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Journal articles on the topic 'Cyclin C'

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Published: 4 June 2021

Last updated: 6 February 2022

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1

Ježek, Jan, Daniel G. J. Smethurst, David C. Stieg, et al. "Cyclin C: The Story of a Non-Cycling Cyclin." Biology 8, no. 1 (2019): 3. http://dx.doi.org/10.3390/biology8010003.

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The class I cyclin family is a well-studied group of structurally conserved proteins that interact with their associated cyclin-dependent kinases (Cdks) to regulate different stages of cell cycle progression depending on their oscillating expression levels. However, the role of class II cyclins, which primarily act as transcription factors and whose expression remains constant throughout the cell cycle, is less well understood. As a classic example of a transcriptional cyclin, cyclin C forms a regulatory sub-complex with its partner kinase Cdk8 and two accessory subunits Med12 and Med13 called

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2

Liu, Zhao-Jun, Takahiro Ueda, Tadaaki Miyazaki, et al. "A Critical Role for Cyclin C in Promotion of the Hematopoietic Cell Cycle by Cooperation with c-Myc." Molecular and Cellular Biology 18, no. 6 (1998): 3445–54. http://dx.doi.org/10.1128/mcb.18.6.3445.

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ABSTRACT Cyclin C, a putative G1 cyclin, was originally isolated through its ability to complement a Saccharomyces cerevisiae strain lacking the G1 cyclin geneCLN1-3. Unlike cyclins D1 and E, the other two G1 cyclins obtained by the same approach and subsequently shown to play important roles during the G1/S transition, there is thus far no evidence to support the hypothesis that cyclin C is indeed critical for the promotion of cell cycle progression. In BAF-B03 cells, an interleukin 3 (IL-3)-dependent murine pro-B-cell line, cyclin C gene mRNA was induced at the G1/S phase upon IL-3 stimulati

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3

Caldon, C. Elizabeth, C. Marcelo Sergio, Judith Schütte, et al. "Estrogen Regulation of Cyclin E2 Requires Cyclin D1 but Not c-Myc." Molecular and Cellular Biology 29, no. 17 (2009): 4623–39. http://dx.doi.org/10.1128/mcb.00269-09.

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ABSTRACT During estrogen-induced proliferation, c-Myc and cyclin D1 initiate independent pathways that activate cyclin E1-Cdk2 by sequestration and/or downregulation of the CDK inhibitor p21Waf1/Cip1, without significant increases in cyclin E1 protein levels. In contrast, cyclin E2 undergoes a marked increase in expression, which occurs within 9 to 12 h of estrogen treatment of antiestrogen-pretreated MCF-7 breast cancer cells. Both E cyclins are important to estrogen action, as small interfering RNA (siRNA)-mediated knockdown of either cyclin E1 or cyclin E2 attenuated estrogen-mediated proli

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4

Jänicke, R. U., X. Y. Lin, F. H. Lee, and A. G. Porter. "Cyclin D3 sensitizes tumor cells to tumor necrosis factor-induced, c-Myc-dependent apoptosis." Molecular and Cellular Biology 16, no. 10 (1996): 5245–53. http://dx.doi.org/10.1128/mcb.16.10.5245.

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c-Myc is an important mediator of apoptosis in cytokine- or serum-deprived cells and sensitizes various cell types to tumor necrosis factor alpha (TNF) cytotoxicity. However, downstream mediators of c-Myc-dependent apoptosis are largely unknown. In this study, we investigated whether one or more cyclins which, like c-Myc, are important regulators of the cell cycle are involved in TNF-induced apoptosis downstream of c-Myc. Cyclin D3 and c-Myc levels in HeLa and fibrosarcoma cells correlated with sensitivity of these cells to TNF-induced apoptosis, as both proteins were highly expressed in TNF-s

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5

Husdal, A., G. Bukholm, and I. R. K. Bukholm. "The Prognostic Value and Overexpression of Cyclin A Is Correlated with Gene Amplification of both Cyclin A and Cyclin E in Breast Cancer Patient." Analytical Cellular Pathology 28, no. 3 (2006): 107–16. http://dx.doi.org/10.1155/2006/721919.

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Deregulation of cell cycle control is a hallmark of cancer. The primary cyclins (A, B1, D1, D3 and E) are crucial for cell cycle progression. Secondary cyclins (C and H) have putative indirect effects on cell cycle propulsion and are not previously evaluated in breast cancer. We have examined protein expression and gene amplification of cyclins in breast carcinomas and correlated the findings with clinical follow-up data. We have previously demonstrated that over-expression of cyclin A is associated with poor prognosis in breast cancer patients. In this study we wanted to evaluate the mechanis

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6

Sudakin, V., D. Ganoth, A. Dahan, et al. "The cyclosome, a large complex containing cyclin-selective ubiquitin ligase activity, targets cyclins for destruction at the end of mitosis." Molecular Biology of the Cell 6, no. 2 (1995): 185–97. http://dx.doi.org/10.1091/mbc.6.2.185.

