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Journal articles on the topic 'Transition G1'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Chen, Zihao, and Chunhe Li. "Quantifying the Landscape and Transition Paths for Proliferation–Quiescence Fate Decisions." Journal of Clinical Medicine 9, no. 8 (2020): 2582. http://dx.doi.org/10.3390/jcm9082582.

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The cell cycle, essential for biological functions, experiences delicate spatiotemporal regulation. The transition between G1 and S phase, which is called the proliferation–quiescence decision, is critical to the cell cycle. However, the stability and underlying stochastic dynamical mechanisms of the proliferation–quiescence decision have not been fully understood. To quantify the process of the proliferation–quiescence decision, we constructed its underlying landscape based on the relevant gene regulatory network. We identified three attractors on the landscape corresponding to the G0, G1, an

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2

Zwijsen, R. M., R. Klompmaker, E. B. Wientjens, P. M. Kristel, B. van der Burg, and R. J. Michalides. "Cyclin D1 triggers autonomous growth of breast cancer cells by governing cell cycle exit." Molecular and Cellular Biology 16, no. 6 (1996): 2554–60. http://dx.doi.org/10.1128/mcb.16.6.2554.

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Cyclin D1 controls G1-associated processes, including G0-to-G1 and G1-to-S transitions. This study demonstrates a novel aspect of cyclin D1 as a regulator of the transition between G1 and G0. Overexpression of cyclin D1 in MCF7 breast tumor cells resulted in a continued proliferation under low-serum conditions, whereas nonoverexpressing cells ceased to grow. This difference in growth was due to a reduced exit from G1 to G0 in cyclin D1-overexpressing cells. Our data therefore suggest a model in which cyclin D1 overexpression in tumor cells is responsible for hyperproliferation under growth fac

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Mattaloni, Stella M., Anabela C. Ferretti, Facundo M. Tonucci, Cristián Favre, James R. Goldenring, and M. Cecilia Larocca. "Centrosomal AKAP350 modulates the G1/S transition." Cellular Logistics 3, no. 4 (2013): e26331. http://dx.doi.org/10.4161/cl.26331.

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4

Bekkal-Brikci, Fadia, Giovanna Chiorino, and Khalid Boushaba. "G1/S transition and cell population dynamics." Networks & Heterogeneous Media 4, no. 1 (2009): 67–90. http://dx.doi.org/10.3934/nhm.2009.4.67.

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5

Dittmer, D., and E. S. Mocarski. "Human cytomegalovirus infection inhibits G1/S transition." Journal of virology 71, no. 2 (1997): 1629–34. http://dx.doi.org/10.1128/jvi.71.2.1629-1634.1997.

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Prathapam, T., S. Tegen, T. Oskarsson, A. Trumpp, and G. S. Martin. "Activated Src abrogates the Myc requirement for the G0/G1 transition but not for the G1/S transition." Proceedings of the National Academy of Sciences 103, no. 8 (2006): 2695–700. http://dx.doi.org/10.1073/pnas.0511186103.

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Ortega, S., M. Malumbres, and M. Barbacid. "Cell Cycle and Cancer: The G1 Restriction Point and the G1 / S Transition." Current Genomics 3, no. 4 (2002): 245–63. http://dx.doi.org/10.2174/1389202023350444.

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8

Ohtsubo, M., A. M. Theodoras, J. Schumacher, J. M. Roberts, and M. Pagano. "Human cyclin E, a nuclear protein essential for the G1-to-S phase transition." Molecular and Cellular Biology 15, no. 5 (1995): 2612–24. http://dx.doi.org/10.1128/mcb.15.5.2612.

