Relevant bibliographies by topics / Cell cycle progression

Academic literature on the topic 'Cell cycle progression'

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Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Cell cycle progression"

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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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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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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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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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Dissertations / Theses on the topic "Cell cycle progression"

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Santos, Carlo Steven. "Circadian Control of Cell Cycle Progression." Thesis, Virginia Tech, 2009. http://hdl.handle.net/10919/76987.

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Tumorigenesis is the result of uncontrolled cell growth due to the deregulation of cell cycle checkpoints 1. Period 2 (Per2) is a tumor suppressor that oscillate in expression in a 24-hour cycle 2, 3. Here, we show that Per2 interacts with the tumor suppressor protein p53. Both G1 and G2 checkpoint pathways involve a p53 dependent pathway which can trigger the cell to go through cell arrest or programmed cell death4. Understanding all the mitigating factors involved in regulating cell cycle progression under DNA damage can offer a better idea in how cells become immortal. Initially discovered through screening of a human liver cDNA library, the novel interaction between p53-Per2 was further documented using co-precipitation. Interestingly, under genotoxic stress conditions, p53 and Per2 were not found to bind which leads us to suspect that Per2 does not affect active p53 which may possibly be due to post translational modifications of its active state. Furthermore we investigated p53's ability to act as a transcription factor in the presence of Per2, showing that the Per2-p53 complex prevents p53 from binding to DNA. This implies that the tetramerization of p53 may also be another factor in Per2's ability to bind to p53. A truncated p53 lacking the last 30 amino acids that theoretically increase p53's ability to form a tetramer showed a drastic reduction in binding to Per2 5, 6. On the other hand, p53 lacking the tetramerization domain showed binding similar to wildtype. Consequently we speculate that the ability of Per2 to modulate p53 and act as a tumor suppressor protein may be dependent on either the post translational modifications of p53 or its oligomeric state.
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Joseph, Alton J. "Regulation of S6KL during cell cycle progression." Thesis, California State University, Long Beach, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=1527714.

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mTOR (Mammalian Target ofRapamycin), PI3K (Phosphatidylinositol3-kinase) and MEK (Mitogen-activated protein kinase/ERK kinase) have been shown to be potent regulators ofS6Kl at G1 phase of the cell cycle. Research has been concentrated at the Gt phase to elucidate mTOR's role in cell growth and proliferation. Limited information is available on the activity ofmTOR, PI3K and ERKl/2 in cell cycle phases other than G1. Since we have observed that S6Kl is active in phases other than G1 our goal was to ascertain ifmTOR, PI3K or ERKl/2 have a role in regulating S6Kl during these cell cycle phases. Using cell cycle analysis and immunoblot analysis we have determined here that mTORand PI3K could play a role in regulating S6Kl at the G1/S transition iQ. the cell cycle but there is also indications that mTOR and PI3K are potentially involved in regulating S6Kl in the phases post-G1/S of the cell cycle, indicating a complex interaction between the kinases used to regulate S6Kl during the cell cycle. ERKl/2 is demonstrated to have limited involvement in the regulation of S6Kl during the cell cycle.

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Fredlund, Jan O. "The role of polyanimes in cell cycle progression." Lund : Lund University Dept. of Animal Physiology, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38100686.html.

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Delorme, Marilyne. "Downregulation of ATRX disrupts cell proliferation and cell cycle progression." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27627.

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ATRX is a chromatin remodelling protein of the SNF2 family of chromatin remodelling proteins. Mutations in the ATRX gene have been shown to cause the ATR-X syndrome, an X-linked mental retardation disorder. ATRX is part of a chromatin-remodelling complex with Daxx that localizes to PML nuclear bodies or pericentromeric heterochromatin and is thought to regulate gene expression. In mice, Atrx inactivation results in embryonic lethality whereas conditional forebrain specific Atrx ablation showed impaired development and disorganization of the cortex. Furthermore, ATRX phosphorylation was shown to be cell cycle dependant, suggesting an important role for ATRX in cell cycle regulation. In this study we investigated the effects of ATRX downregulation in cell culture models, using siRNA transient transfection, a clone expressing an shRNA targeted to ATRX, and Atrxnull MEFs. ATRX downregulated cells showed reduced growth rates and cell cycle defects at the G1 and S phases of the cell cycle. Moreover, ATRX ablation was associated with an altered Rb phosphorylation status and decreased expression of the cyclin A and E2F-1 proteins. Taken together our results suggest that ATRX may play a significant role in cell cycle progression that is pertinent for proper development.
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Stewart, Nancy G. "P53 control over cell cycle progression at G2." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32022.pdf.

