Journal articles: 'Cell cycle progression'

1

Braun-Dullaeus, Ruediger C., Michael J. Mann, and Victor J. Dzau. "Cell Cycle Progression." Circulation 98, no. 1 (July 7, 1998): 82–89. http://dx.doi.org/10.1161/01.cir.98.1.82.

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Tyrcha, Joanna. "Cell cycle progression." Comptes Rendus Biologies 327, no. 3 (March 2004): 193–200. http://dx.doi.org/10.1016/j.crvi.2003.05.002.

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3

Assoian, Richard K. "Anchorage-dependent Cell Cycle Progression." Journal of Cell Biology 136, no. 1 (January 13, 1997): 1–4. http://dx.doi.org/10.1083/jcb.136.1.1.

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4

Giacinti, C., and A. Giordano. "RB and cell cycle progression." Oncogene 25, no. 38 (August 2006): 5220–27. http://dx.doi.org/10.1038/sj.onc.1209615.

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Jazwinski, S. M., B. H. Howard, and R. K. Nayak. "Cell Cycle Progression, Aging, and Cell Death." Journals of Gerontology Series A: Biological Sciences and Medical Sciences 50A, no. 1 (January 1, 1995): B1—B8. http://dx.doi.org/10.1093/gerona/50a.1.b1.

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Trotter, Eleanor Wendy, and Iain Michael Hagan. "Release from cell cycle arrest with Cdk4/6 inhibitors generates highly synchronized cell cycle progression in human cell culture." Open Biology 10, no. 10 (October 2020): 200200. http://dx.doi.org/10.1098/rsob.200200.

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Each approach used to synchronize cell cycle progression of human cell lines presents a unique set of challenges. Induction synchrony with agents that transiently block progression through key cell cycle stages are popular, but change stoichiometries of cell cycle regulators, invoke compensatory changes in growth rate and, for DNA replication inhibitors, damage DNA. The production, replacement or manipulation of a target molecule must be exceptionally rapid if the interpretation of phenotypes in the cycle under study is to remain independent of impacts upon progression through the preceding cycle. We show how these challenges are avoided by exploiting the ability of the Cdk4/6 inhibitors, palbociclib, ribociclib and abemaciclib to arrest cell cycle progression at the natural control point for cell cycle commitment: the restriction point. After previous work found no change in the coupling of growth and division during recovery from CDK4/6 inhibition, we find high degrees of synchrony in cell cycle progression. Although we validate CDK4/6 induction synchronization with hTERT-RPE-1, A549, THP1 and H1299, it is effective in other lines and avoids the DNA damage that accompanies synchronization by thymidine block/release. Competence to return to cycle after 72 h arrest enables out of cycle target induction/manipulation, without impacting upon preceding cycles.

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Baldassarre, Gustavo, Milena Nicoloso, Monica Schiappacassi, Emanuela Chimienti, and Barbara Belletti. "Linking Inflammation to Cell Cycle Progression." Current Pharmaceutical Design 10, no. 14 (May 1, 2004): 1653–66. http://dx.doi.org/10.2174/1381612043384691.

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Bohnsack, Brenda L., and Karen K. Hirschi. "NUTRIENT REGULATION OF CELL CYCLE PROGRESSION." Annual Review of Nutrition 24, no. 1 (July 14, 2004): 433–53. http://dx.doi.org/10.1146/annurev.nutr.23.011702.073203.

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9

David, Rachel. "Keeping cell cycle progression in check." Nature Reviews Molecular Cell Biology 13, no. 6 (May 23, 2012): 341. http://dx.doi.org/10.1038/nrm3363.

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Smink, Luc J. "Acetylation can regulate cell-cycle progression." Trends in Molecular Medicine 7, no. 9 (September 2001): 384. http://dx.doi.org/10.1016/s1471-4914(01)02122-0.

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11

Takuwa, Noriko, Wei Zhou, and Yoh Takuwa. "Calcium, calmodulin and cell cycle progression." Cellular Signalling 7, no. 2 (February 1995): 93–104. http://dx.doi.org/10.1016/0898-6568(94)00074-l.