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The ubiquitin-mediated degradation of mitotic cyclins is required for cells to exit from mitosis. Previous work with cell-free systems has revealed four components required for cyclin-ubiquitin ligation and proteolysis: a nonspecific ubiquitin-activating enzyme E1, a soluble fraction containing a ubiquitin carrier protein activity called E2-C, a crude particulate fraction containing a ubiquitin ligase (E3) activity that is activated during M-phase, and a constitutively active 26S proteasome that degrades ubiquitinated proteins. Here, we identify a novel approximately 1500-kDa complex, termed t

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7

Wang, Guo-Li, Xiurong Shi, Elizabeth Salisbury та ін. "Cyclin D3 Maintains Growth-Inhibitory Activity of C/EBPα by Stabilizing C/EBPα-cdk2 and C/EBPα-Brm Complexes". Molecular and Cellular Biology 26, № 7 (2006): 2570–82. http://dx.doi.org/10.1128/mcb.26.7.2570-2582.2006.

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ABSTRACT C/EBPα arrests proliferation of young livers by inhibition of cdk2. In old mice, C/EBPα inhibits growth by repression of E2F-dependent promoters through the C/EBPα-Brm complex. In this paper, we show that cyclin D3-cdk4/cdk6 supports the ability of C/EBPα to inhibit liver proliferation in both age groups. Although cyclin D3-cdk4/cdk6 kinases are involved in the promotion of growth, they are expressed in terminally differentiated cells, suggesting that they have additional functions in these settings. We demonstrate that C/EBPα represents a target for phosphorylation by cyclin D3-cdk4/

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8

Müller, Carsten, Rong Yang, Gregory Idos, et al. "c-myb Transactivates the Human Cyclin A1 Promoter and Induces Cyclin A1 Gene Expression." Blood 94, no. 12 (1999): 4255–62. http://dx.doi.org/10.1182/blood.v94.12.4255.

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Abstract Cyclin A1 differs from other cyclins in its highly restricted expression pattern. Besides its expression during spermatogenesis, cyclin A1 is also expressed in hematopoietic progenitor cells and in acute myeloid leukemia. We investigated mechanisms that might contribute to cyclin A1 expression in hematopoietic cells. Comparison of cyclin A1 and cyclin A promoter activity in adherent and myeloid leukemia cell lines showed that the cyclin A1 promoter is preferentially active in myeloid cell lines. This preferential activity was present in a small, 335-bp cyclin A1 promoter fragment that

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9

Müller, Carsten, Rong Yang, Gregory Idos, et al. "c-myb Transactivates the Human Cyclin A1 Promoter and Induces Cyclin A1 Gene Expression." Blood 94, no. 12 (1999): 4255–62. http://dx.doi.org/10.1182/blood.v94.12.4255.424k32_4255_4262.

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Cyclin A1 differs from other cyclins in its highly restricted expression pattern. Besides its expression during spermatogenesis, cyclin A1 is also expressed in hematopoietic progenitor cells and in acute myeloid leukemia. We investigated mechanisms that might contribute to cyclin A1 expression in hematopoietic cells. Comparison of cyclin A1 and cyclin A promoter activity in adherent and myeloid leukemia cell lines showed that the cyclin A1 promoter is preferentially active in myeloid cell lines. This preferential activity was present in a small, 335-bp cyclin A1 promoter fragment that containe

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10

Leclerc, V., J. P. Tassan, P. H. O'Farrell, E. A. Nigg, and P. Léopold. "Drosophila Cdk8, a kinase partner of cyclin C that interacts with the large subunit of RNA polymerase II." Molecular Biology of the Cell 7, no. 4 (1996): 505–13. http://dx.doi.org/10.1091/mbc.7.4.505.

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A number of cyclins have been described, most of which act together with their catalytic partners, the cyclin-dependent kinases (Cdks), to regulate events in the eukaryotic cell cycle. Cyclin C was originally identified by a genetic screen for human and Drosophila cDNAs that complement a triple knock-out of the CLN genes in Saccharomyces cerevisiae. Unlike other cyclins identified in this complementation screen, there has been no evidence that cyclin C has a cell-cycle role in the cognate organism. Here we report that cyclin C is a nuclear protein present in a multiprotein complex. It interact

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11

Musgrove, E. A., J. A. Hamilton, C. S. Lee, K. J. Sweeney, C. K. Watts, and R. L. Sutherland. "Growth factor, steroid, and steroid antagonist regulation of cyclin gene expression associated with changes in T-47D human breast cancer cell cycle progression." Molecular and Cellular Biology 13, no. 6 (1993): 3577–87. http://dx.doi.org/10.1128/mcb.13.6.3577.

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Cyclins and proto-oncogenes including c-myc have been implicated in eukaryotic cell cycle control. The role of cyclins in steroidal regulation of cell proliferation is unknown, but a role for c-myc has been suggested. This study investigated the relationship between regulation of T-47D breast cancer cell cycle progression, particularly by steroids and their antagonists, and changes in the levels of expression of these genes. Sequential induction of cyclins D1 (early G1 phase), D3, E, A (late G1-early S phase), and B1 (G2 phase) was observed following insulin stimulation of cell cycle progressi

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12

Musgrove, E. A., J. A. Hamilton, C. S. Lee, K. J. Sweeney, C. K. Watts, and R. L. Sutherland. "Growth factor, steroid, and steroid antagonist regulation of cyclin gene expression associated with changes in T-47D human breast cancer cell cycle progression." Molecular and Cellular Biology 13, no. 6 (1993): 3577–87. http://dx.doi.org/10.1128/mcb.13.6.3577-3587.1993.

