Human cyclin E, a new cyclin that interacts with two members of the CDC2 gene family

Koff, Andrew; Cross, Frederick R.; Fisher, Alfred L.; Schumacher, Jill M.; LeGuellec, Katherine; Maury, Philippe; Roberts, James M.

doi:10.1016/0092-8674(91)90044-y

Cited by 622 publications

(366 citation statements)

References 70 publications

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“…Cyclin E is a major regulator of G1 to S transition in eukaryotic cells (Koff et al, 1991;Ohtsubo et al, 1995) and its increased expression has been reported in a variety of human malignancies (Donnellan and Chetty, 1999;Sandhu and Slingerland, 2000). In this study, we analysed the sensitivity to doxorubicin and to other anticancer drugs of derivatives of Rat-1 fibroblasts that stably overexpress cyclin E and demonstrated that changes in the expression levels of cyclin E can affect cell sensitivity to doxorubicin.…”

Section: Discussionmentioning

confidence: 99%

Increased expression of cyclin E is associated with an increased resistance to doxorubicin in rat fibroblasts

et al. 2003

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Cell cycle progression in eukaryotic cells is regulated by a family of cyclin-dependent kinases (CDKs). Cyclin E is a regulatory subunit of CDK2 and drives cells from G1 to S phase. Increased expression of cyclin E is a frequent event in human malignancies and has been associated with poor prognosis in various cancers. In this study, we evaluated the effects of cyclin E-overexpression on the sensitivity of rat fibroblasts to anticancer drugs. Cyclin E-overexpressing cells were less sensitive to doxorubicin-induced inhibition of cell growth but not to other antineoplastic drugs, such as paclitaxel, vincristine, etoposide and methotrexate. Cyclin E-overexpressing fibroblasts also displayed a reduction in ROS levels and a significantly lower increase following doxorubicin treatment compared with vector control cells. The expression of manganese superoxide dismutase (MnSOD) and its activity were increased (about 1.3-fold) in cyclin E-overexpressing derivatives compared with control cells. These results suggest that cyclin E overexpression might reduce tumour cells sensitivity to doxorubicin by affecting the expression of MnSOD and that determination of cyclin E expression levels might help to select patients to be treated with an anthracycline-based antineoplastic therapy.

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Section: Discussionmentioning

confidence: 99%

Increased expression of cyclin E is associated with an increased resistance to doxorubicin in rat fibroblasts

et al. 2003

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“…Figure 7A shows the typical staining pattern for each of the three populations (G1, S, and G2) of cells within the division cycle. Positive red staining for cyclin E indicates that the cells were in the G1 phase (Koff et al, 1991) at the time of fixation. Since the thymidine analog BrdU is integrated into nuclear DNA only during DNA synthesis during the S phase, the green fluorescence staining for BrdU indicates that the cell was actively synthesizing DNA.…”

Section: Infrared Spectral Heterogeneity Of Exfoliated Cells and Distmentioning

confidence: 99%

Chapter 10 Infrared and Raman Microscopy in Cell Biology

Matthäus

Bird

Miljković

et al. 2008

Methods in Cell Biology

159

119

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This chapter presents novel microscopic methods to monitor cell biological processes of live or fixed cells without the use of any dye, stains, or other contrast agent. These methods are based on spectral techniques that detect inherent spectroscopic properties of biochemical constituents of cells, or parts thereof. Two different modalities have been developed for this task. One of them is infrared micro-spectroscopy, in which an average snapshot of a cell's biochemical composition is collected at a spatial resolution of typically 25 mm. This technique, which is extremely sensitive and can collect such a snapshot in fractions of a second, is particularly suited for studying gross biochemical changes. The other technique, Raman microscopy (also known as Raman microspectroscopy), is ideally suited to study variations of cellular composition on the scale of subcellular organelles, since its spatial resolution is as good as that of fluorescence microscopy. Both techniques exhibit the fingerprint sensitivity of vibrational spectroscopy toward biochemical composition, and can be used to follow a variety of cellular processes.

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“…Inactivation of pRb repression of E2F results in the transcription of Cyclin E, and Cyclin A, as well as E2F itself prior to the G1/S transition stage (Woo and Poon, 2003). At the onset of S phase, Cdk2 (Cdc28 in yeast) is activated by expressed Cyclin E subunits, which then continues the phosphorylation of pRb (Koff et al, 1991;Koff et al, 1992). Accumulating Cyclin A generated from the pRb/E2F…”

Section: A Brief Description Of Cell Cycle Progression From G1 and S mentioning

confidence: 99%

An ATM- and ATR-dependent checkpoint inactivates spindle assembly by targeting CEP63

Smith¹,

Dejsuphong

Balestrini³

et al. 2009

Nat Cell Biol

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The effects of ATM and ATR signalling induced by chromosomal breakage have been described extensively in modulating cell cycle progression up to the onset of mitosis.However, DNA damage checkpoint responses in mitotic cells are not well understood.This thesis reports on the effects of double strand breaks on the progression of mitosis.We found ATM and ATR activation can occur in mitotic Xenopus laevis egg extract and the induction of ATM and ATR by chromosomal breakages inhibits spindle assembly in both Xenopus egg extract and somatic cells. The delay in mitotic progression induced by ATM and ATR was found not to involve major spindle assembly factors activities such as, Cdk1, Plx1 and RCC1/Ran-GTP. However, normal anastral spindles formation around linear DNA coated beads, which can activate ATM and ATR, linked centrosome-driven spindle assembly to ATM and ATR dependent spindle defects. cDNA expression library screening was undertaken to identify novel ATM and ATR targets in this mitotic checkpoint pathway, through which the novel centrosomal protein XCEP63 was identified as a likely candidate. Data obtained from depletion and reconstitution of XCEP63 in Xenopus egg extract established that normal centrosome-driven spindle assembly requires XCEP63. Moreover, ATM and ATR phosphorylates XCEP63 on serine 560 and promotes delocalisation from the centrosome. ATM and ATR inhibition or addition of non-phosphorylable XCEP63 recombinant protein mutated at serine 560 prevents spindle assembly abnormalities.These findings suggest that ATM and ATR regulate mitotic events by targeting XCEP63 and centrosome-dependent spindle assembly. This pathway may provide support for DNA repair processes or regulate cell survival in the presence of mitotic DNA damage. 3

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Human cyclin E, a new cyclin that interacts with two members of the CDC2 gene family

Cited by 622 publications

References 70 publications

Increased expression of cyclin E is associated with an increased resistance to doxorubicin in rat fibroblasts

Increased expression of cyclin E is associated with an increased resistance to doxorubicin in rat fibroblasts

Chapter 10 Infrared and Raman Microscopy in Cell Biology

An ATM- and ATR-dependent checkpoint inactivates spindle assembly by targeting CEP63

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