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Uetake, Yumi, and Greenfield Sluder. "Cell cycle progression after cleavage failure." Journal of Cell Biology 165, no. 5 (June 7, 2004): 609–15. http://dx.doi.org/10.1083/jcb.200403014.

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Failure of cells to cleave at the end of mitosis is dangerous to the organism because it immediately produces tetraploidy and centrosome amplification, which is thought to produce genetic imbalances. Using normal human and rat cells, we reexamined the basis for the attractive and increasingly accepted proposal that normal mammalian cells have a “tetraploidy checkpoint” that arrests binucleate cells in G1, thereby preventing their propagation. Using 10 μM cytochalasin to block cleavage, we confirm that most binucleate cells arrest in G1. However, when we use lower concentrations of cytochalasin, we find that binucleate cells undergo DNA synthesis and later proceed through mitosis in >80% of the cases for the hTERT-RPE1 human cell line, primary human fibroblasts, and the REF52 cell line. These observations provide a functional demonstration that the tetraploidy checkpoint does not exist in normal mammalian somatic cells.

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DIFRANCESCO, P., F. PICA, E. TUBARO, C. FAVALLI, and E. GARACI. "Cocaine effects on cell cycle progression." Cell Biology International Reports 14 (September 1990): 102. http://dx.doi.org/10.1016/0309-1651(90)90507-u.

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Tamanoi, Fuyuhiko, Juran Kato-Stankiewicz, Chen Jiang, Iara Machado, and Nitika Thapar. "Farnesylated proteins and cell cycle progression." Journal of Cellular Biochemistry 84, S37 (2001): 64–70. http://dx.doi.org/10.1002/jcb.10067.

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15

Kelvin, David J., Susan Chance, Mona Shreeve, Arthur A. Axelrad, Joe A. Connolly, and David McLeod. "Interleukin 3 and cell cycle progression." Journal of Cellular Physiology 127, no. 3 (June 1986): 403–9. http://dx.doi.org/10.1002/jcp.1041270308.

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16

Whitaker, M., and R. Patel. "Calcium and cell cycle control." Development 108, no. 4 (April 1, 1990): 525–42. http://dx.doi.org/10.1242/dev.108.4.525.

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The cell division cycle of the early sea urchin embryo is basic. Nonetheless, it has control points in common with the yeast and mammalian cell cycles, at START, mitosis ENTRY and mitosis EXIT. Progression through each control point in sea urchins is triggered by transient increases in intracellular free calcium. The Cai transients control cell cycle progression by translational and post-translational regulation of the cell cycle control proteins pp34 and cyclin. The START Cai transient leads to phosphorylation of pp34 and cyclin synthesis. The mitosis ENTRY Cai transient triggers cyclin phosphorylation. The motosis EXIT transient causes destruction of phosphorylated cyclin. We compare cell cycle regulation by calcium in sea urchin embryos to cell cycle regulation in other eggs and oocytes and in mammalian cells.

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Liu, Joey Z., Christopher J. Lyon, Willa A. Hsueh, and Ronald E. Law. "A Dominant-Negative PPARγMutant Promotes Cell Cycle Progression and Cell Growth in Vascular Smooth Muscle Cells." PPAR Research 2009 (2009): 1–10. http://dx.doi.org/10.1155/2009/438673.