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Rathbone, Christopher R. "Mechanisms regulating skeletal muscle satellite cell cycle progression." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/5866.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2006.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "December 2006" Includes bibliographical references.
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Weber, Tom. "Optimal timing of phase resolved cell cycle progression." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2015. http://dx.doi.org/10.18452/17253.

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Selbstreproduktion ist eines der Kennzeichen aller lebenden Organismen. Der Zellzyklus dient der Selbstreproduktion in einzelligen Organismen. In mehrzelligen Organismen ist der Zellzyklus darüber hinaus für andere lebenswichtige Prozesse, einschließlich Immunreaktionen, unerlässlich. In dieser Arbeit wird eine Methode entwickelt mit der die Dauer der Zellzyklus Phasen bestimmt werden kann. Kenntnis über die Zellzyklusphasendauer ermöglicht vorherzusagen, wie schnell eine Population von proliferierenden Zellen wachsen wird, oder wie viele neue Zellen pro Stunde in einem Gewebe geboren werden. Im Kapitel 1 dieser Arbeit wird ein Zellzyklusmodell aufgestellt und mit experimentellen Bromdesoxyuridin Daten verglichen. Die Analyse zeigt, dass das Modell gut die experimentelle Kinetik beschreibt, hebt jedoch auch hervor dass einige der Parameter nicht identifiziert werden können. Dieses Problem wird in Kapitel 2 bearbeitet, wo zwei Ansätze erforscht werden, um den Informationsgehalt der Experimente zu erhöhen. In einem ersten Ansatz wird die Theorie der Versuchsplanung angewendet, um optimale Versuchspläne zu bestimmen. In einem zweiten Ansatz wird das übliche Bromdesoxyuridin Protokoll durch ein zweites Nukleosid erweitert. Beide Methoden verbessern in silico erheblich die Genauigkeit und Präzision der Abschätzungen. Im dritten Kapitel wird die Methodik in der Analyse der Keimzentrumsreaktion angewendet. Ein erheblicher Zufluss von Zellen in die dunkle Zone von Keimzentren wird vorhergesagt, und die Ansicht einer extrem schellen Zellteilung im Keimzentrum erscheint in dem Modell als ein Artefakt der Zellmigration.
Self-reproduction is one of the distinguishing marks of living organisms. The cell cycle is the underlying process by which self-reproduction is accomplished in single-celled organisms. In multi-cellular organisms, the cell cycle is in addition indispensable for other vital processes, including immune reactions. In this thesis a method is developed that allows to estimate the time it takes for a dividing cells to complete the CC phases. Knowledge of the CC phase durations allows to predict, for example, how fast a population of proliferating cells will grow in size, or how many new cells are born per hour in a given tissue. In Chapter 1 of this thesis, a cell cycle model with delays and variability in the completion times of each phase is developed. Analytical solutions are derived to describe a common experimental technique used for cell cycle analysis, namely pulse labeling with bromodeoxyuridine (BrdU). Comparison with data shows that the model reproduces closely measured cell cycle kinetics, however also reveals that some of the parameter values cannot be identified. This problem is addressed in Chapter 2. In a first approach, the framework of D-optimal experimental designs is employed, in order to choose optimal sampling schemes. In a second approach, the prevailing protocol with a single nucleoside is modified by adding a second nucleoside analog pulse. Both methods are tested and the results suggest that experimental design can significantly improve parameter estimation. In Chapter 3, the model is applied to the germinal center reaction. A substantial influx of cells into the dark zone of germinal centers is predicted. Moreover the wide-held view of rapid proliferation in germinal centers, appears, under this model, as an artifact of cell migration.
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Poli, Alessandro <1985&gt. "New DAG-dependent mechanisms modulate cell cycle progression." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6739/1/Tesi_Alessandro.Poli..pdf.

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Through the years, several studies reported the involvement of nuclear lipid signalling as highly connected with cell cycle progression. Indeed, nuclear Phosphatidylinositol-4,5-Biphosphate (PIP2) hydrolisis mediated by Phospholipases C (PLC), which leads to production of the second messengers Diacylglycerol (DAG) and Inositol-1,4,5-Triphosphate (IP3), is a fundamental event for both G1/S and G2/M checkpoints. In particular, we found that nuclear DAG production was mediated by PLCbeta1, enzyme mainly localized in the nucleus of K562 human erythroleukemia cells. This event triggered the activation and nuclear translocation of PKCalpha, which, in turn, resulted able to affect cell cycle via modulation of Cyclin D3 and Cyclin B1, two important enzymes for G1/S transition and G2/M progression respectively.
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Poli, Alessandro <1985&gt. "New DAG-dependent mechanisms modulate cell cycle progression." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6739/.

