Journal articles: 'Cell division and cell death'

1

Maddox, Amy Shaub, and Jan M. Skotheim. "Cell cycle, cell division, cell death." Molecular Biology of the Cell 30, no. 6 (March 15, 2019): 732. http://dx.doi.org/10.1091/mbc.e18-12-0819.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Coller, Hilary A., and Arshad Desai. "Cell cycle, cell division, and cell death." Molecular Biology of the Cell 28, no. 6 (March 15, 2017): 693–94. http://dx.doi.org/10.1091/mbc.e16-11-0793.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Lewis, Mark. "Cell differentiation; Cell division, growth and death." Current Opinion in Cell Biology 14, no. 6 (December 2002): 671–72. http://dx.doi.org/10.1016/s0955-0674(02)00396-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Yuan, Junying, and David Morgan. "Cell division, growth and death." Current Opinion in Cell Biology 14, no. 6 (December 2002): 673–75. http://dx.doi.org/10.1016/s0955-0674(02)00397-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Kornbluth, Sally, and Jonathon Pines. "Cell division, growth and death." Current Opinion in Cell Biology 15, no. 6 (December 2003): 645–47. http://dx.doi.org/10.1016/j.ceb.2003.10.017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Reed, Steven I., and Joel H. Rothman. "Cell division, growth and death." Current Opinion in Cell Biology 16, no. 6 (December 2004): 599–601. http://dx.doi.org/10.1016/j.ceb.2004.10.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Kaufmann, Scott, and Mike Tyers. "Cell division, growth and death." Current Opinion in Cell Biology 17, no. 6 (December 2005): 565–67. http://dx.doi.org/10.1016/j.ceb.2005.10.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Earnshaw, William C., and Yuri A. Lazebnik. "Cell division, growth and death." Current Opinion in Cell Biology 18, no. 6 (December 2006): 587–88. http://dx.doi.org/10.1016/j.ceb.2006.10.010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Jackson, Peter K., and Jan-Michael Peters. "Cell division, growth and death." Current Opinion in Cell Biology 19, no. 6 (December 2007): 646–48. http://dx.doi.org/10.1016/j.ceb.2007.11.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Barral, Yves, and Jürgen Knoblich. "Cell division, growth and death." Current Opinion in Cell Biology 20, no. 6 (December 2008): 647–49. http://dx.doi.org/10.1016/j.ceb.2008.10.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Sorger, Peter K., Max Dobles, Regis Tournebize, and Anthony A. Hyman. "Coupling cell division and cell death to microtubule dynamics." Current Opinion in Cell Biology 9, no. 6 (December 1997): 807–14. http://dx.doi.org/10.1016/s0955-0674(97)80081-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Li, Wei, Abhijit Kale, and Nicholas E. Baker. "Oriented Cell Division as a Response to Cell Death and Cell Competition." Current Biology 19, no. 21 (November 2009): 1821–26. http://dx.doi.org/10.1016/j.cub.2009.09.023.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Boissonnas, Alexandre, and Behazine Combadiere. "Interplay between cell division and cell death during TCR triggering." European Journal of Immunology 34, no. 9 (September 2004): 2430–38. http://dx.doi.org/10.1002/eji.200425271.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Poulton, John S., John C. Cuningham, and Mark Peifer. "Acentrosomal Drosophila Epithelial Cells Exhibit Abnormal Cell Division, Leading to Cell Death and Compensatory Proliferation." Developmental Cell 30, no. 6 (September 2014): 731–45. http://dx.doi.org/10.1016/j.devcel.2014.08.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Colnaghi, Rita, and Sally P. Wheatley. "Liaisons between Survivin and Plk1 during Cell Division and Cell Death." Journal of Biological Chemistry 285, no. 29 (April 28, 2010): 22592–604. http://dx.doi.org/10.1074/jbc.m109.065003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