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PPARγligands have been shown to have antiproliferative effects on many cell types. We herein report that a synthetic dominant-negative (DN) PPARγmutant functions like a growth factor to promote cell cycle progression and cell proliferation in human coronary artery smooth muscle cells (CASMCs). In quiescent CASMCs, adenovirus-expressed DN-PPARγpromoted G1→S cell cycle progression, enhanced BrdU incorporation, and increased cell proliferation. DN-PPARγexpression also markedly enhanced positive regulators of the cell cycle, increasing Rb and CDC2 phosphorylation and the expression of cyclin A, B1, D1, and MCM7. Conversely, overexpression of wild-type (WT) or constitutively-active (CA) PPARγinhibited cell cycle progression and the activity and expression of positive regulators of the cell cycle. DN-PPARγexpression, however, did not up-regulate positive cell cycle regulators in PPARγ-deficient cells, strongly suggesting that DN-PPARγeffects on cell cycle result from blocking the function of endogenous wild-type PPARγ. DN-PPARγexpression enhanced phosphorylation of ERK MAPKs. Furthermore, the ERK specific-inhibitor PD98059 blocked DN-PPARγ-induced phosphorylation of Rb and expression of cyclin A and MCM7. Our data thus suggest that DN-PPARγpromotes cell cycle progression and cell growth in CASMCs by modulating fundamental cell cycle regulatory proteins and MAPK mitogenic signaling pathways in vascular smooth muscle cells (VSMCs).

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18

Sherr, Charles J., Hitoshi Matsushime, and Martine F. Roussel. "Colony-stimulating factors and cell cycle progression." Current Opinion in Oncology 4 (December 1992): S16—S18. http://dx.doi.org/10.1097/00001622-199212001-00007.

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19

Srsen, Vlastimil, Nadia Korfali, and Eric C. Schirmer. "Nuclear envelope influences on cell-cycle progression." Biochemical Society Transactions 39, no. 6 (November 21, 2011): 1742–46. http://dx.doi.org/10.1042/bst20110656.

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The nuclear envelope is a complex double membrane system that serves as a dynamic interface between the nuclear and cytoplasmic compartments. Among its many roles is to provide an anchor for gene regulatory proteins on its nucleoplasmic surface and for the cytoskeleton on its cytoplasmic surface. Both sets of anchors are proteins called NETs (nuclear envelope transmembrane proteins), embedded respectively in the inner or outer nuclear membranes. Several lines of evidence indicate that the nuclear envelope contributes to cell-cycle regulation. These contributions come from both inner and outer nuclear membrane NETs and appear to operate through several distinct mechanisms ranging from sequestration of gene-regulatory proteins to activating kinase cascades.

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20

Li, Jian, Wei-Ping Qian, and Qing-Yuan Sun. "Cyclins regulating oocyte meiotic cell cycle progression†." Biology of Reproduction 101, no. 5 (July 26, 2019): 878–81. http://dx.doi.org/10.1093/biolre/ioz143.

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Abstract Oocyte meiotic maturation is a vital and final process in oogenesis. Unlike somatic cells， the oocyte needs to undergo two continuous meiotic divisions (meiosis I and meiosis II) to become a haploid gamete. Notably, oocyte meiotic progression includes two rounds of unique meiotic arrest and resumption. The first arrest occurs at the G2 (germinal vesicle) stage and meiosis resumption is stimulated by a gonadotropin surge; the second arrest takes place at the metaphase II stage, the stage from which it is released when fertilization takes place. The maturation-promoting factor, which consists of cyclin B1 (CCNB1) and cyclin-dependent kinase 1 (CDK1), is responsible for regulating meiotic resumption and progression, while CDK1 is the unique CDK that acts as the catalytic subunit of maturation-promoting factor. Recent studies showed that except for cyclin B1, multiple cyclins interact with CDK1 to form complexes, which are involved in the regulation of meiotic progression at different stages. Here, we review and discuss the control of oocyte meiotic progression by cyclins A1, A2, B1, B2, B3, and O.

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21

Molinie, Nicolas, Svetlana N. Rubtsova, Artem Fokin, Sai P. Visweshwaran, Nathalie Rocques, Anna Polesskaya, Anne Schnitzler, et al. "Cortical branched actin determines cell cycle progression." Cell Research 29, no. 6 (April 10, 2019): 432–45. http://dx.doi.org/10.1038/s41422-019-0160-9.

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22

Oredsson, S. M. "Polyamine dependence of normal cell-cycle progression." Biochemical Society Transactions 31, no. 2 (April 1, 2003): 366–70. http://dx.doi.org/10.1042/bst0310366.

