Phosphorylation by p34cdc2 regulates spindle association of human Eg5, a kinesin-related motor essential for bipolar spindle formation in vivo

Blangy, Anne; Lane, Heidi A.; d'Hérin, Pierre; Harper, Maryannick; Kress, Michel; Nigg, Erich A.

doi:10.1016/0092-8674(95)90142-6

Cited by 878 publications

(831 citation statements)

References 67 publications

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“…1B) directly into the Eg5-pRcCMV plasmid coding for the native full-length Eg5 fused to a N-terminal myc-tag [1]. The sequences of the primers used and the unique restriction sites introduced are noted in Table 1 of supplemental material section.…”

Section: Cloning Of Point Mutations and Transfectionmentioning

confidence: 99%

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Mutations in the human kinesin Eg5 that confer resistance to monastrol and S-trityl-l-cysteine in tumor derived cell lines

Tcherniuk

Lis

Kozielski

et al. 2010

Biochemical Pharmacology

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. Mutations in the human kinesin Eg5 that confer resistance to monastrol and S-Trityl-L-Cysteine in tumor derived cell lines.. Biochemical Pharmacology, Elsevier, 2010, 79 (6) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. confirms the target specificity of monastrol and STLC for Eg5. These data also suggest a possible mechanism by which drug resistance may occur in tumors treated with agents targeting Eg5.

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Section: Cloning Of Point Mutations and Transfectionmentioning

confidence: 99%

“…The human kinesin Eg5 (also known as KSP, or Kif11), a member of the kinesin-5 family, is essential for the formation of a bipolar spindle in dividing cells [1]. Eg5 is a homotetrameric motor formed by the antiparallel arrangement of two dimers [2].…”

Section: Introductionmentioning

confidence: 99%

Mutations in the human kinesin Eg5 that confer resistance to monastrol and S-trityl-l-cysteine in tumor derived cell lines

Tcherniuk

Lis

Kozielski

et al. 2010

Biochemical Pharmacology

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“…In prophase, HCAP-G, which is a subunit of condensin, induces chromatin condensation (Kimura et al, 2001). KIF11 is required for centrosome microtubule attachment (Blangy et al, 1995). In prometaphase, CDCA8 is involved in the spindle checkpoint in association with Aurora B and survivin (Gassmann et al, 2004).…”

Section: Green) U-2 Os Rb( þ ) Cells Treated With Doxorubicin (A-c)mentioning

confidence: 99%

RB silencing compromises the DNA damage-induced G2/M checkpoint and causes deregulated expression of the ECT2 oncogene

et al. 2006

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As alterations in retinoblastoma (RB)/E2F pathway are commonly found in human cancers, the molecular mechanism underlying cell cycle deregulation caused by the mutations in the RB/E2F pathway needs to be investigated extensively. Compared with good understanding of RB/E2F functions in G1-S cell cycle progression, it is not fully understood how an abrogated RB pathway affects the G2-M phase of the cell cycle. Here, we report that disruption of RB accelerated G2-M progression in the presence of DNA damage by elevating the expression of a set of mitotic regulatory genes. We generated RB( þ )-and (À)-matched cells using short hairpin RNA. In the RB(À) cells, the G2/M checkpoint mediated by a DNA-damaging agent was over-ridden. With microarray analysis, we found that the expression of key G2-M regulatory genes was upregulated in RB(À) cells. In particular, we demonstrated that the proto-oncogene ECT2 was directly regulated by E2Fs. Furthermore, suppression of ECT2 expression by small interfering RNA in RB(À) cells resulted in cytokinesis arrest, suggesting that RB(À) cells lack the regulation of E2F-mediated cytokinesis. These results indicate that aberrant ECT2 expression, observed in various human tumors, could be the direct result of RB/E2F pathway deficiency, thereby contributing to cell division in cancers.

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“…However, the principal activator of CDK1 as a mitosis-promoting factor is cyclin B. The cyclin B/CDK1 activity is necessary to phosphorylate key proteins (for example, lamins, histones, condensins and microtubuleassociated proteins), leading to the radical reorganization of subcellular structures allowing metaphase to take place (Dessev et al, 1991;Peter et al, 1991;Blangy et al, 1995;Morgan, 1995;Kimura et al, 1998). Nevertheless, CDK1 appears to be dispensable for early mitotic events.…”

Section: Introductionmentioning

confidence: 99%

Cyclin B2 suppresses mitotic failure and DNA re-replication in human somatic cells knocked down for both cyclins B1 and B2

2007

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Cyclin-dependent kinase 1 (CDK1) plays a crucial role in establishing metaphase and has also been shown to prevent DNA re-replication. Cyclins B1 and B2 are two known activators of CDK1 operating during mitosis in human cells. Little is known about the specific roles of each of these cyclins in CDK1 activation, but cyclin B2 is thought to play a minor role and to be unable to replace cyclin B1 for mitosis completion. In our study, we found that severe reduction by separate RNA interference of either cyclin B1 or cyclin B2 protein levels results in little or no alteration of the cell cycle and, more specifically, of mitosis progression. In contrast, simultaneous depletion of both B-type cyclins leads to massive accumulation of 4N cells, mitotic failure, premature mitosis exit and DNA rereplication. These defects can be corrected by the ectopic expression of a cyclin B2 resistant to the short hairpin RNA. Altogether, these data show that, in cycling human cells, cyclin B2 can compensate for the downregulation of cyclin B1 during mitosis. They also clearly implicate cyclins B1 and B2 as crucial activators of CDK1 in its biological function of DNA re-replication prevention.

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Phosphorylation by p34cdc2 regulates spindle association of human Eg5, a kinesin-related motor essential for bipolar spindle formation in vivo

Cited by 878 publications

References 67 publications

Mutations in the human kinesin Eg5 that confer resistance to monastrol and S-trityl-l-cysteine in tumor derived cell lines

Mutations in the human kinesin Eg5 that confer resistance to monastrol and S-trityl-l-cysteine in tumor derived cell lines

RB silencing compromises the DNA damage-induced G2/M checkpoint and causes deregulated expression of the ECT2 oncogene

Cyclin B2 suppresses mitotic failure and DNA re-replication in human somatic cells knocked down for both cyclins B1 and B2

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