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Through the years, several studies reported the involvement of nuclear lipid signalling as highly connected with cell cycle progression. Indeed, nuclear Phosphatidylinositol-4,5-Biphosphate (PIP2) hydrolisis mediated by Phospholipases C (PLC), which leads to production of the second messengers Diacylglycerol (DAG) and Inositol-1,4,5-Triphosphate (IP3), is a fundamental event for both G1/S and G2/M checkpoints. In particular, we found that nuclear DAG production was mediated by PLCbeta1, enzyme mainly localized in the nucleus of K562 human erythroleukemia cells. This event triggered the activation and nuclear translocation of PKCalpha, which, in turn, resulted able to affect cell cycle via modulation of Cyclin D3 and Cyclin B1, two important enzymes for G1/S transition and G2/M progression respectively.
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Ouertani, A. "Determinants of cell cycle progression in human mammary epithelial MCF12 cells." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1362848/.

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Cancer of the mammary gland is the most common type of cancer in women worldwide, and the vast majority of breast cancers originate from a cluster of malignant cells in the epithelial tissue of the breast, which initially confines the ductal carcinoma in situ. Research has shown that the signalling pathways that increase differentiation and maintain proliferation in normal epithelial cells are of utmost importance for sustaining this barrier against malignant cells. As a model for normal mammary epithelial cells, the MCF-12A cell line was used to determine factors that are required for cell cycle progression of these cells. A discontinuous treatment assay was developed in which the MCF-12A cells were treated with epidermal growth factor (EGF) and insulin at two distinct times to induce cell cycle re-entry. The use of these chemically defined growth factors enabled us to determine that continuous stimulation with mitogenic factors is not required for these cells to re-enter the cell cycle. An initial activation of the MAP kinase pathway and an up-regulation of the transcription factor c-Myc, followed by activation of the PI3K pathway, resulted in full competence to progress into S phase. The order in which the growth factors were applied, and thus the sequence in which the subsequent proteins were triggered, was of great importance for successful S phase entry. We found that estradiol (E2) was unable to induce the factors necessary for cell cycle progression. Furthermore, we report for the first time that E2 did not affect estrogen-regulated genes which normally are under the control of a ligand-bound estrogen receptor (ER). We suggest that the mechanism by which the ligand-activated ER usually interferes with the estrogen responsive element in the promoter region of the target genes is defective in the MCF-12A cell line. The results presented here may contribute to new approaches in chemotherapy, taking advantage of the diverse molecular mechanism in place for cell cycle progression and proliferation in malignant cells compared to normal mammary epithelial cells.
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Books on the topic "Cell cycle progression"

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Johannes, Boonstra, ed. G1 phase progression. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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Boonstra, Johannes. G1 phase progression. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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Klein, Alyssa Michelle. A p53-independent role for MDM2-MDMX in cell cycle progression. [New York, N.Y.?]: [publisher not identified], 2021.

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Radeva, Galina. Overexpression of the integrin-linked kinase (ILK) promotes anchorage-independent cell cycle progression. Ottawa: National Library of Canada, 1997.

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G1 phase progression. Georgetown, TX: Landes Bioscience/Eurekah.com ; Kluwer Academic/Plenum, 2004.

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Boonstra, Johannes. Regulation of G1 Phase Progression. Springer, 2003.

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Petrocelli, Teresa. UVB cell cycle checkpoint loss in melanoma progression. 2002.

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Liang, Jiyong. Regulation of p27(KIP1) by the PI3K/PKB pathway and its role in cell cycle progression in human cancer. 2004.

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Turner, Neil. Mechanisms of progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0136.

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Three major hypotheses attempt to explain progressive kidney disease following diverse diseases and injuries. To varying degrees they can explain the observed risk factors for progression and the ability of interventions to lower risk. The hyperfiltration hypothesis argues that progression is due to stress on residual nephrons leading to injury and damage to remaining glomeruli. The toxicity of proteinuria hypothesis proposes that serum proteins or bound substances are toxic to tubular or tubulointerstitial cells. This sets up cycles of damage which lead to tubulointerstitial scarring. The podocyte loss hypothesis contends that proteinuria is simply a biomarker for damaged or dying podocytes, and that it is further podocyte loss that leads to progressive glomerulosclerosis. Renoprotective strategies might have direct effects on podocytes. Importantly these different hypotheses suggest different therapeutic approaches to protecting the function of damaged kidneys. Differences between repair mechanisms may explain why some injuries lead to recovery and others to progressive disease, and may suggest new targets for protective therapy.
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Pozio, Edoardo. Trichinellosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0068.

