Last update 01 Nov 2024

CMPK1

Last update 01 Nov 2024

Basic Info

Synonyms

CK, CMK, CMPK

+ [13]

Introduction

Catalyzes the phosphorylation of pyrimidine nucleoside monophosphates at the expense of ATP. Plays an important role in de novo pyrimidine nucleotide biosynthesis. Has preference for UMP and CMP as phosphate acceptors. Also displays broad nucleoside diphosphate kinase activity.

Drugs associated with CMPK1

JMF4073

Target

CMPK1

Mechanism

CMPK1 inhibitors

Active Org.

National Taiwan University

Originator Org.

National Taiwan University

Active Indication

Acute Myeloid Leukemia

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CMPK1

100 Translational Medicine associated with CMPK1

0 Patents (Medical) associated with CMPK1

259

Literatures (Medical) associated with CMPK1

01 Jul 2024·iScience

Exosomal miRNA 16-5p/29a-3p from pancreatic cancer induce adipose atrophy by inhibiting adipogenesis and promoting lipolysis

Article

Author: Chang, Ming-Chu ; Chang, Chin-Chun ; Hu, Chun-Mei ; Peng, Hsuan-Yu ; Lee, Wen-Hwa ; Tien, Sui-Chih ; Chang, Yu-Ting ; Huang, Ching-Hsuan

Over 80% of the patients with pancreatic ductal adenocarcinoma (PDAC) have cachexia/wasting syndrome. Cachexia is associated with reduced survival, decreased quality of life, and higher metastasis rates. Here, we demonstrate that fat loss is the earliest feature of PDAC-exosome-induced cachexia. MicroRNA sequencing of exosomal components from normal and cancer-derived exosomes revealed enrichment of miR-16-5p, miR-21-5p, miR-29a-3p, and miR-125b-5p in serum exosomes of mice harboring PDAC and patients with PDAC. Further, miR-16-5p and miR-29a-3p inhibited adipogenesis through decreasing Erlin2 and Cmpk1 expression which downregulates C/EBPβ and PPARγ. Synergistically, miR-29a-3p promotes lipolysis through increasing ATGL expression by suppressing MCT1 expression. Furthermore, PDAC-exosomes deprived of miR-16-5p and miR-29a-3p fail to induce fat loss. Hence, miR-16-5p and miR-29a-3p exosomal miRs are essential for PDAC-induced fat loss. Thus, we unravel that PDAC induces adipose atrophy via exosomal miRs. This knowledge may provide new diagnostic and therapeutic strategies for PDAC-induced cachexia.

01 Jul 2024·Acta Pharmaceutica Sinica B

Selectively T cell phosphorylation activation of azvudine in the thymus tissue with immune protection effect

Article

Author: Wang, Lulu ; Li, Yuhuan ; Wang, Zhe ; Zhang, Jinlan ; Jiang, Jiandong ; Li, Rui ; Li, Yang ; Sheng, Ning

Thymus is the important immune organ, responsible for T cell development and differentiation. The lower circulating T counts have been observed in patients who died from COVID-19 compared with survivors. Azvudine, also known as FNC, is a thymus-homing anti-SARS-CoV-2 drug in treating COVID-19 patients. In this study, single-cell transcriptome, proteomics, and parallel reaction monitoring (PRM) were applied to insight into the activation process of FNC in rat and SARS-CoV-2 rhesus monkey thymus. The results indicated that thymic immune cells possess a robust metabolic capacity for cytidine-analogue drugs such as FNC. Key enzymes involved in the FNC phosphorylation process, such as Dck, Cmpk1, and Nme2, were highly expressed in CD4+ T cells, CD8+ T cells, and DP (CD4+ CD8+) cells. Additionally, FNC could upregulate multiple phosphorylated kinases in various cell types while downregulating the phosphatases, phosphoribosyl transferases, and deaminases, respectively. The robust phosphorylation capacity of the thymus for cytidine analogue drug FNC, and the activation effect of FNC on the NAs metabolism system potentially contribute to its enrichment in the thymus and immune protection effect. This suggests that it is crucial to consider the expression level of phosphorylation kinases when evaluating NA drug properties, as an important factor during antiviral drug design.

01 Apr 2023·Bioprocess and Biosystems Engineering

Computational aided design of a halotolerant CMP kinase for enzymatic synthesis of cytidine triphosphate

Article

Author: Zhang, Bingyun ; Wen, Qingshi ; Wang, Junzhi ; Miao, Rongxin ; Yan, Ziyi ; Zhang, Jie ; Ying, Hanjie

The current biocatalytic method of industrial Cytidine triphosphate (CTP) production suffers from reaction rate loss. It is caused by gradually increasing acetate salt concentration, which inhibits enzyme activities and decreases the final yield. This work gave a possible solution to this problem through computational aided design of CMP kinase (CMPK), an enzyme in the CTP production system, to increase its stability in solution with high acetate salt concentration. Enlightened by the features of natural halophilic enzymes, the basic and neutral surface residues were replaced with acidic amino acids. This protein design strategy effectively increased the activity of CMPK in the working condition (acetate concentration over 1200 mM). The halotolerant CMPK was applied in fed-batch production of CTP. The maximum titer was 201.4 ± 1.6 mM, and the productivity was 12.6 mM L^-1 h^-1, increased 26.4% and 27.8% from the process using wild-type CMPK, respectively.

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CMPK1

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