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Journal articles on the topic 'Mammalian cell cycle'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

OKAYAMA, HIROTO. "Mammalian Cell Cycle." RADIOISOTOPES 42, no. 8 (1993): 497–98. http://dx.doi.org/10.3769/radioisotopes.42.497.

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2

Martínez-Alonso, Diego, and Marcos Malumbres. "Mammalian cell cycle cyclins." Seminars in Cell & Developmental Biology 107 (November 2020): 28–35. http://dx.doi.org/10.1016/j.semcdb.2020.03.009.

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3

Noël, Vincent, Sergey Vakulenko, and Ovidiu Radulescu. "A hybrid mammalian cell cycle model." Electronic Proceedings in Theoretical Computer Science 125 (August 27, 2013): 68–83. http://dx.doi.org/10.4204/eptcs.125.5.

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4

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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5

Cooper, S. "Rethinking synchronization of mammalian cells for cell cycle analysis." Cellular and Molecular Life Sciences 60, no. 6 (June 2003): 1099–106. http://dx.doi.org/10.1007/s00018-003-2253-2.

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6

Davis, Penny K., Alan Ho, and Steven F. Dowdy. "Biological Methods for Cell-Cycle Synchronization of Mammalian Cells." BioTechniques 30, no. 6 (June 2001): 1322–31. http://dx.doi.org/10.2144/01306rv01.

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7

Müller, Rolf. "Transcriptional regulation during the mammalian cell cycle." Trends in Genetics 11, no. 5 (May 1995): 173–78. http://dx.doi.org/10.1016/s0168-9525(00)89039-3.

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8

Denhardt, David T., Dylan R. Edwards, and Craig L. J. Parfett. "Gene expression during the mammalian cell cycle." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 865, no. 2 (October 1986): 83–125. http://dx.doi.org/10.1016/0304-419x(86)90024-7.

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9

OSADA, HIROYUKI. "Bioprobes for Investigating Mammalian Cell Cycle Control." Journal of Antibiotics 51, no. 11 (1998): 973–82. http://dx.doi.org/10.7164/antibiotics.51.973.

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10

Rieder, Conly L., and Richard W. Cole. "Cold-Shock and the Mammalian Cell Cycle." Cell Cycle 1, no. 3 (May 2002): 168–74. http://dx.doi.org/10.4161/cc.1.3.119.

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11

Lee, Melanie, and Paul Nurse. "Cell cycle control genes in fission yeast and mammalian cells." Trends in Genetics 4, no. 10 (October 1988): 287–90. http://dx.doi.org/10.1016/0168-9525(88)90171-0.

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12

Lee, Seungmin, Sujeong Kim, Xuejun Sun, Jae-Ho Lee, and Hyeseong Cho. "Cell cycle-dependent mitochondrial biogenesis and dynamics in mammalian cells." Biochemical and Biophysical Research Communications 357, no. 1 (May 2007): 111–17. http://dx.doi.org/10.1016/j.bbrc.2007.03.091.

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13

Stumpf, Craig R., Melissa V. Moreno, Adam B. Olshen, Barry S. Taylor, and Davide Ruggero. "The Translational Landscape of the Mammalian Cell Cycle." Molecular Cell 52, no. 4 (November 2013): 574–82. http://dx.doi.org/10.1016/j.molcel.2013.09.018.

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14

Kim, Jun Hyun, Channabasavaiah Basavaraju Gurumurthy, Mayumi Naramura, Ying Zhang, Andrew T. Dudley, Lynn Doglio, Hamid Band, and Vimla Band. "Role of Mammalian Ecdysoneless in Cell Cycle Regulation." Journal of Biological Chemistry 284, no. 39 (July 29, 2009): 26402–10. http://dx.doi.org/10.1074/jbc.m109.030551.

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15

Marcus, M., A. Fainsod, and G. Diamond. "The Genetic Analysis of Mammalian Cell-Cycle Mutants." Annual Review of Genetics 19, no. 1 (December 1985): 389–421. http://dx.doi.org/10.1146/annurev.ge.19.120185.002133.

