Release of Mps1 from kinetochores is crucial for timely anaphase onset. - Wikidata - wikimedia - TriplyDB

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

http://www.wikidata.org/entity/Q42407469

about

The final link: tapping the power of chemical genetics to connect the molecular and biologic functions of mitotic protein kinases The Renaissance or the cuckoo clock ARHGEF17 is an essential spindle assembly checkpoint factor that targets Mps1 to kinetochores A TPR domain–containing N-terminal module of MPS1 is required for its kinetochore localization by Aurora B Structural and functional insights into the role of the N-terminal Mps1 TPR domain in the SAC (spindle assembly checkpoint)Mad1 kinetochore recruitment by Mps1-mediated phosphorylation of Bub1 signals the spindle checkpoint.Polo-like kinase-1 regulates kinetochore-microtubule dynamics and spindle checkpoint silencing.UV-C irradiation delays mitotic progression by recruiting Mps1 to kinetochores Drosophila Polo regulates the spindle assembly checkpoint through Mps1-dependent BubR1 phosphorylation Bub1 autophosphorylation feeds back to regulate kinetochore docking and promote localized substrate phosphorylation The MPS1 family of protein kinases.Recruitment of Mad1 to metaphase kinetochores is sufficient to reactivate the mitotic checkpoint.Conditional targeting of MAD1 to kinetochores is sufficient to reactivate the spindle assembly checkpoint in metaphase.Dynamic autophosphorylation of mps1 kinase is required for faithful mitotic progression The kinetochore encodes a mechanical switch to disrupt spindle assembly checkpoint signalling.A putative N-terminal nuclear export sequence is sufficient for Mps1 nuclear exclusion during interphase Two LXXLL motifs in the N terminus of Mps1 are required for Mps1 nuclear import during G(2)/M transition and sustained spindle checkpoint responses.Mutual regulation between the spindle checkpoint and APC/C.Centromere-tethered Mps1 pombe homolog (Mph1) kinase is a sufficient marker for recruitment of the spindle checkpoint protein Bub1, but not Mad1.Characterization of spindle checkpoint kinase Mps1 reveals domain with functional and structural similarities to tetratricopeptide repeat motifs of Bub1 and BubR1 checkpoint kinases.Dynamic localization of Mps1 kinase to kinetochores is essential for accurate spindle microtubule attachment Spindle checkpoint-independent inhibition of mitotic chromosome segregation by Drosophila Mps1.Probing the catalytic functions of Bub1 kinase using the small molecule inhibitors BAY-320 and BAY-524.Whole-genome duplication increases tumor cell sensitivity to MPS1 inhibition.Monopolar spindle 1 (MPS1) kinase promotes production of closed MAD2 (C-MAD2) conformer and assembly of the mitotic checkpoint complex Connecting up and clearing out: how kinetochore attachment silences the spindle assembly checkpoint.Function and regulation of dynein in mitotic chromosome segregation."Uno, nessuno e centomila": the different faces of the budding yeast kinetochore.An overview of the spindle assembly checkpoint status in oral cancer.Signalling dynamics in the spindle checkpoint response.Sharpening the anaphase switch.Spatial rule-based modeling: a method and its application to the human mitotic kinetochore.A direct role of Mad1 in the spindle assembly checkpoint beyond Mad2 kinetochore recruitment.Mps1 is SUMO-modified during the cell cycle.ARHGEF17 sets the timer for retention of Mps1 at kinetochores.Playing polo during mitosis: PLK1 takes the lead.Aurora B potentiates Mps1 activation to ensure rapid checkpoint establishment at the onset of mitosis.Synthetic Physical Interactions Map Kinetochore-Checkpoint Activation Regions.Plk1 bound to Bub1 contributes to spindle assembly checkpoint activity during mitosis.All together now: Polo joins the kinase network controlling the spindle assembly checkpoint in Drosophila.

P2860

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P2860

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

http://www.wikidata.org/entity/Q42407469

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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2010年论文

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2010年论文

@zh-cn

name

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

@en

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

@nl

type

label

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

@en

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

@nl

prefLabel

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

@en

Release of Mps1 from kinetochores is crucial for timely anaphase onset.

@nl

P1433

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P1433

Journal of Cell Biology

P1476

Release of Mps1 from kinetochores is crucial for timely anaphase onset

@en

P2093

Nannette Jelluma

http://www.w3.org/2001/XMLSchema#string

Nicholas P Kwiatkowski

http://www.w3.org/2001/XMLSchema#string

Tale Sliedrecht

http://www.w3.org/2001/XMLSchema#string

Tobias B Dansen

http://www.w3.org/2001/XMLSchema#string

P2860

ZW10 links mitotic checkpoint signaling to the structural kinetochore.

A conserved protein network controls assembly of the outer kinetochore and its ability to sustain tension

Determinants of conformational dimerization of Mad2 and its inhibition by p31comet

A conserved Mis12 centromere complex is linked to heterochromatic HP1 and outer kinetochore protein Zwint-1

Mps1 phosphorylates Borealin to control Aurora B activity and chromosome alignment

Timely anaphase onset requires a novel spindle and kinetochore complex comprising Ska1 and Ska2

Stable kinetochore-microtubule interactions depend on the Ska complex and its new component Ska3/C13Orf3.

Human Mps1 kinase is required for the spindle assembly checkpoint but not for centrosome duplication

Conformation-specific binding of p31(comet) antagonizes the function of Mad2 in the spindle checkpoint

Lethality to human cancer cells through massive chromosome loss by inhibition of the mitotic checkpoint.

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281-290

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10.1083/JCB.201003038

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2

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191

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47395495

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20937696

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2958484

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