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Description
p73 alpha + beta Recombinant Rabbit mAb (S-2565-27)Product Specification Host Rabbit Antigen p73 alpha + beta Synonyms Tumor protein p73; p53 like transcription factor; p53 related protein; P73; TP73 Immunogen Synthetic Peptide Location Cytoplasm, Nucleus Accession O15350 Clone Number S 2565 27 Antibody Type Recombinant mAb Isotype IgG Application WB Reactivity Hu Positive Sample HEK293, MCF7 Predicted Reactivity Mk, Ms Purification Protein A Concentration 2 mg ml Conjugation Unconjugated Physical
Product Specification
| Host | Rabbit |
| Antigen | p73 alpha + beta |
| Synonyms | Tumor protein p73; p53-like transcription factor; p53-related protein; P73; TP73 |
| Immunogen | Synthetic Peptide |
| Location | Cytoplasm, Nucleus |
| Accession | O15350 |
| Clone Number | S-2565-27 |
| Antibody Type | Recombinant mAb |
| Isotype | IgG |
| Application | WB |
| Reactivity | Hu |
| Positive Sample | HEK293, MCF7 |
| Predicted Reactivity | Mk, Ms |
| Purification | Protein A |
| Concentration | 2 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, -20 °C as supplied |
Dilution
| application | dilution | species |
| WB | 1:1000 | Hu |
Background
The p73 alpha + beta proteins collectively denote the two major N-terminal transactivation-domain isoforms encoded by the human TP73 gene: the full-length TAp73α (containing an N-terminal TA domain, DNA-binding domain, oligomerization domain, and a long C-terminal sterile α-motif, SAM domain) and its shorter splice variant TAp73β, which retains the TA, DBD and OD but lacks the C-terminal SAM extension; both act as p53-like tumor suppressors, binding canonical p53-response elements to activate transcription of pro-apoptotic and cell-cycle arrest genes, yet they also exhibit isoform-specific roles in neuronal development, DNA damage response, chemosensitivity, and metabolic regulation, with α being more abundant in post-mitotic neurons and β predominating in proliferating epithelia, while their expression is tightly controlled through alternative promoter usage and extensive C-terminal splicing that yields additional dominant-negative ΔNp73 isoforms that antagonize the α/β tumor-suppressive activities under stress conditions.
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