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Cyclin E was first identified by screening human cDNA libraries for genes that would complement G1 cyclin mutations in Saccharomyces cerevisiae and has subsequently been found to have specific biochemical and physiological properties that are consistent with it performing a G1 function in mammalian cells. Most significantly, the cyclin E-Cdk2 complex is maximally active at the G1/S transition, and overexpression of cyclin E decreases the time it takes the cell to complete G1 and enter S phase. We have now found that mammalian cells express two forms of cyclin E protein which differ from each o

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Orr, Stephen J., Rong Wang, Nicholas C. Lea, et al. "Systems Biology Analysis of Human Primary T Cells Identifies SAP145 as Rate Limiting for the G1→S Phase Transition." Blood 110, no. 11 (2007): 3350. http://dx.doi.org/10.1182/blood.v110.11.3350.3350.

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Abstract We identified a G0→G1 commitment point in primary human T cells that controls entry into the cell cycle from quiescence. We demonstrated proof of principle that cellular pathways regulating cell cycle progression and effector functions that normally coincide during CD3/CD28 stimulation can be uncoupled experimentally. We have now used systems biology approaches to identify nuclear protein networks in primary human T cells that are regulated during the transition from quiescence into the cell cycle (G0→G1→S-phase). First we sequenced proteins that became bound to chromatin & nuclea

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10

Chiorino, G., and M. Lupi. "Variability in the timing of G1/S transition." Mathematical Biosciences 177-178 (May 2002): 85–101. http://dx.doi.org/10.1016/s0025-5564(02)00085-8.

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Huang, Fu, Susan M. Abmayr, and Jerry L. Workman. "Limiting PCNA-unloading at the G1/S transition." Cell Cycle 15, no. 22 (2016): 3001–2. http://dx.doi.org/10.1080/15384101.2016.1214036.

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Guevara, Claudia, Wouter Korver, Daniel Mahony, et al. "Regulation of G1/S transition in mammalian cells." Kidney International 56, no. 4 (1999): 1182. http://dx.doi.org/10.1046/j.1523-1755.1999.00711.x.

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13

Hsiung, Chris C. S., Arjun Raj, and Gerd A. Blobel. "Hematopoietic Transcriptional Regulation At The Mitosis-G1 Transition." Blood 122, no. 21 (2013): 2440. http://dx.doi.org/10.1182/blood.v122.21.2440.2440.

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Abstract Normal hematopoiesis involves the coordination of cell division and gene expression to produce physiologically appropriate cell numbers of various developmental stages across lineages. While studies have demonstrated intricate links between cell cycle progression and developmental gene regulation -- two cellular programs whose concomitant dysregulation is central to many malignant and non-malignant hematologic diseases -- researchers currently lack clear, general principles of how intrinsic properties of cell division could influence developmental gene regulation. In each round of div

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14

Rossi, Vincenzo, and Serena Varotto. "Insights into the G1/S transition in plants." Planta 215, no. 3 (2002): 345–56. http://dx.doi.org/10.1007/s00425-002-0780-y.

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DeMali, Kris A., та Andrius Kazlauskas. "Activation of Src Family Members Is Not Required for the Platelet-Derived Growth Factor β Receptor To Initiate Mitogenesis". Molecular and Cellular Biology 18, № 4 (1998): 2014–22. http://dx.doi.org/10.1128/mcb.18.4.2014.

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ABSTRACT The basal activity of Src family kinases is readily detectable throughout the cell cycle and increases by two- to fivefold upon acute stimulation of cells with growth factors such as platelet-derived growth factor. Previous reports have demonstrated a requirement for Src activity for the G1/S and G2/M transitions. With a chimeric α-β PDGF receptor (PDGFR) expressed in fibroblasts, we have investigated the importance of the PDGF-mediated increase in Src activity at the G0/G1 transition for subsequent cell cycle events. A mutant PDGFR chimera that was not able to detectably associate wi

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Pepperkok, R., P. Lorenz, W. Ansorge, and W. Pyerin. "Casein kinase II is required for transition of G0/G1, early G1, and G1/S phases of the cell cycle." Journal of Biological Chemistry 269, no. 9 (1994): 6986–91. http://dx.doi.org/10.1016/s0021-9258(17)37471-9.