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The driving force of the cell cycle is the activities of cyclin-dependent kinases (CDKs). Key steps in the regulation of the cell cycle therefore must impinge upon the activities of the CDKs. CDKs exert their functions when bound to cyclins that are expressed cyclically during the cell cycle. Polyamine biosynthesis varies bicyclically during the cell cycle with peaks in enzyme activities at the G1/S and S/G2 transitions. The enzyme activities are regulated at transcriptional, translational and post-translational levels. When cells are seeded in the presence of drugs that interfere with polyamine biosynthesis, cell cycle progression is affected within one cell cycle after seeding. The cell cycle phase that is most sensitive to polyamine biosynthesis inhibition is the S phase, while effects on the G1 and G2/M phases occur at later time points. The elongation step of DNA replication is negatively affected when polyamine pools are not allowed to increase normally during cell proliferation. Cyclin A is expressed during the S phase and cyclin A/CDK2 is important for a normal rate of DNA elongation. Cyclin A expression is lowered in cells treated with polyamine biosynthesis inhibitors. Thus, polyamines may affect S phase progression by participating in the regulation of cyclin A expression.

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23

Vielfort, Katarina, Linda Weyler, Niklas Söderholm, Mattias Engelbrecht, Sonja Löfmark, and Helena Aro. "Lactobacillus Decelerates Cervical Epithelial Cell Cycle Progression." PLoS ONE 8, no. 5 (May 10, 2013): e63592. http://dx.doi.org/10.1371/journal.pone.0063592.

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24

Fridovich-Keil, Judith L., Linnea J. Hansen, Khandan Keyomarsi, and Arthur B. Pardee. "Progression through the Cell Cycle: An Overview." American Review of Respiratory Disease 142, no. 6_pt_2 (December 1990): S3—S6. http://dx.doi.org/10.1164/ajrccm/142.6_pt_2.s3.

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25

Roci, Irena, Jeramie D. Watrous, Kim A. Lagerborg, Mohit Jain, and Roland Nilsson. "Mapping metabolic oscillations during cell cycle progression." Cell Cycle 19, no. 20 (October 4, 2020): 2676–84. http://dx.doi.org/10.1080/15384101.2020.1825203.

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26

Kukuruzinska, Maria A., and Kelley Lennon-Hopkins. "ALG gene expression and cell cycle progression." Biochimica et Biophysica Acta (BBA) - General Subjects 1426, no. 2 (January 1999): 359–72. http://dx.doi.org/10.1016/s0304-4165(98)00136-6.

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27

Giannini, Marianna, Chiara Primerano, Liron Berger, Martina Giannaccini, Zhigang Wang, Elena Landi, Alfred Cuschieri, Luciana Dente, Giovanni Signore, and Vittoria Raffa. "Nano-topography: Quicksand for cell cycle progression?" Nanomedicine: Nanotechnology, Biology and Medicine 14, no. 8 (November 2018): 2656–65. http://dx.doi.org/10.1016/j.nano.2018.07.002.

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28

Ahmed, Amel, Duane Smoot, George Littleton, Robert Tackey, Curla S. Walters, Fatah Kashanchi, Cornell R. Allen, and Hassan Ashktorab. "Helicobacter pylori inhibits gastric cell cycle progression." Microbes and Infection 2, no. 10 (August 2000): 1159–69. http://dx.doi.org/10.1016/s1286-4579(00)01270-3.

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29

Gladden, Andrew B., and J. Alan Diehl. "Cell cycle progression without cyclin E/CDK2." Cancer Cell 4, no. 3 (September 2003): 160–62. http://dx.doi.org/10.1016/s1535-6108(03)00217-4.

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30

Kapuy, Orsolya, Enuo He, Sandra López-Avilés, Frank Uhlmann, John J. Tyson, and Béla Novák. "System-level feedbacks control cell cycle progression." FEBS Letters 583, no. 24 (August 22, 2009): 3992–98. http://dx.doi.org/10.1016/j.febslet.2009.08.023.

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31

Pomerening, Joseph R. "Positive-feedback loops in cell cycle progression." FEBS Letters 583, no. 21 (October 8, 2009): 3388–96. http://dx.doi.org/10.1016/j.febslet.2009.10.001.