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16

Yao, Guang, Cheemeng Tan, Mike West, Joseph R. Nevins, and Lingchong You. "Origin of bistability underlying mammalian cell cycle entry." Molecular Systems Biology 7, no. 1 (January 2011): 485. http://dx.doi.org/10.1038/msb.2011.19.

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17

Singhania, Rajat, R. Michael Sramkoski, James W. Jacobberger, and John J. Tyson. "A Hybrid Model of Mammalian Cell Cycle Regulation." PLoS Computational Biology 7, no. 2 (February 10, 2011): e1001077. http://dx.doi.org/10.1371/journal.pcbi.1001077.

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18

Eriksson, Staffan, Sven Skog, Bernard Tribukait, and Birgitta Wallström. "Deoxyribonucleoside triphosphate metabolism and the mammalian cell cycle." Experimental Cell Research 168, no. 1 (January 1987): 79–88. http://dx.doi.org/10.1016/0014-4827(87)90417-4.

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19

Fulka, Josef, Judy Bradshaw, and Robert Moor. "Meiotic cycle checkpoints in mammalian oocytes." Zygote 2, no. 4 (November 1994): 351–54. http://dx.doi.org/10.1017/s0967199400002197.

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Recent Spectacular achievements have enabled the identification of key molecules responsible for mitotic cell cycle progression through the stages of G1, the gap before DNA replication; S, the phase of DNA synthesis; G2, the gap before chromosome segregation; and M, mitosis itself. The last stage has been most intensively studied, where MPE, maturation promotion factor, has been found responsible for the nuclear events associated with chromosomal segregation and the prodcution of two identical daughter cells (see Murray & Hunt, 1993).
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20

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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21

Wolgemuth, DJ, K. Rhee, S. Wu, and SE Ravnik. "Genetic control of mitosis, meiosis and cellular differentiation during mammalian spermatogenesis." Reproduction, Fertility and Development 7, no. 4 (1995): 669. http://dx.doi.org/10.1071/rd9950669.

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Gametogenesis in both the male and female mammal represents a specialized and highly regulated series of cell cycle events, involving both mitosis and meiosis as well as subsequent differentiation. Recent advances in our understanding of the genetic control of the eukaryotic cell cycle have underscored the evolutionarily-conserved nature of these regulatory processes. However, most of the data have been obtained from yeast model systems and mammalian cell lines. Furthermore, most of the observations focus on regulation of mitotic cell cycles. In the present paper: (i) aspects of gametogenesis in mammals that represent unique cell-cycle control points are highlighted; (ii) current knowledge on the regulation of the germ cell cycle, in the context of what is known in yeast and other model eukaryotic systems, is summarized; and (iii) strategies that can be used to identify additional cell cycle regulating genes are outlined.
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22

Fertig, G., M. Klöppinger, and H. G. Miltenburger. "Cell cycle kinetics of insect cell cultures compared to mammalian cell cultures." Experimental Cell Research 189, no. 2 (August 1990): 208–12. http://dx.doi.org/10.1016/0014-4827(90)90237-5.

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23

Quarmby, Lynne M., and Jeremy D. K. Parker. "Cilia and the cell cycle?" Journal of Cell Biology 169, no. 5 (May 31, 2005): 707–10. http://dx.doi.org/10.1083/jcb.200503053.

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A recent convergence of data indicating a relationship between cilia and proliferative diseases, such as polycystic kidney disease, has revived the long-standing enigma of the reciprocal regulatory relationship between cilia and the cell cycle. Multiple signaling pathways are localized to cilia in mammalian cells, and some proteins have been shown to act both in the cilium and in cell cycle regulation. Work from the unicellular alga Chlamydomonas is providing novel insights as to how cilia and the cell cycle are coordinately regulated.
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24

Cui, Cheng-Bin, Hideaki Kakeya, and Hiroyuki Osada. "Novel mammalian cell cycle inhibitors, cyclotroprostatins A–D, produced by Aspergillus fumigatus, which inhibit mammalian cell cycle at G2/M phase." Tetrahedron 53, no. 1 (January 1997): 59–72. http://dx.doi.org/10.1016/s0040-4020(96)00978-7.

