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更新于：2025-05-07

DGUOK

更新于：2025-05-07

基本信息

别名

Deoxyadenosine kinase, mitochondrial、deoxyguanosine kinase、Deoxyguanosine kinase, mitochondrial

+ [2]

简介

Phosphorylates deoxyguanosine and deoxyadenosine in the mitochondrial matrix, with the highest efficiency for deoxyguanosine (PubMed:11687801, PubMed:17073823, PubMed:23043144, PubMed:8692979, PubMed:8706825). In non-replicating cells, where cytosolic dNTP synthesis is down-regulated, mtDNA synthesis depends solely on DGUOK and TK2. Phosphorylates certain nucleoside analogs (By similarity). Widely used as target of antiviral and chemotherapeutic agents.

关联

项与 DGUOK 相关的药物

[18F]F-AraG

靶点

DCK x DGUOK

作用机制

DCK inhibitors [+2]

在研机构

CellSight Technologies, Inc. [+1]

原研机构

Stanford University

在研适应症

局部晚期非小细胞肺癌 [+8]

非在研适应症

侵袭性 B 细胞非霍奇金淋巴瘤 [+9]

最高研发阶段临床2期

首次获批国家/地区-

首次获批日期1800-01-20

CERC-913

靶点

DGUOK

作用机制

DGUOK agonists

在研机构

Ichorion Therapeutics, Inc.

原研机构

Ichorion Therapeutics, Inc.

在研适应症

线粒体病

非在研适应症

脱氧鸟苷激酶缺乏症

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

项与 DGUOK 相关的临床试验

NCT06457789

/ RecruitingN/AIIT

Assessment of PET Tracers to Evaluate T Cell Change and Activation in Relation to Immunotherapy Treatment Response in Non-Small Cell Lung Cancer

The iRelate is a PET imaging trial to compare two upcoming and promising T cell PET tracers. Following chemo-immuno therapy, as part of standard care, NSCLC patients will be recruited to receive two PET scans, shortly before their surgery. Both PET scans will be compared to each other, as well as compared to the pathological analysis of the resected tumor.
This study will provide detailed information on the unique as well as additive capacities of imaging biomarkers derived from the immune cell targeting PET tracers.

开始日期2024-12-01

申办/合作机构

Stichting Onderzoek Cancer Center Amsterdam

[+1]

NCT06414902

/ Recruiting早期临床1期IIT

18F-AraG PET/CT as a Non-Invasive Imaging Biomarker for Chemoradiation Treatment Response in Esophageal Cancer

To learn if 18F-FAraG PET scans can find tumors in participants with esophageal cancer and predict a participant's response to treatment.

开始日期2024-09-04

申办/合作机构

The University of Texas MD Anderson Cancer Center

NCT06107374

/ Recruiting临床2期

Imaging of T-cell Activation With [18F]F-araG in Advanced Non-Small Cell Lung Cancer (NSCLC) Patients Undergoing PD-1/PD-L1 Directed Therapy

This pilot study uses [18F]F AraG PET imaging to evaluate the immunological response to checkpoint inhibitor therapy (CkIT) in patients with advanced NSCLC tumors. The study's main objectives are to quantify the change in [18F]F AraG PET signal before and while on CkIT therapy and to correlate this change in [18F]F AraG PET signal with radiographic response.
To explore these objectives, eligible subjects will undergo pre- and on - CkIT treatment [18F]F AraG PET/CT scans, and will be followed up for 12 months for assessment of radiographic and clinical outcomes. This study is a single-site, open label, non randomized, single arm pilot trial. Patients and care providers will not be blinded to any part of the study.

开始日期2023-11-01

申办/合作机构

CellSight Technologies, Inc.

100 项与 DGUOK 相关的临床结果

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100 项与 DGUOK 相关的转化医学

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0 项与 DGUOK 相关的专利（医药）

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218

项与 DGUOK 相关的文献（医药）

2025-03-01·Molecular Therapy Methods & Clinical Development

Gene therapy prevents hepatic mitochondrial dysfunction in murine deoxyguanosine kinase deficiency

Article

作者: Keshavan, Nandaki ; Greenwood, Miriam ; Privolizzi, Riccardo ; Prunty, Helen ; Counsell, John ; Karlsson, Anna ; Waddington, Simon ; Rahman, Shamima ; Diaz, Juan Antinao ; Sebire, Neil ; Karda, Rajvinder

