Mitotic Regulation by NEK Kinase Networks

Fry, Andrew M.; Bayliss, Richard; Roig, Joan

doi:10.3389/fcell.2017.00102

Cited by 80 publications

(80 citation statements)

References 128 publications

(187 reference statements)

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“…The presence of the mutation in the affected lung tissue suggests this mutation may play a role in the etiology of this malformation in this patient. NEK9 may interact with any of the known pathways important in lung morphogenesis or perhaps this could be due to its role in cell cycle regulation (Fry, Bayliss, & Roig, ). However, given the lack of any obvious normal lung tissue in the resected specimen, we were unable to perform genetic analysis in normal lung tissue for direct comparison to abnormal tissue.…”

Section: Discussionmentioning

confidence: 99%

Further delineation of the phenotypic spectrum of nevus comedonicus syndrome to include congenital pulmonary airway malformation of the lung and aneurysm

Sheppard

Smith

Grand

et al. 2020

American J of Med Genetics Pt A

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Nevus comedonicus syndrome (NCS) is a rare epidermal nevus syndrome characterized by ocular, skeletal, and central nervous system anomalies. We present a 23‐month‐old boy with a history of a congenital pulmonary airway malformation (CPAM) of the lung and a congenital cataract who developed progressive linear and curvilinear plaques of dilated follicular openings with keratin plugs (comedones) on parts of his scalp, face, and body consistent with nevus comedonicus. MRI of the brain demonstrated an aneurysm of the right internal carotid artery. Genetic testing identified NEK9 c.1755_1757del (p.Thr586del) at mean allele frequency of 28% in the nevus comedonicus. This same mutation was present in the CPAM tissue. This is the first case of a CPAM in a patient with an epidermal nevus syndrome. This case expands the phenotype of nevus comedonicus syndrome to include CPAM and vascular anomalies.

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Section: Discussionmentioning

confidence: 99%

Further delineation of the phenotypic spectrum of nevus comedonicus syndrome to include congenital pulmonary airway malformation of the lung and aneurysm

Sheppard

Smith

Grand

et al. 2020

American J of Med Genetics Pt A

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“…We will conclude this review with a brief outlook on how and why cancer cells might have changed the G2/M switch system, and how this could be further exploited by therapeutic intervention. For other aspects of mitotic entry dynamics, such as spatial regulation and functions of other mitotic kinases, the reader is referred to excellent recent reviews .…”

Section: The Mitotic Trigger Is An Irreversible Cellular Switchmentioning

confidence: 99%

Triggering mitosis

Crncec

Hochegger

2019

FEBS Letters

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Entry into mitosis is triggered by the activation of cyclin‐dependent kinase 1 (Cdk1). This simple reaction rapidly and irreversibly sets the cell up for division. Even though the core step in triggering mitosis is so simple, the regulation of this cellular switch is highly complex, involving a large number of interconnected signalling cascades. We do have a detailed knowledge of most of the components of this network, but only a poor understanding of how they work together to create a precise and robust system that ensures that mitosis is triggered at the right time and in an orderly fashion. In this review, we will give an overview of the literature that describes the Cdk1 activation network and then address questions relating to the systems biology of this switch. How is the timing of the trigger controlled? How is mitosis insulated from interphase? What determines the sequence of events, following the initial trigger of Cdk1 activation? Which elements ensure robustness in the timing and execution of the switch? How has this system been adapted to the high levels of replication stress in cancer cells?

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“…NIMA‐related kinases, or never in mitosis A‐related kinases (NEKs), are proteins conserved across most eukaryotes . Human cells express 11 NEKs (NEK1‐11).…”

mentioning

confidence: 99%

“…12,19 NIMA-related kinases, or never in mitosis A-related kinases (NEKs), are proteins conserved across most eukaryotes. 20 Human cells express 11 NEKs (NEK1-11). NEK2, NEK5, NEK6, NEK7, and NEK9 have different functions related to control of the centrosome cycle.…”

mentioning

confidence: 99%

Regulation of lung endothelial permeability by NEK kinases

Barabutis

2020

IUBMB Life

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Dysregulation of lung endothelial barrier function may lead to lethal outcomes, as demonstrated in the case of the acute respiratory distress syndrome (ARDS). p53 participates in the regulation of the lung endothelial barrier, and it has been associated both in vivo and in vitro with protective effects against the LPS‐induced hyperpermeability. Family members of the never in mitosis A‐related kinases (NEKs) are crucial mediators of fundamental cellular processes, including mitosis, and have been shown to posttranslationally modify p53. Since such modifications affect p53 stability and activity, it is highly probable that NEK kinases are also regulators of lung endothelial permeability. Thus, they may serve as possible therapeutic targets for treatment of pathologies associated with endothelial barrier dysfunction.

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Mitotic Regulation by NEK Kinase Networks

Cited by 80 publications

References 128 publications

Further delineation of the phenotypic spectrum of nevus comedonicus syndrome to include congenital pulmonary airway malformation of the lung and aneurysm

Further delineation of the phenotypic spectrum of nevus comedonicus syndrome to include congenital pulmonary airway malformation of the lung and aneurysm

Triggering mitosis

Regulation of lung endothelial permeability by NEK kinases

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