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17

MacKay, Vivian L., Bernard Mai, Laurie Waters, and Linda L. Breeden. "Early Cell Cycle Box-Mediated Transcription ofCLN3 and SWI4 Contributes to the Proper Timing of the G1-to-S Transition in Budding Yeast." Molecular and Cellular Biology 21, no. 13 (2001): 4140–48. http://dx.doi.org/10.1128/mcb.21.13.4140-4148.2001.

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ABSTRACT The Cln3-Cdc28 kinase is required to activate the Swi4-Swi6 transcription complex which induces CLN1 andCLN2 transcription in late G1 and drives the transition to S. Cln3 and Swi4 are both rate limiting for G1 progression, and they are coordinately transcribed to peak at the M/G1 boundary. Early cell cycle box (ECB) elements, which confer M/G1-specific transcription, have been found in both promoters, and elimination of all ECB elements from the CLN3 promoter causes both a loss of periodicity and Cln3-deficient phenotypes, which include an extended G1interval and increased cell volume

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18

Nishii, Tomonori, Yu Oikawa, Yasumasa Ishida, Masashi Kawaichi, and Eishou Matsuda. "CtBP-interacting BTB Zinc Finger Protein (CIBZ) Promotes Proliferation and G1/S Transition in Embryonic Stem Cells via Nanog." Journal of Biological Chemistry 287, no. 15 (2012): 12417–24. http://dx.doi.org/10.1074/jbc.m111.333856.

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Mouse embryonic stem cells (ESCs) require transcriptional regulation to ensure rapid proliferation that allows for self-renewal. However, the molecular mechanism by which transcriptional factors regulate this rapid proliferation remains largely unknown. Here we present data showing that CIBZ, a BTB domain zinc finger transcriptional factor, is a key transcriptional regulator for regulation of ESC proliferation. Here we show that deletion or siRNA knockdown of CIBZ inhibits ESC proliferation. Cell cycle analysis shows that loss of CIBZ delays the progression of ESCs through the G1 to S phase tr

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19

Susaki, Etsuo, Keiko Nakayama, and Keiichi I. Nakayama. "Cyclin D2 Translocates p27 out of the Nucleus and Promotes Its Degradation at the G0-G1 Transition." Molecular and Cellular Biology 27, no. 13 (2007): 4626–40. http://dx.doi.org/10.1128/mcb.00862-06.

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ABSTRACT The nuclear export and cytoplasmic degradation of the cyclin-dependent kinase inhibitor p27 are required for effective progression of the cell cycle through the G0-G1 transition. The mechanism responsible for this translocation of p27 has remained unclear, however. We now show that cyclin D2 directly links growth signaling with the nuclear export of p27 at the G0-G1 transition in some cell types. The up-regulation of cyclin D2 in response to mitogenic stimulation was found to occur earlier than that of other D-type cyclins and in parallel with down-regulation of p27 at the G0-G1 trans

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20

Tvegard, T., H. Soltani, H. C. Skjolberg, et al. "A novel checkpoint mechanism regulating the G1/S transition." Genes & Development 21, no. 6 (2007): 649–54. http://dx.doi.org/10.1101/gad.421807.

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21

Krek, Wilhelm. "Proteolysis and the G1-S transition: the SCF connection." Current Opinion in Genetics & Development 8, no. 1 (1998): 36–42. http://dx.doi.org/10.1016/s0959-437x(98)80059-2.

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22

Bøe, Cathrine A., Jon Halvor J. Knutsen, Erik Boye, and Beáta Grallert. "Hpz1 Modulates the G1-S Transition in Fission Yeast." PLoS ONE 7, no. 9 (2012): e44539. http://dx.doi.org/10.1371/journal.pone.0044539.

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23

Li, Yunfang, Jing Pei, Hong Xia, Hengning Ke, Hongyan Wang, and Wufan Tao. "Lats2, a putative tumor suppressor, inhibits G1/S transition." Oncogene 22, no. 28 (2003): 4398–405. http://dx.doi.org/10.1038/sj.onc.1206603.

