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Literature summary for 7.4.2.14 extracted from
- p53 induces TAP1 and enhances the transport of MHC class I peptides (1999), Oncogene, 18, 7740-7747 .
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| additional information | TAP1-Fluc is cotransfected into H-1299 cells with pcDNA3 or a vector that expresses wild-type p73alpha or p73beta. The fold increase in relative luciferase activity is calculated. TAP1-Fluc is co-transfected into H1299 cells with 5 mg of pcDNA3 or a vector that expresses p53(V143A), p53(R175H), p53(R249S), or p53(R273H). p53 mutants are unable to increase the luciferase activity for TAP1-Fluc | Homo sapiens |
Localization
| Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|
| endoplasmic reticulum membrane | - |
Homo sapiens | 5789 | - |
Metals/Ions
| Metals/Ions | Comment | Organism | Structure |
|---|---|---|---|
| Mg2+ | required | Homo sapiens |  |
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ATP + H2O + antigen peptide[side 1] | Homo sapiens | - |
ADP + phosphate + antigen peptide[side 2] | - |
? | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | Q03518 | TAP1 subunit | - |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| 80S14 cell | - |
Homo sapiens | - |
| carcinoma cell | - |
Homo sapiens | - |
| colorectal cancer cell | - |
Homo sapiens | - |
| HCT-116 cell | - |
Homo sapiens | - |
| LNCaP cell | - |
Homo sapiens | - |
| LS-174T cell | - |
Homo sapiens | - |
| MCF-7 cell | - |
Homo sapiens | - |
| RKO cell | - |
Homo sapiens | - |
| WI-38 cell | - |
Homo sapiens | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ATP + H2O + antigen peptide[side 1] | - |
Homo sapiens | ADP + phosphate + antigen peptide[side 2] | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| peptide transporter | - |
Homo sapiens |
| TAP 1 | - |
Homo sapiens |
| TAP1 | - |
Homo sapiens |
| transporter associated with antigen processing 1 | - |
Homo sapiens |
Cofactor
| Cofactor | Comment | Organism | Structure |
|---|---|---|---|
| ATP | - |
Homo sapiens | |
Expression
| Organism | Comment | Expression |
|---|---|---|
| Homo sapiens | p53 and p73 induce TAP1 and enhance the transport of MHC class I peptides. TAP1 is strongly induced by p53 and DNA-damaging agents through a p53-responsive element. p73, which is homologous to p53, is capable of inducing TAP1 and cooperates with p53 to activate TAP1. Both TAP1 and p21 are induced in cells containing wild-type p53 when treated with camptothecin. TAP1 is induced by DNA damage. p53 is required for the increased expression of TAP1 protein in RKO cells by DNA damage. p53 can activate TAP1 independently of p21. TAP1 is not induced in p53-null-like HCT-116-E6 cells. Mutants p53(V143A), p53(R175H), p53(R249S), and p53(R273H), as well as mutant p73alpha292 are incapable of activating TAP1. IFNgamma is a potent inducer of TAP1, most efficiently at 15 U/ml. Identification of a specific p53-responsive element in the TAP1 gene located approximately 300 nucleotides downstream of the TAP1 transcription start site. This sequence (ggg cttg g*cc ctgccg gga cttg cct) has only one mismatch (G* instead of C/T) to the consensus p53-binding site | up |
General Information
| General Information | Comment | Organism |
|---|---|---|
| metabolism | p53 induces TAP1 and enhances the transport of MHC class I peptides. Since more than 50% of tumors have a dysfunctional p53, evasion of tumor surveillance by tumor cells may be linked to loss of p53 function. TAP1 is strongly induced by p53 and DNA-damaging agents through a p53-responsive element. p73, which is homologous to p53, is capable of inducing TAP1 and cooperates with p53 to activate TAP1. By inducing TAP1, p53 enhances the transport of MHC class I peptides and expression of surface MHC-peptide complexes, and cooperates with interferon gamma to activate the MHC class I pathway. Tumor surveillance may be a mechanism by which p53 and/or p73 function as tumor suppressors. The tumor-derived p53 mutant p53(R249S) is defective in transactivation. TAP1, but no other components in the MHC class I pathway, is induced by p53 | Homo sapiens |
| physiological function | the transporter associated with antigen processing (TAP) 1 is required for the major histocompatibility complex (MHC) class I antigen presentation pathway, which plays a key role in host tumor surveillance. Since more than 50% of tumors have a dysfunctional p53, evasion of tumor surveillance by tumor cells may be linked to loss of p53 function. TAP1 is strongly induced by p53 and DNA-damaging agents through a p53-responsive element. p73, which is homologous to p53, is capable of inducing TAP1 and cooperates with p53 to activate TAP1. By inducing TAP1, p53 enhances the transport of MHC class I peptides and expression of surface MHC-peptide complexes, and cooperates with interferon gamma to activate the MHC class I pathway | Homo sapiens |
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