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32

Kühl, N. M., and L. Rensing*. "Heat shock effects on cell cycle progression." Cellular and Molecular Life Sciences 57, no. 3 (March 2000): 450–63. http://dx.doi.org/10.1007/pl00000707.

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33

Lee, G. "Cell cycle: progression from interphase to telophase." Science 245, no. 4919 (August 18, 1989): 766–67. http://dx.doi.org/10.1126/science.2549635.

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34

Koelink, Pim J., and Hein W. Verspaget. "5-ASA and Colorectal Cell-Cycle Progression." Gastroenterology 132, no. 4 (April 2007): 1635–36. http://dx.doi.org/10.1053/j.gastro.2007.03.008.

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35

Pagliuca, Felicia Walton, Mark O. Collins, and Jyoti S. Choudhary. "Coordinating cell cycle progression via cyclin specificity." Cell Cycle 10, no. 24 (December 15, 2011): 4195–96. http://dx.doi.org/10.4161/cc.10.24.18395.

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36

Strum, Jay C., Katherine I. Swenson, J. Eric Turner, and Robert M. Bell. "Ceramide Triggers Meiotic Cell Cycle Progression inXenopusOocytes." Journal of Biological Chemistry 270, no. 22 (June 2, 1995): 13541–47. http://dx.doi.org/10.1074/jbc.270.22.13541.

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37

Juan, Gloria. "In silico analysis of cell cycle progression." Cytometry Part A 85, no. 9 (June 17, 2014): 741–42. http://dx.doi.org/10.1002/cyto.a.22498.

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38

Gut, Gabriele, Michelle D. Tadmor, Dana Pe'er, Lucas Pelkmans, and Prisca Liberali. "Trajectories of cell-cycle progression from fixed cell populations." Nature Methods 12, no. 10 (August 24, 2015): 951–54. http://dx.doi.org/10.1038/nmeth.3545.

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39

Cirera-Salinas, Daniel, Montse Pauta, Ryan M. Allen, Alessandro G. Salerno, Cristina M. Ramírez, Aranzazu Chamorro-Jorganes, Amarylis C. Wanschel, et al. "Mir-33 regulates cell proliferation and cell cycle progression." Cell Cycle 11, no. 5 (March 2012): 922–33. http://dx.doi.org/10.4161/cc.11.5.19421.

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40

Askeland, Eric J., Vincent A. Chehval, Ryan W. Askeland, Placede G. Fosso, Zaina Sangale, Nafei Xu, Saradha Rajamani, Steven Stone, and James A. Brown. "Cell cycle progression score predicts metastatic progression of clear cell renal cell carcinoma after resection." Cancer Biomarkers 15, no. 6 (November 24, 2015): 861–67. http://dx.doi.org/10.3233/cbm-150530.

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41

Germanguz, Igal, Jenny C. Park, Jessica Cinkornpumin, Aryeh Solomon, Minori Ohashi, and William E. Lowry. "TDG regulates cell cycle progression in human neural progenitors." F1000Research 7 (April 26, 2018): 497. http://dx.doi.org/10.12688/f1000research.13801.1.

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Background: As cells divide, they must both replicate their DNA and generate a new set of histone proteins. The newly synthesized daughter strands and histones are unmodified, and must therefore be covalently modified to allow for transmission of important epigenetic marks to daughter cells. Human pluripotent stem cells (hPSCs) display a unique cell cycle profile, and control of the cell cycle is known to be critical for their proper differentiation and survival. A major unresolved question is how hPSCs regulate their DNA methylation status through the cell cycle, namely how passive and active demethylation work to maintain a stable genome. Thymine-DNA glycosylase (TDG), an embryonic essential gene, has been recently implicated as a major enzyme involved in demethylation. Methods: We use human pluripotent stem cells and their derivatives to investigate the role of TDG in differentiation and proliferation. To perform loss of function of TDG, RNA Interference was used. To study the cell cyle, we engineered human pluripotent stem cells to express the FUCCI tool which marks cells at various stages of the cell cycle with distinct patterns of fluorescent proteins. We also used cell cycle profiling by FACS, and DNA methylation analysis to probe a connection between DNA demethylation and cell cycle. Results: Here we present data showing that TDG regulates cell cycle dynamics in human neural progenitors (NPCs) derived from hPSCs, leading to changes in cell cycle related gene expression and neural differentiation capacity. These data show that loss of TDG function can block differentiation by driving proliferation of neural progenitors. We also identify specific cell cycle related genes whose expression changes upon loss of TDG expression. Conclusions: These observations suggest that TDG and active demethylation play an important role in hPSC cell cycle regulation and differentiation.