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Cyclins and proto-oncogenes including c-myc have been implicated in eukaryotic cell cycle control. The role of cyclins in steroidal regulation of cell proliferation is unknown, but a role for c-myc has been suggested. This study investigated the relationship between regulation of T-47D breast cancer cell cycle progression, particularly by steroids and their antagonists, and changes in the levels of expression of these genes. Sequential induction of cyclins D1 (early G1 phase), D3, E, A (late G1-early S phase), and B1 (G2 phase) was observed following insulin stimulation of cell cycle progressi

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13

Che, Hui, Gang Li, Hai-Ying Sun, Guo-Sheng Xiao, Yan Wang, and Gui-Rong Li. "Roles of store-operated Ca2+ channels in regulating cell cycling and migration of human cardiac c-kit+ progenitor cells." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 10 (2015): H1772—H1781. http://dx.doi.org/10.1152/ajpheart.00260.2015.

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Cardiac c-kit+ progenitor cells are important for maintaining cardiac homeostasis and can potentially contribute to myocardial repair. However, cellular physiology of human cardiac c-kit+ progenitor cells is not well understood. The present study investigates the functional store-operated Ca2+ entry (SOCE) channels and the potential role in regulating cell cycling and migration using confocal microscopy, RT-PCR, Western blot, coimmunoprecipitation, cell proliferation, and migration assays. We found that SOCE channels mediated Ca2+ influx, and TRPC1, STIM1, and Orai1 were involved in the format

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14

Geley, Stephan, Edgar Kramer, Christian Gieffers, Julian Gannon, Jan-Michael Peters, and Tim Hunt. "Anaphase-Promoting Complex/Cyclosome–Dependent Proteolysis of Human Cyclin a Starts at the Beginning of Mitosis and Is Not Subject to the Spindle Assembly Checkpoint." Journal of Cell Biology 153, no. 1 (2001): 137–48. http://dx.doi.org/10.1083/jcb.153.1.137.

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Cyclin A is a stable protein in S and G2 phases, but is destabilized when cells enter mitosis and is almost completely degraded before the metaphase to anaphase transition. Microinjection of antibodies against subunits of the anaphase-promoting complex/cyclosome (APC/C) or against human Cdc20 (fizzy) arrested cells at metaphase and stabilized both cyclins A and B1. Cyclin A was efficiently polyubiquitylated by Cdc20 or Cdh1-activated APC/C in vitro, but in contrast to cyclin B1, the proteolysis of cyclin A was not delayed by the spindle assembly checkpoint. The degradation of cyclin B1 was acc

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15

Ofir, Ayala, and Daniel Kornitzer. "Candida albicans Cyclin Clb4 Carries S-Phase Cyclin Activity." Eukaryotic Cell 9, no. 9 (2010): 1311–19. http://dx.doi.org/10.1128/ec.00038-10.

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ABSTRACT Cyclin-dependent kinases (CDKs) are key regulators of eukaryotic cell cycle progression. The cyclin subunit activates the CDK and also imparts to the complex, at least in some cases, substrate specificity. Saccharomyces cerevisiae, an organism in which the roles of individual cyclins are best studied, contains nine cyclins (three G1 cyclins and six B-type cyclins) capable of activating the main cell cycle CDK, Cdc28. Analysis of the genome of the pathogenic yeast Candida albicans revealed only two sequences corresponding to B-type cyclins, C. albicans Clb2 (CaClb2) and CaClb4. Notably

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16

Karasu, Mehmet E., Nora Bouftas, Scott Keeney, and Katja Wassmann. "Cyclin B3 promotes anaphase I onset in oocyte meiosis." Journal of Cell Biology 218, no. 4 (2019): 1265–81. http://dx.doi.org/10.1083/jcb.201808091.

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Meiosis poses unique challenges because two rounds of chromosome segregation must be executed without intervening DNA replication. Mammalian cells express numerous temporally regulated cyclins, but how these proteins collaborate to control meiosis remains poorly understood. Here, we show that female mice genetically ablated for cyclin B3 are viable—indicating that the protein is dispensable for mitotic divisions—but are sterile. Mutant oocytes appear normal until metaphase I but then display a highly penetrant failure to transition to anaphase I. They arrest with hallmarks of defective anaphas

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17

Depoortere, Fabienne, Alexandra Van Keymeulen, Jiri Lukas, et al. "A Requirement for Cyclin D3–Cyclin-dependent Kinase (cdk)-4 Assembly in the Cyclic Adenosine Monophosphate–dependent Proliferation of Thyrocytes." Journal of Cell Biology 140, no. 6 (1998): 1427–39. http://dx.doi.org/10.1083/jcb.140.6.1427.

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In different systems, cyclic adenosine monophosphate (cAMP) either blocks or promotes cell cycle progression in mid to late G1 phase. Dog thyroid epithelial cells in primary culture constitute a model of positive control of DNA synthesis initiation and G0-S prereplicative phase progression by cAMP as a second messenger for thyrotropin (TSH). The cAMP-dependent mitogenic pathway is unique as it is independent of mitogen-activated protein kinase activation and differs from growth factor–dependent pathways at the level of the expression of several protooncogenes/transcription factors. This study

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18

van der Velden, H. M., and M. J. Lohka. "Cell cycle-regulated degradation of Xenopus cyclin B2 requires binding to p34cdc2." Molecular Biology of the Cell 5, no. 7 (1994): 713–24. http://dx.doi.org/10.1091/mbc.5.7.713.

