Recombinant Human p53 protein is a Human Full Length protein, in the 1 to 393 aa range, expressed in Baculovirus, with >95% purity and suitable for SDS-PAGE, mobility shift assay.
M E E P Q S D P S V E P P L S Q E T F S D L W K L L P E N N V L S P L P S Q A M D D L M L S P D D I E Q W F T E D P G P D E A P R M P E A A P P V A P A P A A P T P A A P A P A P S W P L S S S V P S Q K T Y Q G S Y G F R L G F L H S G T A K S V T C T Y S P A L N K M F C Q L A K T C P V Q L W V D S T P P P G T R V R A M A I Y K Q S Q H M T E V V R R C P H H E R C S D S D G L A P P Q H L I R V E G N L R V E Y L D D R N T F R H S V V V P Y E P P E V G S D C T T I H Y N Y M C N S S C M G G M N R R P I L T I I T L E D S S G N L L G R N S F E V R V C A C P G R D R R T E E E N L R K K G E P H H E L P P G S T K R A L P N N T S S S P Q P K K K P L D G E Y F T L Q I R G R E R F E M F R E L N E A L E L K D A Q A G K E P G G S R A H S S H L K S K K G Q S T S R H K K L M F K T E G P D S D
Application | Reactivity | Dilution info | Notes |
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Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application mobility shift assay | Reactivity Reacts | Dilution info - | Notes 1 unit equals 1 nanogram of purified protein. 1 unit is sufficient for a gel mobility shift assay in a 20 μl reaction. |
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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
Recombinant Human p53 protein is a Human Full Length protein, in the 1 to 393 aa range, expressed in Baculovirus, with >95% purity and suitable for SDS-PAGE, mobility shift assay.
pH: 7.9
Constituents: 20% Glycerol (glycerin, glycerine), 0.75% Potassium chloride, 0.316% Tris HCl, 0.0154% (R*,R*)-1,4-Dimercaptobutan-2,3-diol, 0.00584% EDTA
ab82201 is greater than 95% homogeneous based on SDS-PAGE gel analysis, purified by affinity and FPLC chromatography.
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).
Belongs to the p53 family.
Acetylation of Lys-382 by CREBBP enhances transcriptional activity (PubMed:10656795, PubMed:15448695, PubMed:20228809, PubMed:23431171). Acetylation of Lys-382 by EP300 (PubMed:10656795, PubMed:15448695, PubMed:20228809, PubMed:23431171). Deacetylation of Lys-382 by SIRT1 impairs its ability to induce proapoptotic program and modulate cell senescence (PubMed:10656795, PubMed:15448695, PubMed:20228809, PubMed:23431171). Deacetylation by SIRT2 impairs its ability to induce transcription activation in a AKT-dependent manner (PubMed:10656795, PubMed:15448695, PubMed:20228809, PubMed:23431171, PubMed:29681526). Acetylation at Lys-381 increases stability (PubMed:29474172). Deacetylation at Lys-381 by SIRT6 decreases its stability, thereby regulating cell senescence (PubMed:29474172). Acetylated at Lys-120 by KAT5, KAT6A and KAT8; regulating its ability to induce proapoptotic program (PubMed:17189187, PubMed:19854137, PubMed:23431171).
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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SDS-PAGE analysis of ab82201.
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