CREPT and p15RS, also named RPRD1B and RPRD1A, are RPRD (regulation of nuclear pre-mRNA-domain-containing) proteins containing C-terminal domain (CTD)-interacting domain (CID), which mediates the binding to the CTD of Rpb1, the largest subunit of RNA polymerase II (RNAPII). CREPT and p15RS are highly conserved, with a common yeast orthologue Rtt103. Intriguingly, human CREPT and p15RS possess opposite functions in the regulation of cell proliferation and tumorigenesis. While p15RS inhibits cell proliferation, CREPT promotes cell cycle and tumor growth. Aberrant expression of both CREPT and p15RS was found in numerous types of cancers. At the molecular level, both CREPT and p15RS were reported to regulate gene transcription by interacting with RNAPII. However, CREPT also exerts a key function in the processes linked to DNA damage repairs. In this review, we summarized the recent studies regarding the biological roles of CREPT and p15RS, as well as the molecular mechanisms underlying their activities. Fully revealing the mechanisms of CREPT and p15RS functions will not only provide new insights into understanding gene transcription and maintenance of DNA stability in tumors, but also promote new approach development for tumor diagnosis and therapy.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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