A bifurcated signaling cascade of NIMA-related kinases controls distinct kinesins in anaphase

Cullati, Sierra; Kabeche, Lilian; Kettenbach, Arminja N.; Gerber, Scott A.

doi:10.1083/jcb.201512055

Cited by 28 publications

(33 citation statements)

References 49 publications

(90 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…, 2015 ), a finding consistent with our results. Also consistent with our results is the observation that directly impairing MKlp2’s ability to target the midzone does not completely abolish CPC targeting to the cell middle ( Cullati et al. , 2017 ).…”

Section: Discussionsupporting

confidence: 91%

Two mechanisms coordinate the recruitment of the chromosomal passenger complex to the plane of cell division

Landino

Norris

et al. 2017

MBoC

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 91%

Two mechanisms coordinate the recruitment of the chromosomal passenger complex to the plane of cell division

Landino

Norris

et al. 2017

MBoC

View full text Add to dashboard Cite

show abstract

“…However, NEK7 can phosphorylate other motor proteins to control microtubule organization, and interacts with additional regulators of both the microtubule and actin networks, offering alternative mechanisms through which these kinases can influence cell movement 45,46 . consisting of an NTD that encompasses a trimerization motif and basic region that binds microtubules, and a C-terminal TAPE domain that binds tubulin heterodimers 15,16 .…”

Section: Discussionmentioning

confidence: 99%

EML4-ALK V3 drives cell migration through NEK9 and NEK7 kinases in non-small-cell lung cancer

O’Regan

Barone

Adib

et al. 2019

Preprint

View full text Add to dashboard Cite

EML4-ALK is an oncogenic fusion present in ~5% lung adenocarcinomas. However, distinct EML4-ALK variants differ in the length of the EML4 microtubule-associated protein encoded within the fusion and are associated with a poorly understood variability in disease progression and therapeutic response. Here, we show that EML4-ALK variant 3, which is linked to accelerated metastatic spread and worse patient outcome, causes microtubule stabilization, formation of extended cytoplasmic protrusions, loss of cell polarity and increased cell migration. Strikingly, this is dependent upon the NEK9 kinase that interacts with the Nterminal region of EML4. Overexpression of wild-type EML4, as well as constitutive activation of NEK9, also perturbs cell morphology and accelerates cell migration in a manner that requires the downstream kinase NEK7 but not ALK activity. Moreover, elevated NEK9 is associated in patients with EML4-ALK V3 expression, as well as reduced progression-free and overall survival. Hence, we propose that EML4-ALK V3 promotes microtubule stabilization through recruitment of NEK9 and NEK7 to increase cell migration and that this represents a novel actionable pathway that drives disease progression in lung cancer.

show abstract

“…14,36,37 Conversely, it has been proposed that KIF14 may be crucial to localize CIT-K to the midzone. 14,50 Although the inter-dependence between CIT-K and KIF14 for their correct localization to the midbody may be context-dependent, a strong functional link between the two proteins is suggested by the finding that KIF14 knockout mice seem to phenocopy CIT-K knockout. 51 Thus, CIT-K may contribute to the stability of midbody by bridging CPC proteins with midbody ring kinesins MKLP1 and KIF14.…”

Section: Molecular Complexes and Mechanisms Of Cit Proteins At The Imentioning

confidence: 99%

Of rings and spines: The multiple facets of Citron proteins in neural development

et al. 2017

View full text Add to dashboard Cite

The Citron protein was originally identified for its capability to specifically bind the active form of RhoA small GTPase, leading to the simplistic hypothesis that it may work as a RhoA downstream effector in actin remodeling. More than two decades later, a much more complex picture has emerged. In particular, it has become clear that in animals, and especially in mammals, the functions of the Citron gene (CIT) are intimately linked to many aspects of central nervous system (CNS) development and function, although the gene is broadly expressed. More specifically, CIT encodes two main isoforms, Citron-kinase (CIT-K) and Citron-N (CIT-N), characterized by complementary expression pattern and different functions. Moreover, in many of their activities, CIT proteins act more as upstream regulators than as downstream effectors of RhoA. Finally it has been found that, besides working through actin, CIT proteins have many crucial functional interactions with the microtubule cytoskeleton and may directly affect genome stability. In this review, we will summarize these advances and illustrate their actual or potential relevance for CNS diseases, including microcephaly and psychiatric disorders.

show abstract

A bifurcated signaling cascade of NIMA-related kinases controls distinct kinesins in anaphase

Cited by 28 publications

References 49 publications

Two mechanisms coordinate the recruitment of the chromosomal passenger complex to the plane of cell division

Two mechanisms coordinate the recruitment of the chromosomal passenger complex to the plane of cell division

EML4-ALK V3 drives cell migration through NEK9 and NEK7 kinases in non-small-cell lung cancer

Of rings and spines: The multiple facets of Citron proteins in neural development

Contact Info

Product

Resources

About