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25

TANAKA, Arowu, Fumi KANO, and Masayuki MURATA. "Organelle Inheritance-Cell Cycle Dependent Dynamics of Organelles in Mammalian Cells." Seibutsu Butsuri 42, no. 3 (2002): 116–21. http://dx.doi.org/10.2142/biophys.42.116.

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26

Fujita, Masatoshi. "Cell cycle regulation of DNA replication initiation proteins in mammalian cells." Frontiers in Bioscience 4, no. 1-3 (1999): d816. http://dx.doi.org/10.2741/fujita.

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27

Schorl, Christoph, and John M. Sedivy. "Analysis of cell cycle phases and progression in cultured mammalian cells." Methods 41, no. 2 (February 2007): 143–50. http://dx.doi.org/10.1016/j.ymeth.2006.07.022.

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28

Fujita, Masatoshi. "Cell cycle regulation of DNA replication initiation proteins in mammalian cells." Frontiers in Bioscience 4, no. 4 (1999): d816–823. http://dx.doi.org/10.2741/a398.

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29

Reddy, G. Prem Veer. "Cell cycle: Regulatory events in G1 → S transition of mammalian cells." Journal of Cellular Biochemistry 54, no. 4 (April 1994): 379–86. http://dx.doi.org/10.1002/jcb.240540404.

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30

Wagner, R. W., and K. Nishikura. "Cell cycle expression of RNA duplex unwindase activity in mammalian cells." Molecular and Cellular Biology 8, no. 2 (February 1988): 770–77. http://dx.doi.org/10.1128/mcb.8.2.770.

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An RNA duplex unwindase activity has been found by using an in vitro assay with various types of mammalian, somatic cells, including HeLa, mouse plasmacytoma, and Burkitt lymphoma. The unwindase activity is very low in mouse fibroblast 3T3 cells arrested into quiescence, but increases when the cells are released into renewed growth by serum. In addition, a gel retardation assay proved to be specific and sensitive for detection of RNA duplex-unwindase complexes.
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31

Aprea, Julieta, and Federico Calegari. "Bioelectric State and Cell Cycle Control of Mammalian Neural Stem Cells." Stem Cells International 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/816049.

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The concerted action of ion channels and pumps establishing a resting membrane potential has been most thoroughly studied in the context of excitable cells, most notably neurons, but emerging evidences indicate that they are also involved in controlling proliferation and differentiation of nonexcitable somatic stem cells. The importance of understanding stem cell contribution to tissue formation during embryonic development, adult homeostasis, and regeneration in disease has prompted many groups to study and manipulate the membrane potential of stem cells in a variety of systems. In this paper we aimed at summarizing the current knowledge on the role of ion channels and pumps in the context of mammalian corticogenesis with particular emphasis on their contribution to the switch of neural stem cells from proliferation to differentiation and generation of more committed progenitors and neurons, whose lineage during brain development has been recently elucidated.
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32

Wagner, R. W., and K. Nishikura. "Cell cycle expression of RNA duplex unwindase activity in mammalian cells." Molecular and Cellular Biology 8, no. 2 (February 1988): 770–77. http://dx.doi.org/10.1128/mcb.8.2.770-777.1988.

