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Deoxycytidine kinase (DCK) is required for the phosphorylation of several deoxyribonucleosides and their nucleoside analogs. Zusätzlich bieten wir Ihnen DCK Antikörper (151) und DCK Proteine (16) und viele weitere Produktgruppen zu diesem Protein an.
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study suggests that DCK knockdown facilitates apoptosis while inhibiting proliferation and tumorigenicity in vivo of cervical cancer HeLa cells.
Phosphorylated and activated DCK can inhibit radiation-induced cell death including apoptosis and mitotic catastrophe, and promote radiation-induced autophagy through PI3K (zeige PIK3CA ELISA Kits)/Akt (zeige AKT1 ELISA Kits)/mTOR (zeige FRAP1 ELISA Kits) pathway.
Low deoxycytidine kinase expression is associated with periampullary adenocarcinoma.
recently described a human deoxycytidine kinase mutant (G12 (zeige TCF3 ELISA Kits)) that sensitizes cancer cell lines to treatment with gemcitabine. Here, starting from the G12 (zeige TCF3 ELISA Kits) variant, we identified a mutant that triggers even greater sensitisation to gemcitabine than G12 (zeige TCF3 ELISA Kits).
RNA expression of deoxycytidine kinase (DCK), human equilibrative nucleoside transporter-1 (ENT1 (zeige SLC29A1 ELISA Kits)) and ribonucleotide reductase M1 (RRM1 (zeige RRM1 ELISA Kits)) were significantly higher and cytidine deaminase (CDA (zeige CDA ELISA Kits)) was significantly lower in ex vivo Ara (zeige FOXC1 ELISA Kits)-C sensitive samples.
n the multivariate Cox regression analysis, we found that age at diagnosis, wild-type genotype of the CDA (zeige CDA ELISA Kits) A79C polymorphism, and wild-type genotype of the dCK C360G polymorphism were the most significant prognostic factors for predicting the risk of death
results strongly suggest that (1) the E197K alteration in DCK causes inactivation of DCK, and that (2) loss of the normal E197 allele is the crucial mechanism in acquisition of gemcitabine resistance in the RMKN28 tumor cell line
DCK rs12648166 and DCK rs4694362 SNPs were associated with hematologic toxicity (OR = 2.63, CI 95% = 1.37-5.04, P = 0.0036 and OR = 2.53, CI 95% = 1.34-4.80, P = 0.0044, respectively).
These findings indicate that the decitabine metabolic pathway affects its therapeutic effects, lower hENT1 expression may induce primary resistance and down-regulated DCK expression may be related to secondary resistance.
DCK expression levels are prognostic and had predictive value for sensitivity to 5-FU in pancreatic cancer.
Mutation of a single serine 74 residue has profound effects on murine T and B lymphocyte (zeige AKAP17A ELISA Kits) development, suggesting that post-translational regulation of dCK has a role in maintaining genomic stability during hematopoiesis.
activating the dAdo-DCK-dATP pathway directly results in increased apoptosis in the lungs of mice with air-space enlargement and suggests a novel therapeutic target for the treatment of COPD (zeige ARCN1 ELISA Kits)
Deoxycytidine kinase is a new regulator of hematopoietic integrity and lymphocyte quiescence and survival.
The severe impact of dCK inactivation on lymphopoiesis was unexpected given that nucleoside salvage has been thought to play a limited, "fine-tuning" role in regulating deoxyribonucleotide triphosphate pools produced by the de novo pathway.
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.
, Deoxycytidine kinase
, deoxycytidine kinase
, deoxycytidine kinase 1
, deoxyribonucleoside kinase