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Trichinellosis is caused by nematodes of the genus Trichinella. These zoonotic parasites show a cosmopolitan distribution in all the continents, but Antarctica. They circulate in nature by synanthropic-domestic and sylvatic cycles. Today, eight species and four genotypes are recognized, all of which infect mammals, including humans, one species also infects birds, and two other species infect also reptiles.Parasites of the genus Trichinella are unusual among the other nematodes in that the worm undergoes a complete developmental cycle, from larva to adult to larva, in the body of a single host, which has a profound influence on the epidemiology of trichinellosis. When the cycle is complete, the muscles of the infected animal contain a reservoir of larvae, capable of long-term survival. Humans and other hosts become infected by ingesting muscle tissuescontaining viable larvae.The symptoms associated with trichinellosis vary with the severity of infection, i.e. the number of viable larvae ingested, and the time after infection. The capacity of the worm population to undergo massive multiplication in the body is a major determinant. Progression of disease follows the biological development of the parasite. Symptoms are associated first with the gastrointestinal tract, as the worms invade and establish in the small intestine, become more general as the body responds immunologically, and finally focus on the muscles as the larvae penetrate the muscle cells and develop there. Although Trichinella worms cause pathological changes directly by mechanical damage, most of the clinical features of trichinellosis are immunopathological in origin and can be related to the capacity of the parasite to induce allergic responses.The main source of human infection is raw or under-cooked meat products from pig, wild boar, bear, walrus, and horses, but meat products from other animals have been implicated. In humans, the diagnosis of infection is made by immunological tests or by direct examination of muscle biopsies using microscopy or by recovery of larvae after artificial digestion. Treatment requires both the use of anthelmintic drugs to kill the parasite itself and symptomatic treatment to minimize inflammatory responses.Both pre-slaughter prevention and post-slaughter control can be used to prevent Trichinella infections in animals. The first involves pig management control as well as continuous surveillance programmes. Meat inspection is a successful post-slaughter strategy. However, a continuous consumer education is of great importance in countries where meat inspection is not mandatory.
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Book chapters on the topic "Cell cycle progression"

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Wang, Zhixiang. "Cell Cycle Progression and Synchronization: An Overview." In Cell-Cycle Synchronization, 3–23. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2736-5_1.

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DeRan, Michael, Mary Pulvino, and Jiyong Zhao. "Assessing G1-to-S-Phase Progression After Genotoxic Stress." In Cell Cycle Checkpoints, 221–30. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_16.

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Sherr, Charles J., Hitoshi Matsushime, Jun-ya Kato, Dawn E. Quelle, and Martine F. Roussel. "Control of G1 Progression by Mammalian D-Type Cyclins." In The Cell Cycle, 17–23. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_2.

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Kianfard, Zohreh, Kyle Cheung, Daniel Rappaport, Sirasie P. Magalage, and Sarah A. Sabatinos. "Detecting Cell Cycle Stage and Progression in Fission Yeast, Schizosaccharomyces pombe." In Cell-Cycle Synchronization, 235–46. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2736-5_18.

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Alberts, Arthur S., and Axel Schönthal. "Positive and Negative Regulation of Cell Cycle Progression by Serine/Threonine Protein Phosphatases." In The Cell Cycle, 33–40. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_4.

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Greenwood, Brianna L., and David T. Stuart. "Synchronization of Saccharomyces cerevisiae Cells for Analysis of Progression Through the Cell Cycle." In Cell-Cycle Synchronization, 145–68. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2736-5_12.

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Lee, Jongkuen, and David Dominguez-Sola. "Mammalian Cell Fusion Assays for the Study of Cell Cycle Progression by Functional Complementation." In Cell Cycle Checkpoints, 145–57. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1217-0_9.

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Prall, Owen W. J., Eileen M. Rogan, Elizabeth A. Musgrove, Colin K. W. Watts, and Robert L. Sutherland. "Estrogen Regulation of Cell Cycle Progression." In Hormonal Carcinogenesis III, 220–27. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4612-2092-3_21.

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Sutherland, Robert L., Jenny A. Hamilton, Kimberley J. E. Sweeney, Colin K. W. Watts, and Elizabeth A. Musgrove. "Steroidal Regulation of Cell Cycle Progression." In Novartis Foundation Symposia, 218–34. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514757.ch13.

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Vitale, Ilio, Mohamed Jemaà, Lorenzo Galluzzi, Didier Metivier, Maria Castedo, and Guido Kroemer. "Cytofluorometric Assessment of Cell Cycle Progression." In Methods in Molecular Biology, 93–120. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-239-1_6.