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24

Guadagno, T. M., and R. K. Assoian. "G1/S control of anchorage-independent growth in the fibroblast cell cycle." Journal of Cell Biology 115, no. 5 (1991): 1419–25. http://dx.doi.org/10.1083/jcb.115.5.1419.

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We have developed methodology to identify the block to anchorage-independent growth and position it within the fibroblast cell cycle. Results with NRK fibroblasts show that mitogen stimulation of the G0/G1 transition and G1-associated increases in cell size are minimally affected by loss of cell anchorage. In contrast, the induction of G1/S cell cycle genes and DNA synthesis is markedly inhibited when anchorage is blocked. Moreover, we demonstrate that the anchorage-dependent transition maps to late G1 and shortly before activation of the G1/S p34cdc2-like kinase. The G1/S block was also detec

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Zamir, E., Z. Kam, and A. Yarden. "Transcription-dependent induction of G1 phase during the zebra fish midblastula transition." Molecular and Cellular Biology 17, no. 2 (1997): 529–36. http://dx.doi.org/10.1128/mcb.17.2.529.

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The early development of the zebra fish (Danio rerio) embryo is characterized by a series of rapid and synchronous cell cycles with no detectable transcription. This period is followed by the midblastula transition (MBT), during which the cell cycle gradually lengthens, cell synchrony is lost, and zygotic transcription is initially detected. In this work, we examined the changes in the pattern of the cell cycle during MBT in zebra fish and whether these changes are dependent on the initiation of zygotic transcription. To characterize the pattern of the early zebra fish cell cycles, the embryon

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26

Resnitzky, D., and S. I. Reed. "Different roles for cyclins D1 and E in regulation of the G1-to-S transition." Molecular and Cellular Biology 15, no. 7 (1995): 3463–69. http://dx.doi.org/10.1128/mcb.15.7.3463.

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Ectopic expression of cyclins D1 and E was previously shown to accelerate the G1/S-phase transition, indicating that both classes of G1 cyclin control an event(s) that is rate limiting for entry into S phase. In order to determine whether cyclins D1 and E control the same or two different rate-limiting events, we have created cell lines that express both cyclins in an inducible manner. We show here that ectopic expression of both cyclins E and D1 in the same cell has an additive effect on shortening of the G1 interval relative to expression of any single cyclin. In order to further explore the

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Deng, Xingming, Fengqin Gao, and W. Stratford May. "Bcl2 retards G1/S cell cycle transition by regulating intracellular ROS." Blood 102, no. 9 (2003): 3179–85. http://dx.doi.org/10.1182/blood-2003-04-1027.

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AbstractBcl2's antiapoptotic function is regulated by phosphorylation. Bcl2 also regulates cell cycle progression, but the molecular mechanism is unclear. Bcl2 is functionally expressed in mitochondria where it can act as an antioxidant that may regulate intracellular reactive oxygen species (ROS). Since ROS have been reported to act as second messengers in cell signaling, we tested whether Bcl2 phosphorylation regulates ROS and cell cycle progression. G1 → S transition and ROS levels were measured in cells expressing either the gain of function phosphomimetic Bcl2 mutants S70E and T69E/S70E/S

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Sørensen, Claus Storgaard, Claudia Lukas, Edgar R. Kramer, Jan-Michael Peters, Jiri Bartek, and Jiri Lukas. "Nonperiodic Activity of the Human Anaphase-Promoting Complex–Cdh1 Ubiquitin Ligase Results in Continuous DNA Synthesis Uncoupled from Mitosis." Molecular and Cellular Biology 20, no. 20 (2000): 7613–23. http://dx.doi.org/10.1128/mcb.20.20.7613-7623.2000.