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42

Gookin, Sara, Mingwei Min, Harsha Phadke, Mingyu Chung, Justin Moser, Iain Miller, Dylan Carter, and Sabrina L. Spencer. "A map of protein dynamics during cell-cycle progression and cell-cycle exit." PLOS Biology 15, no. 9 (September 11, 2017): e2003268. http://dx.doi.org/10.1371/journal.pbio.2003268.

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43

Sun, Jing, Run Shi, Sha Zhao, Xiaona Li, Shan Lu, Hemei Bu, and Xianghua Ma. "Cell division cycle 45 promotes papillary thyroid cancer progression via regulating cell cycle." Tumor Biology 39, no. 5 (May 2017): 101042831770534. http://dx.doi.org/10.1177/1010428317705342.

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Cell division cycle 45 was reported to be overexpressed in some cancer-derived cell lines and was predicted to be a candidate oncogene in cervical cancer. However, the clinical and biological significance of cell division cycle 45 in papillary thyroid cancer has never been investigated. We determined the expression level and clinical significance of cell division cycle 45 using The Cancer Genome Atlas, quantitative real-time polymerase chain reaction, and immunohistochemistry. A great upregulation of cell division cycle 45 was observed in papillary thyroid cancer tissues compared with adjacent normal tissues. Furthermore, overexpression of cell division cycle 45 positively correlates with more advanced clinical characteristics. Silence of cell division cycle 45 suppressed proliferation of papillary thyroid cancer cells via G1-phase arrest and inducing apoptosis. The oncogenic activity of cell division cycle 45 was also confirmed in vivo. In conclusion, cell division cycle 45 may serve as a novel biomarker and a potential therapeutic target for papillary thyroid cancer.

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Wang, Zhixiang. "Regulation of Cell Cycle Progression by Growth Factor-Induced Cell Signaling." Cells 10, no. 12 (November 26, 2021): 3327. http://dx.doi.org/10.3390/cells10123327.

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The cell cycle is the series of events that take place in a cell, which drives it to divide and produce two new daughter cells. The typical cell cycle in eukaryotes is composed of the following phases: G1, S, G2, and M phase. Cell cycle progression is mediated by cyclin-dependent kinases (Cdks) and their regulatory cyclin subunits. However, the driving force of cell cycle progression is growth factor-initiated signaling pathways that control the activity of various Cdk–cyclin complexes. While the mechanism underlying the role of growth factor signaling in G1 phase of cell cycle progression has been largely revealed due to early extensive research, little is known regarding the function and mechanism of growth factor signaling in regulating other phases of the cell cycle, including S, G2, and M phase. In this review, we briefly discuss the process of cell cycle progression through various phases, and we focus on the role of signaling pathways activated by growth factors and their receptor (mostly receptor tyrosine kinases) in regulating cell cycle progression through various phases.

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45

Kheir, Tony Bou, and Anders H. Lund. "Epigenetic dynamics across the cell cycle." Essays in Biochemistry 48 (September 20, 2010): 107–20. http://dx.doi.org/10.1042/bse0480107.

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Progression of the mammalian cell cycle depends on correct timing and co-ordination of a series of events, which are managed by the cellular transcriptional machinery and epigenetic mechanisms governing genome accessibility. Epigenetic chromatin modifications are dynamic across the cell cycle, and are shown to influence and be influenced by cell-cycle progression. Chromatin modifiers regulate cell-cycle progression locally by controlling the expression of individual genes and globally by controlling chromatin condensation and chromosome segregation. The cell cycle, on the other hand, ensures a correct inheritance of epigenetic chromatin modifications to daughter cells. In this chapter, we summarize the current knowledge on the dynamics of epigenetic chromatin modifications during progression of the cell cycle.