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The protein kinase activity of the cell cycle regulator p34cdc2 is inactivated when the mitotic cyclin to which it is bound is degraded. The amino (N)-terminus of mitotic cyclins includes a conserved "destruction box" sequence that is essential for degradation. Although the N-terminus of sea urchin cyclin B confer cell cycle-regulated degradation to a fusion protein, a truncated protein containing only the N-terminus of Xenopus cyclin B2, including the destruction box, is stable under conditions where full length molecules are degraded. In an attempt to identify regions of cyclin B2, other tha

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19

Mateyak, Maria K., Alvaro J. Obaya, and John M. Sedivy. "c-Myc Regulates Cyclin D-Cdk4 and -Cdk6 Activity but Affects Cell Cycle Progression at Multiple Independent Points." Molecular and Cellular Biology 19, no. 7 (1999): 4672–83. http://dx.doi.org/10.1128/mcb.19.7.4672.

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ABSTRACT c-myc is a cellular proto-oncogene associated with a variety of human cancers and is strongly implicated in the control of cellular proliferation, programmed cell death, and differentiation. We have previously reported the first isolation of a c-myc-null cell line. Loss of c-Myc causes a profound growth defect manifested by the lengthening of both the G1and G2 phases of the cell cycle. To gain a clearer understanding of the role of c-Myc in cellular proliferation, we have performed a comprehensive analysis of the components that regulate cell cycle progression. The largest defect obse

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20

Hochegger, Helfrid, Andrea Klotzbücher, Jane Kirk, et al. "New B-type cyclin synthesis is required between meiosis I and II duringXenopusoocyte maturation." Development 128, no. 19 (2001): 3795–807. http://dx.doi.org/10.1242/dev.128.19.3795.

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Progression through meiosis requires two waves of maturation promoting factor (MPF) activity corresponding to meiosis I and meiosis II. Frog oocytes contain a pool of inactive ‘pre-MPF’ consisting of cyclin-dependent kinase 1 bound to B-type cyclins, of which we now find three previously unsuspected members, cyclins B3, B4 and B5. Protein synthesis is required to activate pre-MPF, and we show here that this does not require new B-type cyclin synthesis, probably because of a large maternal stockpile of cyclins B2 and B5. This stockpile is degraded after meiosis I and consequently, the activatio

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Hautbergue, Guillaume, and Valérie Goguel. "The Yeast C-Type Cyclin Ctk2p Is Phosphorylated and Rapidly Degraded by the Ubiquitin-Proteasome Pathway." Molecular and Cellular Biology 19, no. 4 (1999): 2527–34. http://dx.doi.org/10.1128/mcb.19.4.2527.

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ABSTRACT The yeast CTDK-I complex has been implicated in phosphorylation of the carboxy-terminal domain of the RNA polymerase II and in transcription control. It is composed of three polypeptides: Ctk1p and Ctk2p, a cyclin-dependent kinase and a C-type cyclin subunit, respectively; and Ctk3p, a third subunit of unknown function. Cyclins are regulatory proteins whose expression is tightly controlled at the protein level. In this study, we examined the regulation of Ctk2p expression in vivo. Surprisingly, unlike what has been described for cell cycle cyclins, steady-state levels of Ctk2p are com

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Maridor, G., P. Gallant, R. Golsteyn, and E. A. Nigg. "Nuclear localization of vertebrate cyclin A correlates with its ability to form complexes with cdk catalytic subunits." Journal of Cell Science 106, no. 2 (1993): 535–44. http://dx.doi.org/10.1242/jcs.106.2.535.

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Cyclins control the activities of cyclin-dependent protein kinases (cdks) and hence play a key role in cell cycle regulation. While B-type cyclins associate with p34cdc2 to trigger entry into mitosis, progression through S phase requires cyclin A, presumably in association with p33cdk2. Vertebrate A- and B-type cyclins display strikingly distinct subcellular localizations, but the mechanisms underlying these differential distributions are unknown. Here, we have begun to study the requirements for nuclear localization of cyclin A. We have isolated a cDNA coding for chicken cyclin A and construc

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23

Pennanen, Mirkka, Jaana Hagström, Ilkka Heiskanen, et al. "C-myc expression in adrenocortical tumours." Journal of Clinical Pathology 71, no. 2 (2017): 129–34. http://dx.doi.org/10.1136/jclinpath-2017-204503.

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AimsWidespread use of high-resolution imaging techniques and thus increased prevalence of adrenal lesions has made diagnostics of adrenocortical tumours an increasingly important clinical issue. In non-metastatic tumours, diagnosis is based on histology. New or enhanced information for clinicopathological diagnosis, revealing the malignant potential of the tumour, could emerge by means of biomarkers. The connection of proto-oncogene c-myc to adrenocortical neoplasias is poorly known, although the Wnt/beta-catenin pathway, one of the signalling pathways leading to induction of c-myc expression,

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Abrieu, A., T. Brassac, S. Galas, D. Fisher, J. C. Labbe, and M. Doree. "The Polo-like kinase Plx1 is a component of the MPF amplification loop at the G2/M-phase transition of the cell cycle in Xenopus eggs." Journal of Cell Science 111, no. 12 (1998): 1751–57. http://dx.doi.org/10.1242/jcs.111.12.1751.