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ABSTRACT Ubiquitin-proteasome-mediated destruction of rate-limiting proteins is required for timely progression through the main cell cycle transitions. The anaphase-promoting complex (APC), periodically activated by the Cdh1 subunit, represents one of the major cellular ubiquitin ligases which, in Saccharomyces cerevisiae andDrosophila spp., triggers exit from mitosis and during G1 prevents unscheduled DNA replication. In this study we investigated the importance of periodic oscillation of the APC-Cdh1 activity for the cell cycle progression in human cells. We show that conditional interferen

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Arco, Pablo Gómez-del, Kazushige Maki, and Katia Georgopoulos. "Phosphorylation Controls Ikaros's Ability To Negatively Regulate the G1-S Transition." Molecular and Cellular Biology 24, no. 7 (2004): 2797–807. http://dx.doi.org/10.1128/mcb.24.7.2797-2807.2004.

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ABSTRACT Ikaros is a key regulator of lymphocyte proliferative responses. Inactivating mutations in Ikaros cause antigen-mediated lymphocyte hyperproliferation and the rapid development of leukemia and lymphoma. Here we show that Ikaros's ability to negatively regulate the G1-S transition can be modulated by phosphorylation of a serine/threonine-rich conserved region (p1) in exon 8. Ikaros phosphorylation in p1 is induced during the G1-S transition. Mutations that prevent phosphorylation in p1 increase Ikaros's ability to impede cell cycle progression and its affinity for DNA. Casein kinase II

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Miele, Angela, Corey D. Braastad, William F. Holmes, et al. "HiNF-P Directly Links the Cyclin E/CDK2/p220NPAT Pathway to Histone H4 Gene Regulation at the G1/S Phase Cell Cycle Transition." Molecular and Cellular Biology 25, no. 14 (2005): 6140–53. http://dx.doi.org/10.1128/mcb.25.14.6140-6153.2005.

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ABSTRACT Genome replication in eukaryotic cells necessitates the stringent coupling of histone biosynthesis with the onset of DNA replication at the G1/S phase transition. A fundamental question is the mechanism that links the restriction (R) point late in G1 with histone gene expression at the onset of S phase. Here we demonstrate that HiNF-P, a transcriptional regulator of replication-dependent histone H4 genes, interacts directly with p220NPAT, a substrate of cyclin E/CDK2, to coactivate histone genes during S phase. HiNF-P and p220 are targeted to, and colocalize at, subnuclear foci (Cajal

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Tu, Xiaoming, and Ching C. Wang. "Coupling of Posterior Cytoskeletal Morphogenesis to the G1/S Transition in theTrypanosoma bruceiCell Cycle." Molecular Biology of the Cell 16, no. 1 (2005): 97–105. http://dx.doi.org/10.1091/mbc.e04-05-0368.

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The expression levels of four Cdc2-related kinases (CRK1, 2, 4, and 6) in the procyclic form of Trypanosoma brucei were knocked down in pairs using the RNA interference (RNAi) technique. A double knockdown of CRK1 and CRK2 resulted in arrested cell growth in the G1 phase accompanied by an apparent cessation of nuclear DNA synthesis. The arrested cells became elongated at the posterior end like the G1-phase cells generated by knockdown of CycE1/CYC2 in a previous study. However, ∼5% of the G1 cells in the current study also possessed multiply branched posterior ends, which have not previously b

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Gu, Jinming, Xiaobo Xia, Peijun Yan, et al. "Cell Cycle-dependent Regulation of a Human DNA Helicase That Localizes in DNA Damage Foci." Molecular Biology of the Cell 15, no. 7 (2004): 3320–32. http://dx.doi.org/10.1091/mbc.e04-03-0227.

