Cellular tumor antigen P53/TP53, Human (His-SUMO)

Cellular tumor antigen P53/TP53, a tumor suppressor, induces growth arrest or apoptosis across tumor types. It regulates the cell cycle by negatively controlling genes crucial for division. TP53's pro-apoptotic activity involves BAX and FAS antigen stimulation or Bcl-2 repression. It induces apoptosis through interactions with PPP1R13B/ASPP1 or TP53BP2/ASPP2, inhibited by PPP1R13L/iASPP. Coordinating with mitochondrial PPIF, TP53 activates oxidative stress-induced necrosis independent of transcription. It induces long intergenic non-coding RNA transcription, contributing to TP53-dependent repression and apoptosis. TP53's involvement in Notch signaling, DNA damage response, and circadian clock regulation adds to its complex regulatory functions. Cellular tumor antigen P53/TP53, Human (His-SUMO) is the recombinant human-derived Cellular tumor antigen P53/TP53, expressed by E. coli, with N-SUMO, N-6*His labeled tag. The total length of Cellular tumor antigen P53/TP53, Human (His-SUMO) is 393 a.a., with molecular weight of 66 kDa.

Cellular tumor antigen P53/TP53 functions as a tumor suppressor across various tumor types, exhibiting the ability to induce growth arrest or apoptosis depending on the physiological context and cell type. Involved in cell cycle regulation, TP53 acts as a trans-activator that negatively regulates cell division by controlling a set of genes essential for this process. Its pro-apoptotic activity is mediated through the stimulation of BAX and FAS antigen expression or repression of Bcl-2 expression. TP53 induces apoptosis by interacting with PPP1R13B/ASPP1 or TP53BP2/ASPP2, and this activity is inhibited by PPP1R13L/iASPP. In cooperation with mitochondrial PPIF, TP53 participates in activating oxidative stress-induced necrosis, independent of transcription. It induces the transcription of long intergenic non-coding RNAs, such as lincRNA-p21 and lincRNA-Mkln1, which contribute to TP53-dependent transcriptional repression and apoptosis. Additionally, TP53 is implicated in Notch signaling cross-over, prevents CDK7 kinase activity in response to DNA damage, and regulates the circadian clock by repressing CLOCK-BMAL1-mediated transcriptional activation of PER2. Different isoforms of TP53 exhibit variations in transactivation activity, apoptosis induction, and growth suppression, showcasing the complexity of its regulatory functions.

Human

E. coli

N-SUMO;N-6*His

P04637 (M1-D393)

7157  [NCBI]

MEEPQSDPSVEPPLSQETFSDLWKLLPENNVLSPLPSQAMDDLMLSPDDIEQWFTEDPGPDEAPRMPEAAPPVAPAPAAPTPAAPAPAPSWPLSSSVPSQKTYQGSYGFRLGFLHSGTAKSVTCTYSPALNKMFCQLAKTCPVQLWVDSTPPPGTRVRAMAIYKQSQHMTEVVRRCPHHERCSDSDGLAPPQHLIRVEGNLRVEYLDDRNTFRHSVVVPYEPPEVGSDCTTIHYNYMCNSSCMGGMNRRPILTIITLEDSSGNLLGRNSFEVRVCACPGRDRRTEEENLRKKGEPHHELPPGSTKRALPNNTSSSPQPKKKPLDGEYFTLQIRGRERFEMFRELNEALELKDAQAGKEPGGSRAHSSHLKSKKGQSTSRHKKLMFKTEGPDSD

66 kDa

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  Greater than 90% as determined by reducing SDS-PAGE.

Lyophilized powder

Lyophilized from 0.2 μm filtered solution in PBS, 6% Trehalose, pH 7.4 or 20 mM Tris-HCl, 0.5 M NaCl, 6% Trehalose, pH 8.0.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O.

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.