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We have investigated whether Plx1, a kinase recently shown to phosphorylate cdc25c in vitro, is required for activation of cdc25c at the G2/M-phase transition of the cell cycle in Xenopus. Using immunodepletion or the mere addition of an antibody against the C terminus of Plx1, which suppressed its activation (not its activity) at G2/M, we show that Plx1 activity is required for activation of cyclin B-cdc2 kinase in both interphase egg extracts receiving recombinant cyclin B, and cycling extracts that spontaneously oscillate between interphase and mitosis. Furthermore, a positive feedback loop

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Rao, S. S., C. Chu, and D. S. Kohtz. "Ectopic expression of cyclin D1 prevents activation of gene transcription by myogenic basic helix-loop-helix regulators." Molecular and Cellular Biology 14, no. 8 (1994): 5259–67. http://dx.doi.org/10.1128/mcb.14.8.5259.

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Activation of muscle gene transcription in differentiating skeletal myoblasts requires their withdrawal from the cell cycle. The effects of ectopic cyclin expression on activation of muscle gene transcription by myogenic basic helix-loop-helix (bHLH) regulators were investigated. Ectopic expression of cyclin D1, but not cyclins A, B1, B2, C, D3, and E, inhibited transcriptional activation of muscle gene reporter constructs by myogenic bHLH regulators in a dose-dependent manner. Ectopic expression of cyclin D1 inhibited the activity of a myogenic bHLH regulator mutant lacking the basic region p

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Rao, S. S., C. Chu, and D. S. Kohtz. "Ectopic expression of cyclin D1 prevents activation of gene transcription by myogenic basic helix-loop-helix regulators." Molecular and Cellular Biology 14, no. 8 (1994): 5259–67. http://dx.doi.org/10.1128/mcb.14.8.5259-5267.1994.

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Activation of muscle gene transcription in differentiating skeletal myoblasts requires their withdrawal from the cell cycle. The effects of ectopic cyclin expression on activation of muscle gene transcription by myogenic basic helix-loop-helix (bHLH) regulators were investigated. Ectopic expression of cyclin D1, but not cyclins A, B1, B2, C, D3, and E, inhibited transcriptional activation of muscle gene reporter constructs by myogenic bHLH regulators in a dose-dependent manner. Ectopic expression of cyclin D1 inhibited the activity of a myogenic bHLH regulator mutant lacking the basic region p

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Wang, Kun, Ruilan Yan, Katrina F. Cooper, and Randy Strich. "Cyclin C mediates stress-induced mitochondrial fission and apoptosis." Molecular Biology of the Cell 26, no. 6 (2015): 1030–43. http://dx.doi.org/10.1091/mbc.e14-08-1315.

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Mitochondria are dynamic organelles that undergo constant fission and fusion cycles. In response to cellular damage, this balance is shifted dramatically toward fission. Cyclin C–Cdk8 kinase regulates transcription of diverse gene sets. Using knockout mouse embryonic fibroblasts (MEFs), we demonstrate that cyclin C directs the extensive mitochondrial scission induced by the anticancer drug cisplatin or oxidative stress. This activity is independent of transcriptional regulation, as Cdk8 is not required for this activity. Furthermore, adding purified cyclin C to unstressed permeabilized MEF cul

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28

Trakala, Marianna, and Marcos Malumbres. "Cyclin C surprises in tumour suppression." Nature Cell Biology 16, no. 11 (2014): 1031–33. http://dx.doi.org/10.1038/ncb3055.

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Aamodt, Rolf, Kristin Jonsdottir, Solveig Norheim Andersen, Johan Bondi, Geir Bukholm, and Ida R. K. Bukholm. "Differences in Protein Expression and Gene Amplification of Cyclins between Colon and Rectal Adenocarcinomas." Gastroenterology Research and Practice 2009 (2009): 1–9. http://dx.doi.org/10.1155/2009/285830.

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Adenocarcinomas of rectum and colon may be different with regard to the cellular biological basis for cancer development. A material of 246 rectal cancers removed surgically at Akershus University Hospital in the years 1992–2000 was investigated and was compared to a material of 219 colon cancers operated on at Akershus University Hospital during the years 1988, 1990 and 1997–2000. There were highly significant differences between the rectal and the colon cancers in the protein expression of cyclin D1, cyclin D3, cyclin E, nuclearβ-catenin, and c-Myc and in gene amplification of cyclin A2, cyc

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30

Ray, L. B. "Who Hid the Cyclin D2?" Science 336, no. 6083 (2012): 778–80. http://dx.doi.org/10.1126/science.336.6083.778-c.

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Huang, James N., Iha Park, Eric Ellingson, Laurie E. Littlepage, and David Pellman. "Activity of the APCCdh1 form of the anaphase-promoting complex persists until S phase and prevents the premature expression of Cdc20p." Journal of Cell Biology 154, no. 1 (2001): 85–94. http://dx.doi.org/10.1083/jcb.200102007.