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Mutational studies of human DNA helicase B (HDHB) have suggested that its activity is critical for the G1/S transition of the cell cycle, but the nature of its role remains unknown. In this study, we show that during G1, ectopically expressed HDHB localizes in nuclear foci induced by DNA damaging agents and that this focal pattern requires active HDHB. During S and G2/M, HDHB localizes primarily in the cytoplasm. A carboxy-terminal domain from HDHB confers cell cycle-dependent localization, but not the focal pattern, to a reporter protein. A cluster of potential cyclin-dependent kinase phospho

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MOU, Sherry, and Diana LINNEKIN. "Lyn is activated during late G1 of stem-cell-factor-induced cell cycle progression in haemopoietic cells." Biochemical Journal 342, no. 1 (1999): 163–70. http://dx.doi.org/10.1042/bj3420163.

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Stem cell factor (SCF) binds the receptor tyrosine kinase c-Kit and is critical in haemopoiesis. Recently we found that the Src family member Lyn is highly expressed in SCF-responsive cells, associates with c-Kit and is activated within minutes of the addition of SCF. Here we show that SCF activates Lyn a second time, hours later, during SCF-induced cell cycle progression. In cells arrested at specific phases of the cell cycle with the drugs mimosine, aphidicolin and nocodazole, maximal Lyn kinase activity occurred in late G1 and through the G1/S transition. Similarly, kinetic studies of SCF-i

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Ho, Yuen, Michael Costanzo, Lynda Moore, Ryuji Kobayashi, and Brenda J. Andrews. "Regulation of Transcription at theSaccharomyces cerevisiae Start Transition by Stb1, a Swi6-Binding Protein." Molecular and Cellular Biology 19, no. 8 (1999): 5267–78. http://dx.doi.org/10.1128/mcb.19.8.5267.

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ABSTRACT In Saccharomyces cerevisiae, gene expression in the late G1 phase is activated by two transcription factors, SBF and MBF. SBF contains the Swi4 and Swi6 proteins and activates the transcription of G1 cyclin genes, cell wall biosynthesis genes, and the HO gene. MBF is composed of Mbp1 and Swi6 and activates the transcription of genes required for DNA synthesis. Mbp1 and Swi4 are the DNA binding subunits for MBF and SBF, while the common subunit, Swi6, is presumed to play a regulatory role in both complexes. We show that Stb1, a protein first identified in a two-hybrid screen with the t

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Lemasters, John J. "V. Necrapoptosis and the mitochondrial permeability transition: shared pathways to necrosis and apoptosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 1 (1999): G1—G6. http://dx.doi.org/10.1152/ajpgi.1999.276.1.g1.

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Opening of a high-conductance pore conducting solutes of molecular mass <1,500 Da causes onset of the mitochondrial permeability transition (MPT). Cyclosporin A blocks this pore and prevents acute necrotic cell death in several models. Confocal microscopy directly visualizes onset of the MPT during acute cytotoxicity from the movement of the green-fluorescing fluorophore, calcein, into the mitochondria from the cytosol. The MPT also plays a causative role in tumor necrosis factor-α-induced apoptosis in hepatocytes. Progression to apoptosis or necrosis after the MPT may depend on the presenc

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Galarneau, Luc, Anne Loranger, Stéphane Gilbert, and Normand Marceau. "Keratins modulate hepatic cell adhesion, size and G1/S transition." Experimental Cell Research 313, no. 1 (2007): 179–94. http://dx.doi.org/10.1016/j.yexcr.2006.10.007.

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Aleem, Eiman, Hiroaki Kiyokawa, and Philipp Kaldis. "Cdc2–cyclin E complexes regulate the G1/S phase transition." Nature Cell Biology 7, no. 8 (2005): 831–36. http://dx.doi.org/10.1038/ncb1284.

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Zhang, Haoyue, Daniel J. Emerson, Thomas G. Gilgenast, et al. "Chromatin structure dynamics during the mitosis-to-G1 phase transition." Nature 576, no. 7785 (2019): 158–62. http://dx.doi.org/10.1038/s41586-019-1778-y.

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Ussar, Siegfried, and Tilman Voss. "MEK1 and MEK2, Different Regulators of the G1/S Transition." Journal of Biological Chemistry 279, no. 42 (2004): 43861–69. http://dx.doi.org/10.1074/jbc.m406240200.

