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Last update 08 May 2025

MOK

Last update 08 May 2025

Basic Info

Synonyms

MAPK/MAK/MRK overlapping kinase, MOK, MOK protein kinase

+ [6]

Introduction

Able to phosphorylate several exogenous substrates and to undergo autophosphorylation. Negatively regulates cilium length in a cAMP and mTORC1 signaling-dependent manner.

Drugs associated with MOK

rCT-S100A8/A9

Target

MOK x TLR4

Mechanism

MOK antagonists [+1]

Active Org.

Hanyang University

Originator Org.

Hanyang University

Active Indication

Colitis [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MOK

100 Translational Medicine associated with MOK

0 Patents (Medical) associated with MOK

Literatures (Medical) associated with MOK

11 Jul 2023·Proceedings of the National Academy of Sciences of the United States of AmericaQ1 · CROSS-FIELD

MAPK/MAK/MRK overlapping kinase (MOK) controls microglial inflammatory/type-I IFN responses via Brd4 and is involved in ALS.

Q1 · CROSS-FIELD

Article

Author: Leal-Lasarte, Magdalena ; García-García, Raquel ; Franco, Jaime M ; Silvera-Carrasco, Lucía ; García-Domínguez, Mario ; Miyata, Yoshihiko ; Roodveldt, Cintia ; Armaos, Alexandros ; Gómez-Lima, María ; Pozo, David ; Baloh, Robert H ; Pérez-Cabello, Jesús A ; Yap, Xin Wen ; Capilla-González, Vivian ; Sawarkar, Ritwick ; Tartaglia, Gian G ; Martínez, Salvador ; Lall, Deepti

Amyotrophic lateral sclerosis (ALS) is a fatal and incurable neurodegenerative disease affecting motor neurons and characterized by microglia-mediated neurotoxic inflammation whose underlying mechanisms remain incompletely understood. In this work, we reveal that MAPK/MAK/MRK overlapping kinase (MOK), with an unknown physiological substrate, displays an immune function by controlling inflammatory and type-I interferon (IFN) responses in microglia which are detrimental to primary motor neurons. Moreover, we uncover the epigenetic reader bromodomain-containing protein 4 (Brd4) as an effector protein regulated by MOK, by promoting Ser⁴⁹²-phospho-Brd4 levels. We further demonstrate that MOK regulates Brd4 functions by supporting its binding to cytokine gene promoters, therefore enabling innate immune responses. Remarkably, we show that MOK levels are increased in the ALS spinal cord, particularly in microglial cells, and that administration of a chemical MOK inhibitor to ALS model mice can modulate Ser⁴⁹²-phospho-Brd4 levels, suppress microglial activation, and modify the disease course, indicating a pathophysiological role of MOK kinase in ALS and neuroinflammation.

31 Dec 2022·RNA Biology

The A to I editing landscape in melanoma and its relation to clinical outcome

Article

Author: Guenova, Emmanuella ; Levesque, Mitchell P ; Cheng, Phil ; Tusup, Marina ; Kundig, Thomas ; Läuchli, Severin ; French, Lars E ; Mellett, Mark ; Amweg, Austeja ; Dummer, Reinhard ; Picardi, Ernesto ; Pascolo, Steve

RNA editing refers to non-transient RNA modifications that occur after transcription and prior to translation by the ribosomes. RNA editing is more widespread in cancer cells than in non-transformed cells and is associated with tumorigenesis of various cancer tissues. However, RNA editing can also generate neo-antigens that expose tumour cells to host immunosurveillance. Global RNA editing in melanoma and its relevance to clinical outcome currently remain poorly characterized. The present study compared RNA editing as well as gene expression in tumour cell lines from melanoma patients of short or long metastasis-free survival, patients relapsing or not after immuno- and targeted therapy and tumours harbouring BRAF or NRAS mutations. Overall, our results showed that NTRK gene expression can be a marker of resistance to BRAF and MEK inhibition and gives some insights of candidate genes as potential biomarkers. In addition, this study revealed an increase in Adenosine-to-Inosine editing in Alu regions and in non-repetitive regions, including the hyperediting of the MOK and DZIP3 genes in relapsed tumour samples during targeted therapy and of the ZBTB11 gene in NRAS mutated melanoma cells. Therefore, RNA editing could be a promising tool for identifying predictive markers, tumour neoantigens and targetable pathways that could help in preventing relapses during immuno- or targeted therapies.

01 Aug 2022·Developmental & Comparative Immunology

MAPK/MAK/MRK overlapping kinase mediated apoptosis through caspase signaling pathway from Cristaria plicata

Article

Author: Jian, Shaoqing ; Wu, Jielian ; Wen, Chungen ; Hu, Baoqing ; Feng, Maolin ; Cao, Xinying ; An, Jinhua ; Gang, Yang

MAPK/MAK/MRK Overlapping Kinase (MOK) belongs to MAP kinase superfamily, which plays an important role in regulating cell growth, division, and differentiation. Caspase-3, as the final executor of apoptosis, has an important position in the caspase-mediated apoptotic signaling pathway. The full-length cDNA of MOK and caspase-3 were cloned from Cristaria plicata (designated CpMOK and CpCaspase-3). The CpMOK gene was sequence with a full-length of 1413 bp, encoding a total of 470 amino acids, and containing an S_TKc structural domain. CpCaspase-3 has a sequence of 2425 bp, encoding 322 amino acids, containing a CASc domain. Real-time fluorescence quantitative PCR analysis showed that CpMOK and CpCaspase-3 distributed in various tissues of C. plicata, and the highest expression of CpMOK and CpCaspase-3 mRNA was in hepatopancreas. The expression of CpMOK was significantly changed in hepatopancreas, gills, and kidneys by the construction of wound model as well as stimulation of LPS, PGN, Poly I: C and Aeromonas hydrophila. Subcellular localization experiments confirmed that CpMOK was localized in the nucleus. Furthermore, the double-stranded RNA (dsRNA) of CpMOK was constructed for interference experiment, and the results showed that the mRNA expression of apoptotic gene signals caspase-1, caspase-3, caspase-7, caspase-8, and caspase-9 were increased. The expression of caspase-1, -3, -7, -9, cytochrome C (Cyt-c) and tumor necrosis factor-α (TNF-α) was detected by ELISA. Fluorescent staining of apoptotic cells using the Tunnel method revealed an increase in the number of apoptotic cells after interference. These results suggested that CpMOK knockdown could induce caspase-mediated apoptosis in C. plicata, and the phosphorylation of the kinase was disrupted during the process.

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