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46

Urrego, Diana, Adam P. Tomczak, Farrah Zahed, Walter Stühmer, and Luis A. Pardo. "Potassium channels in cell cycle and cell proliferation." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1638 (March 19, 2014): 20130094. http://dx.doi.org/10.1098/rstb.2013.0094.

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Normal cell-cycle progression is a crucial task for every multicellular organism, as it determines body size and shape, tissue renewal and senescence, and is also crucial for reproduction. On the other hand, dysregulation of the cell-cycle progression leading to uncontrolled cell proliferation is the hallmark of cancer. Therefore, it is not surprising that it is a tightly regulated process, with multifaceted and very complex control mechanisms. It is now well established that one of those mechanisms relies on ion channels, and in many cases specifically on potassium channels. Here, we summarize the possible mechanisms underlying the importance of potassium channels in cell-cycle control and briefly review some of the identified channels that illustrate the multiple ways in which this group of proteins can influence cell proliferation and modulate cell-cycle progression.

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Bruno, Silvia, Bernardetta Ledda, Claudya Tenca, Silvia Ravera, Anna Maria Orengo, Andrea Nicola Mazzarello, Elisa Pesenti, et al. "Metformin inhibits cell cycle progression of B-cell chronic lymphocytic leukemia cells." Oncotarget 6, no. 26 (June 5, 2015): 22624–40. http://dx.doi.org/10.18632/oncotarget.4168.

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48

Douglas, Robert M., Tian Xu, and Gabriel G. Haddad. "Cell cycle progression and cell division are sensitive to hypoxia in Drosophila melanogaster embryos." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 5 (May 1, 2001): R1555—R1563. http://dx.doi.org/10.1152/ajpregu.2001.280.5.r1555.

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We and others recently demonstrated that Drosophila melanogaster embryos arrest development and embryonic cells cease dividing when they are deprived of O2. To further characterize the behavior of these embryos in response to O2 deprivation and to define the O2-sensitive checkpoints in the cell cycle, embryos undergoing nuclear cycles 3–13 were subjected to O2deprivation and examined by confocal microscopy under control, hypoxic, and reoxygenation conditions. In vivo, real-time analysis of embryos carrying green fluorescent protein-kinesin demonstrated that cells arrest at two major points of the cell cycle, either at the interphase (before DNA duplication) or at metaphase, depending on the cell cycle phase at which O2 deprivation was induced. Immunoblot analysis of embryos whose cell divisions are synchronized by inducible String (cdc25 homolog) demonstrated that cyclin B was degraded during low O2 conditions in interphase-arrested embryos but not in those arrested in metaphase. Embryos resumed cell cycle activity within ∼20 min of reoxygenation, with very little apparent change in cell cycle kinetics. We conclude that there are specific points during the embryonic cell cycle that are sensitive to the O2 level in D. melanogaster. Given the fact that O2deprivation also influences the growth and development of other species, we suggest that similar hypoxia-sensitive cell cycle checkpoints may also exist in mammalian cells.

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49

Uroz, Marina, Sabrina Wistorf, Xavier Serra-Picamal, Vito Conte, Marta Sales-Pardo, Pere Roca-Cusachs, Roger Guimerà, and Xavier Trepat. "Regulation of cell cycle progression by cell–cell and cell–matrix forces." Nature Cell Biology 20, no. 6 (May 25, 2018): 646–54. http://dx.doi.org/10.1038/s41556-018-0107-2.

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50

Singh, Rana, and Rajesh Agarwal. "Natural Flavonoids Targeting Deregulated Cell Cycle Progression in Cancer Cells." Current Drug Targets 7, no. 3 (March 1, 2006): 345–54. http://dx.doi.org/10.2174/138945006776055004.

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Journal articles on the topic 'Cell cycle progression'

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