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Conference papers on the topic "Cell cycle progression"

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Tamura, Rodrigo E., Juliano D. Paccez, Mirian G. Morale, Xuesong Gu, Towia Libermann, Luiz F. Zerbini, and Kristal Duncan. "cdk11p58 regulation of cell cycle progression in cancer development." In AACR International Conference: Molecular Diagnostics in Cancer Therapeutic Development– Sep 27-30, 2010; Denver, CO. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/diag-10-a37.

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Taylor-Harding, Barbie, Hasmik Agadjanian, Sandra Orsulic, Christine Walsh, Beth Y. Karlan, and Wolf-Ruprecht Wiedemeyer. "Abstract 1749: Cell cycle requirements shape ovarian cancer progression." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1749.

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de Souza Cruz, André Luiz, Patricia Torres Bozza, and João Paulo de Biaso Viola. "Abstract 1744: Role of lipid bodies on cell cycle progression." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1744.

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Choi, Byeong Hyeok, Xun Che, Changyan Chen, Luo Lu, and Wei Dai. "Abstract 2726: WWP2 is required for normal cell cycle progression." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2726.

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Dovat, Elanora, Jonathon Payne, Carlos M. Casiano, Justin Sloane, Chandrika Gowda, Kimberly J. Payne, Sinisa Dovat, and Chunhua Song. "Abstract 3504: Regulation of cell cycle progression by Ikaros in leukemia." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3504.

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Muralidharan, Somsundar Veppil, Joydeep Bhadury, Lydia Green, Lisa M. Nilsson, Kevin G. Mclure, and Jonas A. Nilsson. "Abstract 4565: Bet bromodomain inhibitors affects replication & cell cycle progression." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4565.

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Ibla, Juan C., Yan Su, Assefa Wondimu, Stephan Ladisch, and Robert Freishtat. "Modulation Of Cell Cycle Progression By Continuous Hypoxia In Bronchial Epithelium." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5293.

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SHA, YOBAO, Lavannya M. Pandit, shenyan zeng, Li-Yuan Yu-Lee, and Tony N. Eissa. "CHIP Is A Novel Centrosomal Protein Involved In Cell Cycle Progression." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4933.

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Yang, Yingzi, Wantae Kim, and Xiaohui Wang. "Abstract IA11: Hippo signaling Is Intrinsically regulated during cell cycle progression." In Abstracts: AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; May 8-11, 2019; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.hippo19-ia11.

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Almiman, Abeer, Daotai Nie, and Jamila Adom. "Abstract 307: TRIB3 regulates cell cycle progression and programmed cell death in non-small cell lung cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-307.

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Reports on the topic "Cell cycle progression"

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Kuhne, Wendy, Candace Langan, Lucas Angelette, and Lesleyann Hawthorne. Deuterium Concentration Effects on Cell Cycle Progression. Office of Scientific and Technical Information (OSTI), August 2020. http://dx.doi.org/10.2172/1651107.

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KUHNE, WENDY, and LUCAS ANGELETTE. DEUTERIUM CONCENTRATION EFFECTS ON CELL CYCLE PROGRESSION. Office of Scientific and Technical Information (OSTI), October 2021. http://dx.doi.org/10.2172/1827682.

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KUHNE, WENDY. DEUTERIUM CONCENTRATION EFFECTS ON CELL CYCLE PROGRESSION. Office of Scientific and Technical Information (OSTI), October 2021. http://dx.doi.org/10.2172/1827952.

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Direnzo, James. Differential Regulation of Cell Cycle Progression in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1998. http://dx.doi.org/10.21236/adb240737.

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Rajasekaran, Ayyappan K. Role of PSMA in Aberrant Cell Cycle Progression in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2004. http://dx.doi.org/10.21236/ada433876.

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Rajasekaran, Ayyappan. Role of PSMA in Aberrant Cell Cycle Progression in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada560904.

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Direnzo, James, and Myles Brown. Differential Regulation of Cell Cycle Progression in Human Breast Cancer Cell Lines by the Estrogen Receptor. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada394036.

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Lew, Brian. The Loss of Pin1 Deregulates Cell Cycle Progression and Promotes the Development of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada488883.

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Lew, Brian. The Loss of Pin1 Deregulates Cell Cycle Progression and Promotes the Development of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada511532.

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Stiles, Bangyan, and Hong Wu. Functional Analysis of Oncogene Akt: Its Role in Tumorigenesis In Vivo and Cell Cycle Progression In Vitro. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407666.

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You might also be interested in the extended bibliographies on the topic 'Cell cycle progression' for particular source types:
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