Molecule Information
General Information of the Molecule (ID: Mol04023)
| Name |
Deoxycytidine kinase (DCK)
,Homo sapiens
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| Synonyms |
Deoxyadenosine kinase; Deoxyguanosine kinase
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| Molecule Type |
Protein
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| Gene Name |
DCK
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| Gene ID | |||||
| Location |
chr4:70992538-71030914[+]
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| Sequence |
MATPPKRSCPSFSASSEGTRIKKISIEGNIAAGKSTFVNILKQLCEDWEVVPEPVARWCN
VQSTQDEFEELTMSQKNGGNVLQMMYEKPERWSFTFQTYACLSRIRAQLASLNGKLKDAE KPVLFFERSVYSDRYIFASNLYESECMNETEWTIYQDWHDWMNNQFGQSLELDGIIYLQA TPETCLHRIYLRGRNEEQGIPLEYLEKLHYKHESWLLHRTLKTNFDYLQEVPILTLDVNE DFKDKYESLVEKVKEFLSTL Click to Show/Hide
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| 3D-structure |
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| Function |
Phosphorylates the deoxyribonucleosides deoxycytidine, deoxyguanosine and deoxyadenosine (PubMed:12808445, PubMed:18377927, PubMed:19159229, PubMed:1996353, PubMed:20614893, PubMed:20637175). Has broad substrate specificity, and does not display selectivity based on the chirality of the substrate. It is also an essential enzyme for the phosphorylation of numerous nucleoside analogs widely employed as antiviral and chemotherapeutic agents (PubMed:12808445). .
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Type(s) of Resistant Mechanism of This Molecule
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | [1] | |||
| Metabolic Type | Mitochondrial metabolism | |||
| Resistant Disease | Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | |||
| Resistant Drug | Gemcitabine | |||
| Molecule Alteration | Mutation | . |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | CFPAC-1 cells | Pancreas | Homo sapiens (Human) | CVCL_1119 |
| Experiment for Molecule Alteration |
qRT-PCR | |||
| Experiment for Drug Resistance |
Cell viability assay | |||
| Mechanism Description | Moreover, enrichment of oxidative phosphorylation (OXPHOS)-associated genes was a common property shared by PDAC cell lines, and patient clinical samples coupled with low DCK expression was also demonstrated, which implicates DCK in cancer metabolism. In this article, we reveal that the expression of most genes encoding mitochondrial complexes is remarkably upregulated in PDAC patients with low DCK expression. The DCK-knockout (DCK KO) CFPAC-1 PDAC cell line model reiterated this observation. | |||
References
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