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Cell cycle progression is driven by waves of cyclin expression coupled with regulated protein degradation. An essential step for initiating mitosis is the inactivation of proteolysis mediated by the anaphase-promoting complex/cyclosome (APC/C) bound to its regulator Cdh1p/Hct1p. Yeast APCCdh1 was proposed previously to be inactivated at Start by G1 cyclin/cyclin-dependent kinase (CDK). Here, we demonstrate that in a normal cell cycle APCCdh1 is inactivated in a graded manner and is not extinguished until S phase. Complete inactivation of APCCdh1 requires S phase cyclins. Further, persistent AP

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van Zon, Wouter, Janneke Ogink, Bas ter Riet, René H. Medema, Hein te Riele, and Rob M. F. Wolthuis. "The APC/C recruits cyclin B1–Cdk1–Cks in prometaphase before D box recognition to control mitotic exit." Journal of Cell Biology 190, no. 4 (2010): 587–602. http://dx.doi.org/10.1083/jcb.200912084.

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The ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) is activated at prometaphase by mitotic phosphorylation and binding of its activator, Cdc20. This initiates cyclin A degradation, whereas cyclin B1 is stabilized by the spindle checkpoint. Upon checkpoint release, the RXXL destruction box (D box) was proposed to direct cyclin B1 to core APC/C or Cdc20. In this study, we report that endogenous cyclin B1–Cdk1 is recruited to checkpoint-inhibited, phosphorylated APC/C in prometaphase independently of Cdc20 or the cyclin B1 D box. Like cyclin A, cyclin B1 binds the APC/C by the Cdk

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Rovnak, Joel, and Sandra L. Quackenbush. "Walleye Dermal Sarcoma Virus Cyclin Interacts with Components of the Mediator Complex and the RNA Polymerase II Holoenzyme." Journal of Virology 76, no. 16 (2002): 8031–39. http://dx.doi.org/10.1128/jvi.76.16.8031-8039.2002.

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ABSTRACT Walleye dermal sarcoma virus (WDSV) encodes an accessory protein, OrfA, with sequence homology to cyclins (retrovirus cyclin). In cells transfected with an expression construct, OrfA was localized to the nucleus and was concentrated in interchromatin granule clusters (IGCs), sites where splicing factors are concentrated. Other proteins identified in IGCs include transcription factors, the large subunit of RNA polymerase II (Pol II), and cyclin-dependent kinase 8 (cdk8). cdk8 is the kinase partner of cyclin C and a component of the mediator complex, associated with the Pol II holoenzym

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Khakhina, Svetlana, Katrina F. Cooper, and Randy Strich. "Med13p prevents mitochondrial fission and programmed cell death in yeast through nuclear retention of cyclin C." Molecular Biology of the Cell 25, no. 18 (2014): 2807–16. http://dx.doi.org/10.1091/mbc.e14-05-0953.

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The yeast cyclin C-Cdk8 kinase forms a complex with Med13p to repress the transcription of genes involved in the stress response and meiosis. In response to oxidative stress, cyclin C displays nuclear to cytoplasmic relocalization that triggers mitochondrial fission and promotes programmed cell death. In this report, we demonstrate that Med13p mediates cyclin C nuclear retention in unstressed cells. Deleting MED13 allows aberrant cytoplasmic cyclin C localization and extensive mitochondrial fragmentation. Loss of Med13p function resulted in mitochondrial dysfunction and hypersensitivity to oxi

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Wilhide, CC, C. Van Dang, J. Dipersio, AA Kenedy, and PF Bray. "Overexpression of cyclin D1 in the Dami megakaryocytic cell line causes growth arrest." Blood 86, no. 1 (1995): 294–304. http://dx.doi.org/10.1182/blood.v86.1.294.bloodjournal861294.

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The maturation of megakaryocytes in vivo requires polyploidization or repeated duplication of DNA without cytokinesis. As DNA replication and cytokinesis are tightly regulated in somatic cells by cyclins and cyclin-dependent kinases, we sought to determine the pattern of cyclin gene expression in cells that undergo megakaryocytic differentiation and polyploidization. The Dami megakaryocytic cell line differentiates and increases ploidy in response to phorbol 12-myristate 13-acetate (PMA) stimulation in vitro. We used Northern blotting to analyze mRNA levels of cyclins A, B, C, D1, and E in PMA

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Lin, Xueying, Peter Nelson, and Irwin H. Gelman. "SSeCKS, a Major Protein Kinase C Substrate with Tumor Suppressor Activity, Regulates G1→S Progression by Controlling the Expression and Cellular Compartmentalization of Cyclin D." Molecular and Cellular Biology 20, no. 19 (2000): 7259–72. http://dx.doi.org/10.1128/mcb.20.19.7259-7272.2000.