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An RNA duplex unwindase activity has been found by using an in vitro assay with various types of mammalian, somatic cells, including HeLa, mouse plasmacytoma, and Burkitt lymphoma. The unwindase activity is very low in mouse fibroblast 3T3 cells arrested into quiescence, but increases when the cells are released into renewed growth by serum. In addition, a gel retardation assay proved to be specific and sensitive for detection of RNA duplex-unwindase complexes.
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33

Rosner, M., C. Fuchs, N. Siegel, A. Valli, and M. Hengstschlager. "Functional interaction of mammalian target of rapamycin complexes in regulating mammalian cell size and cell cycle." Human Molecular Genetics 18, no. 17 (June 8, 2009): 3298–310. http://dx.doi.org/10.1093/hmg/ddp271.

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34

Orlowski, Craig C., and Richard W. Furlanetto. "THE MAMMALIAN CELL CYCLE IN NORMAL AND ABNORMAL GROWTH." Endocrinology and Metabolism Clinics of North America 25, no. 3 (September 1996): 491–502. http://dx.doi.org/10.1016/s0889-8529(05)70337-6.

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35

Gil-Ranedo, Jon, Eva Hernando, Laura Riolobos, Carlos Domínguez, Michael Kann, and José M. Almendral. "The Mammalian Cell Cycle Regulates Parvovirus Nuclear Capsid Assembly." PLOS Pathogens 11, no. 6 (June 11, 2015): e1004920. http://dx.doi.org/10.1371/journal.ppat.1004920.

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36

Tanaka, Hideaki, Adrien Fauré, and Hiroshi Matsuno. "Boolean modeling of mammalian cell cycle and cancer pathways." Proceedings of International Conference on Artificial Life and Robotics 22 (January 19, 2017): 507–10. http://dx.doi.org/10.5954/icarob.2017.gs4-3.

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37

Santamaría, David, Cédric Barrière, Antonio Cerqueira, Sarah Hunt, Claudine Tardy, Kathryn Newton, Javier F. Cáceres, Pierre Dubus, Marcos Malumbres, and Mariano Barbacid. "Cdk1 is sufficient to drive the mammalian cell cycle." Nature 448, no. 7155 (August 2007): 811–15. http://dx.doi.org/10.1038/nature06046.

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38

Osada, Hiroyuki. "ChemInform Abstract: Bioprobes for Investigating Mammalian Cell Cycle Control." ChemInform 30, no. 14 (June 16, 2010): no. http://dx.doi.org/10.1002/chin.199914337.

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39

Sandal, T. "Molecular Aspects of the Mammalian Cell Cycle and Cancer." Oncologist 7, no. 1 (February 2002): 73–81. http://dx.doi.org/10.1634/theoncologist.7-1-73.

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40

Almeida, S., M. Chaves, F. Delaunay, and C. Feillet. "A comprehensive reduced model of the mammalian cell cycle." IFAC-PapersOnLine 50, no. 1 (July 2017): 12617–22. http://dx.doi.org/10.1016/j.ifacol.2017.08.2204.

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41

Pearl, Sivan, Oded Sandler, Oded Agam, Itamar Simon, and Nathalie Q. Balaban. "Deterministic Versus Stochastic Variability in the Mammalian Cell Cycle." Biophysical Journal 106, no. 2 (January 2014): 232a. http://dx.doi.org/10.1016/j.bpj.2013.11.1357.

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42

Cooper, S., and J. A. Shayman. "Revisiting retinoblastoma protein phosphorylation during the mammalian cell cycle." Cellular and Molecular Life Sciences 58, no. 4 (April 2001): 580–95. http://dx.doi.org/10.1007/pl00000883.

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43

Farnham, Peggy J., Jill E. Slansky, and Richard Kollamar. "The role of E2F in the mammalian cell cycle." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1155, no. 2 (August 1993): 125–31. http://dx.doi.org/10.1016/0304-419x(93)90001-s.

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44

Cui, Cheng-Bin, Hideaki Kakeya, and Hiroyuki Osada. "Novel mammalian cell cycle inhibitors, spirotryprostatins A and B, produced by Aspergillus fumigatus, which inhibit mammalian cell cycle at G2/M phase." Tetrahedron 52, no. 39 (September 1996): 12651–66. http://dx.doi.org/10.1016/0040-4020(96)00737-5.