McDonnell, Timothy J. "Cell division versus cell death: A functional model of multistep neoplasia." Molecular Carcinogenesis 8, no. 4 (1993): 209–13. http://dx.doi.org/10.1002/mc.2940080402.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Miska, Eric A. "How microRNAs control cell division, differentiation and death." Current Opinion in Genetics & Development 15, no. 5 (October 2005): 563–68. http://dx.doi.org/10.1016/j.gde.2005.08.005.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Tyson, John J., and Bela Novak. "Control of cell growth, division and death: information processing in living cells." Interface Focus 4, no. 3 (June 6, 2014): 20130070. http://dx.doi.org/10.1098/rsfs.2013.0070.

Full text

Abstract:

By way of surface receptor molecules and internal surveillance mechanisms, the living cell receives information about its external environment and internal state. In light of this information, the cell must determine its most appropriate course of action under the circumstances and initiate the relevant response pathways. Typical responses include growth and division, sexual reproduction, movement, differentiation and programmed cell death. Similar to a digital computer that uses bistable electrical switches to store and process information, the living cell uses bistable biochemical switches to implement its decision-making capabilities. In this review article, we describe some of the lines of thought that led, over the last 50 years, to our current understanding of cellular information processing, particularly related to cell growth, division and death.

APA, Harvard, Vancouver, ISO, and other styles

19

Chai, Yongping, Dong Tian, Yihong Yang, Guoxin Feng, Ze Cheng, Wei Li, and Guangshuo Ou. "Apoptotic regulators promote cytokinetic midbody degradation in C. elegans." Journal of Cell Biology 199, no. 7 (December 17, 2012): 1047–55. http://dx.doi.org/10.1083/jcb.201209050.

Full text

Abstract:

Cell death genes are essential for apoptosis and other cellular events, but their nonapoptotic functions are not well understood. The midbody is an important cytokinetic structure required for daughter cell abscission, but its fate after cell division remains elusive in metazoans. In this paper, we show through live-imaging analysis that midbodies generated by Q cell divisions in Caenorhabditis elegans were released to the extracellular space after abscission and subsequently internalized and degraded by the phagocyte that digests apoptotic Q cell corpses. We further show that midbody degradation is defective in apoptotic cell engulfment mutants. Externalized phosphatidylserine (PS), an engulfment signal for corpse phagocytosis, exists on the outer surface of the midbody, and inhibiting PS signaling delayed midbody clearance. Thus, our findings uncover a novel function of cell death genes in midbody internalization and degradation after cell division.

APA, Harvard, Vancouver, ISO, and other styles

20

Kato, K., T. Awasaki, and K. Ito. "Neuronal programmed cell death induces glial cell division in the adult Drosophila brain." Development 136, no. 1 (November 19, 2008): 51–59. http://dx.doi.org/10.1242/dev.023366.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Orgogozo, Virginie, François Schweisguth, and Yohanns Bellaïche. "Binary cell death decision regulated by unequal partitioning of Numb at mitosis." Development 129, no. 20 (October 15, 2002): 4677–84. http://dx.doi.org/10.1242/dev.129.20.4677.

Full text

Abstract:

An important issue in Metazoan development is to understand the mechanisms that lead to stereotyped patterns of programmed cell death. In particular, cells programmed to die may arise from asymmetric cell divisions. The mechanisms underlying such binary cell death decisions are unknown. We describe here a Drosophila sensory organ lineage that generates a single multidentritic neuron in the embryo. This lineage involves two asymmetric divisions. Following each division, one of the two daughter cells expresses the pro-apoptotic genes reaper and grim and subsequently dies. The protein Numb appears to be specifically inherited by the daughter cell that does not die. Numb is necessary and sufficient to prevent apoptosis in this lineage. Conversely, activated Notch is sufficient to trigger death in this lineage. These results show that binary cell death decision can be regulated by the unequal segregation of Numb at mitosis. Our study also indicates that regulation of programmed cell death modulates the final pattern of sensory organs in a segment-specific manner.