Primary mitochondrial disorders are a cause of neonatal liver failure. Biallelic pathogenic variants of the gene encoding the mitochondrial localizing enzyme deoxyguanosine kinase (DGUOK) cause hepatocerebral mitochondrial DNA depletion syndrome, leading to acute neonatal liver failure and early mortality. There are currently no effective disease-modifying therapies. In this study, we developed an adeno-associated virus 9 (AAV9) gene therapy approach to treat a mouse model of DGUOK deficiency that recapitulates human disease. We delivered AAV9-hDGUOK intravenously to newborn Dguok knock-out mice and showed that liver dysfunction was prevented in a dose-dependent manner. Unexpectedly for neonatal delivery, durable and long-lasting liver transduction and RNA expression were observed. Liver mitochondrial DNA depletion, deficiencies of oxidative phosphorylation complexes I, III, and IV and liver transaminitis and survival were ameliorated in a dose-dependent manner.

2025-03-01·Current Cancer Drug Targets

Mitochondrial Deoxyguanosine Kinase Induces 5-Fluorouracil Chemotherapy Sensitivity through Autophagy

Article

作者: Sun, Wenjing ; Liu, Sifan ; Zhang, Nan ; Zhang, Shutian ; Dong, Lu ; Liu, Siying

Aims:The purpose of this study was to investigate the role of DGUOK in the pro-gression of colorectal cancer (CRC) and its impact on the sensitivity of CRC cells to 5-FU treatment.Methods:We conducted bioinformatics analysis and qRT-PCR to evaluate DGUOK expression in CRC tissues/cells. Cell viability of CRC cells treated with 5-FU was assessed using CCK-8 and colony formation assays. Autophagy levels were determined through immunofluorescence assays and Western blot analysis. Additionally, the influence of p-p38 on autophagy was inves-tigated via Western blotting. A rescue assay was performed to confirm whether DGUOK/p38 affects 5-FU sensitivity in CRC cells through autophagy.Results:Our findings indicate that DGUOK is upregulated in CRC tissues compared to normal tissues, correlating with increased cell proliferation and migration. Functionally, inhibition of DGUOK enhances autophagy, thereby decreasing the sensitivity of CRC cells to 5-FU. This ef-fect is partly mediated by DGUOK's impact on the mitogen-activated protein kinase (MAPK) pathway, specifically promoting the phosphorylation of p38 MAPK, a crucial regulator in au-tophagy pathways.Conclusion:These results suggest that DGUOK could serve as a novel marker for predicting the efficacy of 5-FU in CRC treatment.

2025-02-01·Molecular Biotechnology

LncRNA DGUOK-AS1 Promotes Cell Progression in Lung Squamous Cell Carcinoma by Regulation of miR-653-5p/SLC6A15 Axis

Article

作者: Wu, Nan ; Wei, Lijuan ; Li, Shixia ; Teng, Yan ; Zhang, Jing ; Huang, Jinchao ; Wang, Shuang ; Zhang, Chi ; Liu, Juntian ; Li, Lijuan ; Zhang, Huan

Long noncoding RNA (lncRNA) plays a key role in regulating cancer development. LncRNA deoxyguanosine kinase antisense RNA 1 (DGUOK-AS1) has been reported as a promoter in tumor. The work was designed to further investigate the mechanism of action of DGUOK-AS1 in lung squamous cell carcinoma (LUSC). DGUOK-AS1 level in LUSC cells was measured using RT-qPCR. Counting Kit-8 assays and colony forming assays were performed to evaluate LUSC cell viability and proliferation. Transwell assays were performed to detect cell migration and invasion. Luciferase reporter and RNA pulldown assays were used to verify the binding capacity of DGUOK-AS1 and miR-653-5p. RNA immunoprecipitation assays were performed to verify the relationship of DGUOK-AS1, miR-653-5p, and SLC6A15. DGUOK-AS1 was highly expressed in LUSC cells. DGUOK-AS1 knockdown suppressed LUSC cell proliferation, migration, and invasion. SLC6A15 was demonstrated to be targeted by miR-653-5p, and DGUOK-AS1 interacted with miR-653-5p to modulate SLC6A15 level in LUSC cells. Overexpression of SLC6A15 reversed the suppressive effects of DGUOK-AS1 knockdown on LUSC cell processes. In conclusion, DGUOK-AS1 promotes malignant behaviors of LUSC cells by upregulating SLC6A15 level through interaction with miR-653-5p.

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