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45

Magno, A. C. G., I. L. Oliveira, and J. V. S. Hauck. "Relation Between the Cell Volume and the Cell Cycle Dynamics in Mammalian cell." Journal of Physics: Conference Series 738 (August 2016): 012061. http://dx.doi.org/10.1088/1742-6596/738/1/012061.

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46

Ahn, Eunyong, Praveen Kumar, Dzmitry Mukha, Amit Tzur, and Tomer Shlomi. "Temporal fluxomics reveals oscillations in TCA cycle flux throughout the mammalian cell cycle." Molecular Systems Biology 13, no. 11 (November 2017): 953. http://dx.doi.org/10.15252/msb.20177763.

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47

McClelland, Sarah E. "Single-cell approaches to understand genome organisation throughout the cell cycle." Essays in Biochemistry 63, no. 2 (May 15, 2019): 209–16. http://dx.doi.org/10.1042/ebc20180043.

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Abstract Mammalian genomes are ordered at several scales, ranging from nucleosomes (beads on a string), to topologically associated domains (TADs), laminar associated domains (LADs), and chromosome territories. These are described briefly below and we refer the reader to some recent comprehensive reviews on genome architecture summarising the current state of knowledge of the organisational principles of the nucleus [1,2]. Biological observations from populations of millions of individual cells can reveal consensus behaviour. New methods to study and interpret biological data at the single-cell level have recently been instrumental in revealing new understanding of cell-to-cell variation and novel biology. Here we will summarise the recent advances in single-cell technology that have provided insights into the behaviour of the mammalian genome during a cell cycle. We will focus on the interphase domain structure of chromosomes, including TADs and LADs, and how chromosome architecture changes during the cell cycle. The role of genome architecture relating to gene expression has been reviewed elsewhere [3].
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48

CUI, C. B., H. KAKEYA, and H. OSADA. "ChemInform Abstract: Novel Mammalian Cell Cycle Inhibitors, Cyclotryprostatins A-D, Produced by Aspergillus fumigatus, Which Inhibit Mammalian Cell Cycle at G2/M Phase." ChemInform 28, no. 14 (August 4, 2010): no. http://dx.doi.org/10.1002/chin.199714185.

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49

Lange, B. M., and K. Gull. "A molecular marker for centriole maturation in the mammalian cell cycle." Journal of Cell Biology 130, no. 4 (August 15, 1995): 919–27. http://dx.doi.org/10.1083/jcb.130.4.919.

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The centriole pair in animals shows duplication and structural maturation at specific cell cycle points. In G1, a cell has two centrioles. One of the centrioles is mature and was generated at least two cell cycles ago. The other centriole was produced in the previous cell cycle and is immature. Both centrioles then nucleate one procentriole each which subsequently elongate to full-length centrioles, usually in S or G2 phase. However, the point in the cell cycle at which maturation of the immature centriole occurs is open to question. Furthermore, the molecular events underlying this process are entirely unknown. Here, using monoclonal and polyclonal antibody approaches, we describe for the first time a molecular marker which localizes exclusively to one centriole of the centriolar pair and provides biochemical evidence that the two centrioles are different. Moreover, this 96-kD protein, which we name Cenexin (derived from the Latin, senex for "old man," and Cenexin for centriole) defines very precisely the mature centriole of a pair and is acquired by the immature centriole at the G2/M transition in prophase. Thus the acquisition of Cenexin marks the functional maturation of the centriole and may indicate a change in centriolar potential such as its ability to act as a basal body for axoneme development or as a congregating site for microtubule-organizing material.
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50

Scholz, M., W. Kraft-Weyrather, S. Ritter, and G. Kraft. "Cell Cycle Delays Induced by Heavy Ion Irradiation of Synchronous Mammalian Cells." International Journal of Radiation Biology 66, no. 1 (January 1994): 59–75. http://dx.doi.org/10.1080/09553009414550951.

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