DCK

Official Full Name

deoxycytidine kinase

Organism

Homo sapiens

Gene ID

1633

Background

Deoxycytidine kinase (DCK) is required for the phosphorylation of several deoxyribonucleosides and their nucleoside analogs. Deficiency of DCK is associated with resistance to antiviral and anticancer chemotherapeutic agents. Conversely, increased deoxycytidine kinase activity is associated with increased activation of these compounds to cytotoxic nucleoside triphosphate derivatives. DCK is clinically important because of its relationship to drug resistance and sensitivity. [provided by RefSeq, Jul 2008]

Synonyms

DCK; deoxycytidine kinase; DCK protein; DCK_HUMAN; OTTHUMP00000160356; OTTHUMP00000219118; OTTHUMP00000219119; deoxynucleoside kinase; MGC117410; MGC138632; wu:fc15f06; zgc:101771

Bio Chemical Class

Kinase

Protein Sequence

MATPPKRSCPSFSASSEGTRIKKISIEGNIAAGKSTFVNILKQLCEDWEVVPEPVARWCNVQSTQDEFEELTMSQKNGGNVLQMMYEKPERWSFTFQTYACLSRIRAQLASLNGKLKDAEKPVLFFERSVYSDRYIFASNLYESECMNETEWTIYQDWHDWMNNQFGQSLELDGIIYLQATPETCLHRIYLRGRNEEQGIPLEYLEKLHYKHESWLLHRTLKTNFDYLQEVPILTLDVNEDFKDKYESLVEKVKEFLSTL

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Approved Drug

Clinical Trial Drug

Discontinued Drug

Cat.No.	Product Name	Price
CSC-DC004083	Panoply™ Human DCK Knockdown Stable Cell Line	Inquiry
CSC-SC004083	Panoply™ Human DCK Over-expressing Stable Cell Line	Inquiry

Cat.No.	Product Name	Price
LV10386L	human DCK (NM_000788) lentivirus particles	Inquiry

Cat.No.	Product Name	Price
SHG223831	shRNA set against Rat Dck(NM_024158.1)	Inquiry
SHG223849	shRNA set against Mouse Dck(NM_007832.4)	Inquiry
SHH275157	shRNA set against Human DCK (NM_000788.2)	Inquiry
SHH275161	shRNA set against Mouse DCK (NM_007832.4)	Inquiry
SHH275165	shRNA set against Rat DCK (NM_024158.1)	Inquiry
SHW000533	shRNA set against Chicken DCK (NM_001006451)	Inquiry
SHW007512	shRNA set against Danio rerio DCK (NM_001007056)	Inquiry

Cat.No.	Product Name	Price
RP00209	Recombinant Human DCK (N-6His-T7)	Inquiry

Cat.No.	Product Name	Price
CDCS405903	Human DCK ORF Clone (BC114617)	Inquiry
CDFG022138	Mouse Dck cDNA Clone(BC060062)	Inquiry
CDFR012288	Rat Dck cDNA Clone(NM_024158.1)	Inquiry
MiUTR1M-03711	DCK miRNA 3'UTR clone	Inquiry
MiUTR1R-01390	DCK miRNA 3'UTR clone	Inquiry
MiUTR3H-00652	DCK miRNA 3'UTR clone	Inquiry
CDCB157642	Human DCK ORF clone (BC114617)	Inquiry
CDCB162008	Chicken DCK ORF Clone (NM_001006451)	Inquiry
CDCB168987	Danio rerio DCK ORF Clone (NM_001007056)	Inquiry
CDCB188685	Rabbit DCK ORF clone (XM_008267765.1)	Inquiry
CDCR244242	Mouse Dck ORF Clone(NM_007832.4)	Inquiry
CDCR379365	Rat Dck ORF Clone(NM_024158.1)	Inquiry

Cat.No.	Product Name	Price
CC-388	DCK Easy KO Kit	Inquiry

Detailed Information

Deoxycytidine kinase (DCK) is an essential enzyme involved in the metabolism of deoxyribonucleosides and plays a crucial role in the nucleoside salvage pathway.

Structure And Function of Deoxycytidine Kinase (DCK)

DCK is a member of the nucleoside kinase family, which is composed of a diverse group of enzymes that phosphorylate deoxyribonucleosides and their phosphates. The crystal structure of DCK has been determined, which has revealed that the enzyme is organized into two domains. The N-terminal domain is responsible for binding the deoxyribonucleoside substrate, while the C-terminal domain is involved in catalysis. The active site of DCK contains a conserved aspartate residue, which is crucial for the phosphorylation of the substrate.

The physiological role of DCK is to phosphorylate deoxyribonucleosides, generating deoxyribonucleotides, which are essential for DNA synthesis. In addition to its role in nucleoside metabolism, DCK also plays a role in the regulation of nucleoside levels in the cell. Over-expression of DCK has been associated with increased nucleoside levels, which can lead to increased nucleotide synthesis and cell growth.

Regulation of Deoxycytidine Kinase (DCK)

DCK is subject to regulation at multiple levels, including transcriptional, post-transcriptional, and post-translational regulation. The expression of DCK is regulated by various transcription factors, including AP-1, Sp1, and nuclear factor-κB (NF-κB). Post-transcriptional regulation of DCK occurs through the action of microRNAs, which can target the mRNA of DCK and reduce its expression. Post-translational regulation of DCK involves the phosphorylation of the enzyme by various kinases, including protein kinase C and mitogen-activated protein kinase (MAPK).

DCK Is Involved in The Inflammatory Response

The gene DCK, also known as DNA-dependent protein kinase, is a crucial regulator of inflammation pathways. DCK is an enzyme that phosphorylates various targets within the cell, including nuclear factors and cytoplasmic proteins, which play essential roles in the initiation and propagation of inflammation. DCK is activated during inflammation, and its expression promotes the activation of nuclear factors, such as NF-κB, which is a primary regulator of inflammation. DCK phosphorylates IκB, a protein that inhibits the nuclear translocation of NF-κB. Upon phosphorylation, IκB is targeted for degradation, allowing NF-κB to enter the nucleus and activate inflammatory genes. This process leads to the expression of various pro-inflammatory cytokines and enzymes, promoting inflammation. Moreover, DCK interacts with cytoplasmic proteins, such as heat shock proteins (HSPs), which play a role in the presentation of antigens to immune cells. This interaction enhances the immune response against pathogens, further contributing to the initiation and propagation of inflammation.

References:

Wu, Biao et al. "Deoxycytidine Kinase (DCK) Mutations in Human Acute Myeloid Leukemia Resistant to Cytarabine." Acta haematologica vol. 144,5 (2021): 534-541. doi:10.1159/000513696
Guantay, Laura et al. "Deoxycytidine kinase (dCK) inhibition is synthetic lethal with BRCA2 deficiency." Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy vol. 67 (2023): 100932. doi:10.1016/j.drup.2023.100932
Han, Zheng et al. "Molecular Imaging of Deoxycytidine Kinase Activity Using Deoxycytidine-Enhanced CEST MRI." Cancer research vol. 79,10 (2019): 2775-2783. doi:10.1158/0008-5472.CAN-18-3565

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