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ABSTRACT SSeCKS, first isolated as a G1→S inhibitor that is downregulated in src- and ras-transformed cells, is a major cytoskeleton-associated PKC substrate with tumor suppressor and kinase-scaffolding activities. Previous attempts at constitutive expression resulted in cell variants with truncated ectopic SSeCKS products. Here, we show that tetracycline-regulated SSeCKS expression in NIH 3T3 cells induces G1 arrest marked by extracellular signal-regulated kinase 2-dependent decreases in cyclin D1 expression and pRb phosphorylation. Unexpectedly, the forced reexpression of cyclin D1 failed to

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Feng, Daorong, Dou Yeon Youn, Xiaoping Zhao, et al. "mTORC1 Down-Regulates Cyclin-Dependent Kinase 8 (CDK8) and Cyclin C (CycC)." PLOS ONE 10, no. 6 (2015): e0126240. http://dx.doi.org/10.1371/journal.pone.0126240.

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Saxena, Utsav H., Christina M. H. Powell, Jill K. Fecko, et al. "Phosphorylation by Cyclin C/Cyclin-Dependent Kinase 2 following Mitogenic Stimulation of Murine Fibroblasts Inhibits Transcriptional Activity of LSF during G1 Progression." Molecular and Cellular Biology 29, no. 9 (2009): 2335–45. http://dx.doi.org/10.1128/mcb.00687-08.

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ABSTRACT Transcription factor LSF is required for progression from quiescence through the cell cycle, regulating thymidylate synthase (Tyms) expression at the G1/S boundary. Given the constant level of LSF protein from G0 through S, we investigated whether LSF is regulated by phosphorylation in G1. In vitro, LSF is phosphorylated by cyclin E/cyclin-dependent kinase 2 (CDK2), cyclin C/CDK2, and cyclin C/CDK3, predominantly on S309. Phosphorylation of LSF on S309 is maximal 1 to 2 h after mitogenic stimulation of quiescent mouse fibroblasts. This phosphorylation is mediated by cyclin C-dependent

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Jin, Chunyan, Randy Strich, and Katrina F. Cooper. "Slt2p phosphorylation induces cyclin C nuclear-to-cytoplasmic translocation in response to oxidative stress." Molecular Biology of the Cell 25, no. 8 (2014): 1396–407. http://dx.doi.org/10.1091/mbc.e13-09-0550.

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The yeast C-type cyclin represses the transcription of genes required for the stress response and meiosis. To relieve this repression, cyclin C undergoes nuclear-to-cytoplasmic translocation in response to many stressors, including hydrogen peroxide, where it is destroyed by ubiquitin-mediated proteolysis. Before its destruction, cyclin C promotes stress-induced mitochondrial fission and programmed cell death, indicating that relocalization is an important cell fate regulator. Here we show that cyclin C cytoplasmic translocation requires the cell wall integrity (CWI) mitogen-activated protein

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Albrecht, J. H., J. S. Hoffman, B. T. Kren, and C. J. Steer. "Cyclin and cyclin-dependent kinase 1 mRNA expression in models of regenerating liver and human liver diseases." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 5 (1993): G857—G864. http://dx.doi.org/10.1152/ajpgi.1993.265.5.g857.

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There is compelling evidence that the eukaryotic cell cycle is controlled by a family of proteins called cyclins, which complex with cyclin-dependent kinases (CDK) to modulate key events during cell division. We have examined the regulation of these genes in models of experimental liver regeneration and their expression in human liver diseases. Seventy percent partial hepatectomy (PH) was performed on rats and normal BALB/c and athymic nude mice to determine patterns of cyclin and CDK1 mRNA expression. It has been previously shown by [3H]thymidine incorporation that athymic nude mice manifest

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Prall, Owen W. J., Eileen M. Rogan, Elizabeth A. Musgrove, Colin K. W. Watts, and Robert L. Sutherland. "c-Myc or Cyclin D1 Mimics Estrogen Effects on Cyclin E-Cdk2 Activation and Cell Cycle Reentry." Molecular and Cellular Biology 18, no. 8 (1998): 4499–508. http://dx.doi.org/10.1128/mcb.18.8.4499.

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ABSTRACT Estrogen-induced progression through G1 phase of the cell cycle is preceded by increased expression of the G1-phase regulatory proteins c-Myc and cyclin D1. To investigate the potential contribution of these proteins to estrogen action, we derived clonal MCF-7 breast cancer cell lines in which c-Myc or cyclin D1 was expressed under the control of the metal-inducible metallothionein promoter. Inducible expression of either c-Myc or cyclin D1 was sufficient for S-phase entry in cells previously arrested in G1 phase by pretreatment with ICI 182780, a potent estrogen antagonist. c-Myc exp

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Dong, Feng, Deepak Agrawal, Tapan Bagui, and W. J. Pledger. "Cyclin D3-associated Kinase Activity Is Regulated by p27kip1 in BALB/c 3T3 Cells." Molecular Biology of the Cell 9, no. 8 (1998): 2081–92. http://dx.doi.org/10.1091/mbc.9.8.2081.

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We report that cyclin D3/cdk4 kinase activity is regulated by p27kip1 in BALB/c 3T3 cells. The association of p27kip1 was found to result in inhibition of cyclin D3 activity as measured by immune complex kinase assays utilizing cyclin D3-specific antibodies. The ternary p27kip1/cyclin D3/cdk4 complexes do exhibit kinase activity when measured in immune complex kinase assays utilizing p27kip1-specific antibodies. The association of p27kip1 with cyclin D3 was highest in quiescent cells and declined upon mitogenic stimulation, concomitantly with declines in the total level of p27kip1 protein. The

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Aviram, Sharon, Einav Simon, Tsvia Gildor, Fabian Glaser, and Daniel Kornitzer. "Autophosphorylation-Induced Degradation of the Pho85 Cyclin Pcl5 Is Essential for Response to Amino Acid Limitation." Molecular and Cellular Biology 28, no. 22 (2008): 6858–69. http://dx.doi.org/10.1128/mcb.00367-08.