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Chesters, John K., Linda Petrie, and Kenneth E. Lipson. "Two zinc-dependent steps during G1 to S phase transition." Journal of Cellular Physiology 155, no. 3 (1993): 445–51. http://dx.doi.org/10.1002/jcp.1041550303.

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Schweinfest, C. W., S. Fujiwara, L. F. Lau, and T. S. Papas. "c-myc can induce expression of G0/G1 transition genes." Molecular and Cellular Biology 8, no. 8 (1988): 3080–87. http://dx.doi.org/10.1128/mcb.8.8.3080.

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The human c-myc oncogene was linked to the heat shock-inducible Drosophila hsp70 promoter and used to stably transfect mouse BALB/c 3T3 cells. Heat shock of the transfectants at 42 degrees C followed by recovery at 37 degrees C resulted in the appearance of the human c-myc protein which was appropriately localized to the nuclear fraction. Two-dimensional analysis of the proteins of density-arrested cells which had been heat shock treated revealed the induction of eight protein species and the repression of five protein species. All of the induced and repressed proteins were nonabundant. cDNA c

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Hume, Samuel, Grigory L. Dianov, and Kristijan Ramadan. "A unified model for the G1/S cell cycle transition." Nucleic Acids Research 48, no. 22 (2020): 12483–501. http://dx.doi.org/10.1093/nar/gkaa1002.

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Abstract Efficient S phase entry is essential for development, tissue repair, and immune defences. However, hyperactive or expedited S phase entry causes replication stress, DNA damage and oncogenesis, highlighting the need for strict regulation. Recent paradigm shifts and conflicting reports demonstrate the requirement for a discussion of the G1/S transition literature. Here, we review the recent studies, and propose a unified model for the S phase entry decision. In this model, competition between mitogen and DNA damage signalling over the course of the mother cell cycle constitutes the pred

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Gardner, Lawrence B., Qing Li, Michele S. Park, W. Michael Flanagan, Gregg L. Semenza, and Chi V. Dang. "Hypoxia Inhibits G1/S Transition through Regulation of p27 Expression." Journal of Biological Chemistry 276, no. 11 (2000): 7919–26. http://dx.doi.org/10.1074/jbc.m010189200.

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Pillai, Malini S., S. Sapna, and K. Shivakumar. "p38 MAPK regulates G1-S transition in hypoxic cardiac fibroblasts." International Journal of Biochemistry & Cell Biology 43, no. 6 (2011): 919–27. http://dx.doi.org/10.1016/j.biocel.2011.03.007.

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Schweinfest, C. W., S. Fujiwara, L. F. Lau, and T. S. Papas. "c-myc can induce expression of G0/G1 transition genes." Molecular and Cellular Biology 8, no. 8 (1988): 3080–87. http://dx.doi.org/10.1128/mcb.8.8.3080-3087.1988.

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The human c-myc oncogene was linked to the heat shock-inducible Drosophila hsp70 promoter and used to stably transfect mouse BALB/c 3T3 cells. Heat shock of the transfectants at 42 degrees C followed by recovery at 37 degrees C resulted in the appearance of the human c-myc protein which was appropriately localized to the nuclear fraction. Two-dimensional analysis of the proteins of density-arrested cells which had been heat shock treated revealed the induction of eight protein species and the repression of five protein species. All of the induced and repressed proteins were nonabundant. cDNA c

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Wang, Jiangfang, Emma L. Reuschel, Jason M. Shackelford, et al. "HIV-1 Vif promotes the G1- to S-phase cell-cycle transition." Blood 117, no. 4 (2011): 1260–69. http://dx.doi.org/10.1182/blood-2010-06-289215.

