Rules to replicate by

Heichman, Karen A.; Roberts, James M.

doi:10.1016/0092-8674(94)90541-x

Cited by 238 publications

(152 citation statements)

References 39 publications

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“…Cells must precisely duplicate their chromosomal DNA during S phase, segregate the sister chromatids to opposite poles of the mitotic spindle during mitosis, assemble two nuclei, and then divide their organelles, cytoplasm, plasma membrane, and other cell contents into two daughter cells in the process known as cytokinesis. Recent studies indicated that cyclin-dependent kinases (CDKs) play important roles in the regulation of this complex process (Heichman and Roberts, 1994;King et al, 1994;Sherr, 1994). The mechanisms of CDK activation and inactivation have been extensively studied (Pines, 1995;Morgan, 1997).…”

Section: Introductionmentioning

confidence: 99%

Cell cycle regulated expression and phosphorylation of hpttg proto-oncogene product

et al. 2000

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We recently isolated a cDNA for hpttg, the human homolog of rat pituitary tumor transforming gene. Now we have analysed the expression of hpttg as a function of cell proliferation. hPTTG protein level is up-regulated in rapidly proliferating cells, is down-regulated in response to serum starvation or cell con¯uence, and is regulated in a cell cycle-dependent manner, peaking in mitosis. In addition, we show that hPTTG is phosphorylated during mitosis. Immunodepletion and in vitro phosphorylation experiments, together with the use of a speci®c inhibitor, indicate that Cdc2 is the kinase that phosphorylates hPTTG. These results suggest that hpttg is induced by, and may have a role in, regulatory pathways involved in the control of cell proliferation. Oncogene (2000) 19, 403 ± 409.

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Section: Introductionmentioning

confidence: 99%

Cell cycle regulated expression and phosphorylation of hpttg proto-oncogene product

et al. 2000

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“…Many cyclins have been shown to associate with catalytic partners, cyclindependent kinases (cdks), to comprise active kinase complexes. These cyclin-cdk kinase complexes exert profound e ects on the progression of the cell cycle (Heichman and Roberts, 1994;Sherr, 1994). However, the physiological or biochemical function(s) of cyclin G remains obscure so far.…”

Section: Introductionmentioning

confidence: 99%

A role of cyclin G in the process of apoptosis

1999

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Cyclin G was previously identi®ed as a target gene of the p53 tumor suppresser protein, and levels of cyclin G are increased after induction of p53 by DNA damage. However, the function of cyclin G has not been established. To determine the e ect of increased expression of cyclin G, retroviruses encoding cyclin G were constructed and used to infect three di erent murine cell lines. Cyclin G protein levels induced by the retroviruses were within the range seen after DNA damage induction of p53. In each case we observed that such over-expression of cyclin G augments the apoptotic process. TNF-a induction of apoptosis is increased by expression of cyclin G in NIH3T3 ®broblasts which express p53, as well as in 10.1 ®broblasts which contain no p53 allele. Additionally, we observed that while cyclin G expression is markedly reduced upon aggregate formation in embryonic carcinoma P19 cells, retrovirus-mediated over-expression of cyclin G enhances apoptotic cell death in aggregated P19 cells, and increases the extent of apoptosis caused by retinoic acid or serum starvation of these cells. These data demonstrate that cyclin G plays a facilitating role in modulating apoptosis induced by di erent stimuli. Moreover, we have discovered that cyclin G expression is rapidly induced in P19 cells after exposure to Bone Morphogenic Protein-4 (BMP-4), suggesting that cyclin G may mediate apoptotic signals generated by BMP-4.

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“…It has been demonstrated that cell cycle regulation in mammalian cells is implemented through a family of proteins, cyclins, that bind and activate latent protein kinases, cyclin dependent kinases (cdk), which phosphorylate key targets, such as Rb family members, that bind and regulate components of the transcriptional machinery, such as E2Fs. The family of cyclin proteins can be subdivided on the basis of the cdks with which they interact and the period of the cell cycle in which they function (for review see: Heichman and Roberts, 1994;Sherr, 1994). Thus, D-type cyclins bind and activate cdk4 or cdk6, forming an activity that has been demonstrated to play a key role during G 1 traverse.…”

Section: Introductionmentioning

confidence: 99%

Primary keratinocytes have an adhesion dependent S phase checkpoint that is absent in immortalized cell lines

1998

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In order to understand the mechanism through which loss of anchorage inhibits growth, we have investigated the events that occur in murine keratinocytes upon substratum detachment utilizing both primary cells and established immortalized cell lines. Our data has revealed that while both primary and immortalized cells undergo growth arrest in suspension, the nature of this arrest is markedly di erent. Primary cells exhibit a growth arrest that is characterized by rapid cessation of DNA synthesis resulting in a static S phase population. In contrast, an immortalized non-tumorgenic cell line, Balb MK, exhibits growth arrest as measured by thymidine incorporation, but does not prevent cells that have entered S phase from continuing into G 2 /M, and accumulating as a 4N population. In contrast to both primary and MK cells, the tumorigenic SLC-1 cell line did not accumulate in a speci®c cell cycle interval and were able to undergo continuous growth in suspension. Examination of cyclin A protein and its associated activity revealed that cyclin A protein levels decreased in primary but not MK cells; suggesting the continued presence of cyclin A may allow continued DNA synthesis observed in MK cells. Furthermore, we demonstrate the accumulation of suspension cultured MK cells as a 4N population correlated with the loss of cyclin A/cdk2 kinase activity, which in turn occurred through the accumulation of p27 kip1 , whereas neither p27 kip1 accumulation nor loss of cyclin A activity was observed in SLC-1 cells. Our results clearly reveal that the process of growth inhibition in suspension cultured cells may occur in several forms with distinct characteristics that are dependent on the status of cyclin/cdk complexes and CKI proteins. Tumor derived cells in suspension did not lose cyclin A dependent kinase activity and thus continued to grow and divide.

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Rules to replicate by

Cited by 238 publications

References 39 publications

Cell cycle regulated expression and phosphorylation of hpttg proto-oncogene product

Cell cycle regulated expression and phosphorylation of hpttg proto-oncogene product

A role of cyclin G in the process of apoptosis

Primary keratinocytes have an adhesion dependent S phase checkpoint that is absent in immortalized cell lines

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