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ABSTRACT Pho85 cyclins (Pcls), activators of the yeast cyclin-dependent kinase (CDK) Pho85, belong together with the p35 activator of mammalian CDK5 to a distinct structural cyclin class. Different Pcls target Pho85 to distinct substrates. Pcl5 targets Pho85 specifically to Gcn4, a yeast transcription factor involved in the response to amino acid starvation, eventually causing the degradation of Gcn4. Pcl5 is itself highly unstable, an instability that was postulated to be important for regulation of Gcn4 degradation. We used hybrids between different Pcls to circumscribe the substrate recogni

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VanHook, A. M. "Cyclin C Moves Out of the Nucleus." Science Signaling 7, no. 311 (2014): ec33-ec33. http://dx.doi.org/10.1126/scisignal.2005148.

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Stieg, David. "Cyclin C Regulated Transcriptional Response to Stress." FASEB Journal 34, S1 (2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.03196.

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Li, Na, Anne Fassl, Joel Chick, et al. "Cyclin C is a haploinsufficient tumour suppressor." Nature Cell Biology 16, no. 11 (2014): 1080–91. http://dx.doi.org/10.1038/ncb3046.

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Edwards, Michael C., Calvin Wong, and Stephen J. Elledge. "Human Cyclin K, a Novel RNA Polymerase II-Associated Cyclin Possessing Both Carboxy-Terminal Domain Kinase and Cdk-Activating Kinase Activity." Molecular and Cellular Biology 18, no. 7 (1998): 4291–300. http://dx.doi.org/10.1128/mcb.18.7.4291.

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ABSTRACT The gene coding for human cyclin K was isolated as aCPR (cell-cycle progression restoration) gene by virtue of its ability to impart a Far− phenotype to the budding yeast Saccharomyces cerevisiae and to rescue the lethality of a deletion of the G1 cyclin genes CLN1,CLN2, and CLN3. The cyclin K gene encodes a 357-amino-acid protein most closely related to human cyclins C and H, which have been proposed to play a role in regulating basal transcription through their association with and activation of cyclin-dependent kinases (Cdks) that phosphorylate the carboxyl-terminal domain (CTD) of

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Nakata, Yuji, Susan Shetzline, Chizuko Sakashita, Anna Kalota, Stephen I. Rudnick, and Alan M. Gewirtz. "Myb Family Transcription Factors Contribute to G2/M Cell Cycle Transition in Normal and Malignant Hematopoietic Cells by Direct Regulation of Cyclin B1 Expression." Blood 108, no. 11 (2006): 1115. http://dx.doi.org/10.1182/blood.v108.11.1115.1115.

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Abstract Myb family transcription factors are ubiquitously expressed, and are known to play a critical role in regulating G1/S cell cycle transition. Recently, Myb-like proteins have been found to regulate G2/M transit in plants, yeast, and Drosophila. A recent study in human T98G ganglioblastoma cells revealed that E2F, together with B-Myb, but not c-Myb, regulated cyclin B1 expression directly. However, in hematopoietic cells Myb’s role in regulating cell cycle check points other than G1/S is less well defined. Herein we report that c-Myb, as well as B-Myb, up-regulates cyclin B1 expression

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Willis, Stephen D., Sara E. Hanley, Thomas Beishke, Prasanna D. Tati, and Katrina F. Cooper. "Ubiquitin–proteasome-mediated cyclin C degradation promotes cell survival following nitrogen starvation." Molecular Biology of the Cell 31, no. 10 (2020): 1015–31. http://dx.doi.org/10.1091/mbc.e19-11-0622.

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Cyclin C-Cdk8 kinase negatively regulates the yeast phagophore gene ATG8. After nitrogen starvation, repression is relieved by ubiquitin proteasome degradation of cyclin C. This is important for survival as degradation occurs prior to cyclin C translocation to the mitochondria where it induces mitochondrial fragmentation and promotes cell death.

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Jiménez-Palomares, Margarita, José Francisco López-Acosta, Pablo Villa-Pérez та ін. "Cyclin C stimulates β-cell proliferation in rat and human pancreatic β-cells". American Journal of Physiology-Endocrinology and Metabolism 308, № 6 (2015): E450—E459. http://dx.doi.org/10.1152/ajpendo.00260.2014.

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Activation of pancreatic β-cell proliferation has been proposed as an approach to replace reduced functional β-cell mass in diabetes. Quiescent fibroblasts exit from G0 (quiescence) to G1 through pRb phosphorylation mediated by cyclin C/cdk3 complexes. Overexpression of cyclin D1, D2, D3, or cyclin E induces pancreatic β-cell proliferation. We hypothesized that cyclin C overexpression would induce β-cell proliferation through G0 exit, thus being a potential therapeutic target to recover functional β-cell mass. We used isolated rat and human islets transduced with adenovirus expressing cyclin C

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