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AbstractHIV-1 depends on host-cell resources for replication, access to which may be limited to a particular phase of the cell cycle. The HIV-encoded proteins Vpr (viral protein R) and Vif (viral infectivity factor) arrest cells in the G2 phase; however, alteration of other cell-cycle phases has not been reported. We show that Vif drives cells out of G1 and into the S phase. The effect of Vif on the G1-to-S transition is distinct from its effect on G2, because G2 arrest is Cullin5-dependent, whereas the G1-to-S progression is Cullin5-independent. Using mass spectrometry, we identified 2 novel

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Molnar, G., A. Crozat, and A. B. Pardee. "The immediate-early gene Egr-1 regulates the activity of the thymidine kinase promoter at the G0-to-G1 transition of the cell cycle." Molecular and Cellular Biology 14, no. 8 (1994): 5242–48. http://dx.doi.org/10.1128/mcb.14.8.5242.

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Production of thymidine kinase (TK) protein parallels the onset of DNA synthesis during the cell cycle. This process is regulated at transcriptional, posttranscriptional, and translational levels to cause a 40- to 50-fold increase in cytosolic enzymatic activity as cells progress from G1 to S phase. Transcriptional activation of the mouse TK gene through the cell cycle is dependent upon previously characterized cis elements of the proximal promoter, called MT1, MT2, and MT3, that bind at least two different complexes: TKE during the transition of cells from quiescence (G0) to G1, and Yi later

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48

Molnar, G., A. Crozat, and A. B. Pardee. "The immediate-early gene Egr-1 regulates the activity of the thymidine kinase promoter at the G0-to-G1 transition of the cell cycle." Molecular and Cellular Biology 14, no. 8 (1994): 5242–48. http://dx.doi.org/10.1128/mcb.14.8.5242-5248.1994.

Full text

Abstract:

Production of thymidine kinase (TK) protein parallels the onset of DNA synthesis during the cell cycle. This process is regulated at transcriptional, posttranscriptional, and translational levels to cause a 40- to 50-fold increase in cytosolic enzymatic activity as cells progress from G1 to S phase. Transcriptional activation of the mouse TK gene through the cell cycle is dependent upon previously characterized cis elements of the proximal promoter, called MT1, MT2, and MT3, that bind at least two different complexes: TKE during the transition of cells from quiescence (G0) to G1, and Yi later

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Gonzalez-Fernandez, A., J. Sans, P. Aller, and C. De La Torre. "The involvement of discrete genome regions in post-mitotic chromosome decondensation and in G1 timing in Allium cepa L. meristematic cells." Journal of Cell Science 103, no. 4 (1992): 1047–51. http://dx.doi.org/10.1242/jcs.103.4.1047.

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The role of DNA regions replicated at different times during the S period in the process of chromatin decondensation that takes place in the next G1 period, as well as in the timing of the G1 to S transition, was analyzed in synchronous populations of cells in Allium cepa L. root meristems. For this analysis, DNA bromosubstitution (10-7 M 5-bromo-2′-deoxyuridine feeding) was carried out at similar times corresponding to the first, middle and last thirds of the S period prior to telophase when anoxic 313 nm irradiation was carried out. Evaluation, after Feulgen staining, of the chromatin patter

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Resnitzky, D., L. Hengst, and S. I. Reed. "Cyclin A-associated kinase activity is rate limiting for entrance into S phase and is negatively regulated in G1 by p27Kip1." Molecular and Cellular Biology 15, no. 8 (1995): 4347–52. http://dx.doi.org/10.1128/mcb.15.8.4347.

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We have created fibroblast cell lines that express cyclin A under the control of a tetracycline-repressible promoter. When stimulated to reenter the cell cycle after serum withdrawal, these cells were advanced prematurely into S phase by induction of cyclin A. In an asynchronous population, induction of cyclin A caused a decrease in the percentage of cells in G1. These results demonstrate that expression of cyclin A is rate limiting for the G1-to-S transition and suggest that cyclin A can function as a G1 cyclin. Although the level of exogenous cyclin A was constant throughout the cell cycle,

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