaction with proteins like MDM2 which regulates p53 through ubiquitin-mediated degradation and ATM kinase which phosphorylates p53 in response to DNA damage. These interactions ensure appropriate cellular responses during stress and are vital for maintaining homeostasis.
P53 mutation or inactivation is often associated with the development of cancer given its role in controlling cell division and preventing tumor formation. Specifically its dysfunction has been linked to cancers such as breast cancer and lung cancer. Additionally p53 can interact with other mutant proteins like Ras compounding mutations that contribute to tumor progression and aggressive cancer phenotypes. Understanding these interactions and the status of p53 can be important in developing targeted cancer therapies.
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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.
All lanes: Western blot - Anti-p53 (acetyl K120) antibody [10E5] (ab78316)
Predicted band size: 43 kDa
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) (Goat Anti-Mouse IgG H&L (DyLight® 488) preadsorbed ab96879) at 1/500 dilution for 30 min at 22ºC. Isotype control antibody (black line) was mouse IgG1 [ICIGG1] (Mouse IgG1, Kappa Monoclonal [B11/6] - Isotype Control 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.
All lanes: Western blot - Anti-p53 (acetyl K120) antibody [10E5] (ab78316)
Predicted band size: 43 kDa
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