APA, Harvard, Vancouver, ISO, and other styles

22

Trifunovic, Nikola. "Earth’s Arth’s Magnetic Field is Factor that Frges Cell Divsion. Reducing Cell’s Magnetic Characteristics Occurs Aging and Death." Journal of Cancer Research Reviews & Reports 2, no. 1 (March 31, 2020): 1–7. http://dx.doi.org/10.47363/jcrr/2020(2)102.

Full text

Abstract:

Introduction Despite many studies on cell division, formation and treatment of cancer (Ca), there is not full explication of aging and death of cells. Everything in the Earth’s magnetic field (EMF) has paramagnetic and ferromagnetic characteristics. Hence tissue cells and organs have magnetic characteristics (Mc). This paper shows that EMF is a factor that impacts cell division. Anomalous magnetic fields (AMF) and unnatural EMF contributes to continuous cell division that causes cancer. Moreover, it shows that the magnetic characteristics of the nuclei, organelles and substances are tightly related to the metabolism of the cells. The article also explains when the immune system works the best, why it fails in preventing the formation of cancerous cells, and how aging reduces the defense of the organism against intruders. Results EMF influences all parts of the cells magnetic characteristics, which in turn impact metabolism. The sequences of the nucleotides in the construction of DNA and RNA match only by magnetic code. EMF impacts the process of crossing over which causes polymorphism and contributes to the evolution. A factor that stimulates cell division is EMF which boosts the metabolism and the immune system. All manifestations of aging are clearly explained by magnetic properties of cells. Intermolecular magnetic force (Mf) in cell varies because they depend on the number of divisions and temperature. With each division, telomeres lose 100-200 nucleotides which reduce the nucleus Mf and metabolism in the cells. The immune system weakens, because of the impact of Mf. Conclusion Natural EMF is a factor that infulences cell division. Magnetic characteristics of nuclei, organelles and substances enable metabolism in cell. EMF and magnetic characteristics of cells have a decisive contribution to the world’s evolutionary process. During cell division, Mf are decreasing in nucleus so less water enters the cell, resulting in accumulation of toxins. The functions of organs and particularly hormonal activity are declining, which leads to deposition of calcium salts in cartilage (in and around chondrocytes), and lower function of the immune system. All of the above are a manifestation of aging

APA, Harvard, Vancouver, ISO, and other styles

23

Hall, Zach, Tri Luu, Dan Moore, and Garret Yount. "Radiation Response of Cultured Human Cells Is Unaffected by Johrei." Evidence-Based Complementary and Alternative Medicine 4, no. 2 (2007): 191–94. http://dx.doi.org/10.1093/ecam/nel078.

Full text

Abstract:

Johrei has been credited with healing thousands from radiation wounds after the Hiroshima and Nagasaki bombs in 1945. This alternative medical therapy is becoming increasingly popular in the United States, as are other Energy Medicine modalities that purport to influence a universal healing energy. Human brain cells were cultured and exposed to increasing doses of ionizing radiation. Experienced Johrei practitioners directed healing intentionality toward the cells for 30 min from a distance of 20 cm and the fate of the cells was observed by computerized time-lapse microscopy. Cell death and cell divisions were tallied every 30 min before, during and after Johrei treatment for a total of 22.5 h. An equal number of control experiments were conducted in which cells were irradiated but did not receive Johrei treatment. Samples were assigned to treatment conditions randomly and data analysis was conducted in a blinded fashion. Radiation exposure decreased the rate of cell division (cell cycle arrest) in a dose-dependent manner. Division rates were estimated for each 30 min and averaged over 8 independent experiments (4 control and 4 with Johrei treatment) for each of 4 doses of X-rays (0, 2, 4 and 8 Gy). Because few cell deaths were observed, pooled data from the entire observation period were used to estimate death rates. Analysis of variance did not reveal any significant differences on division rate or death rate between treatment groups. Only radiation dose was statistically significant. We found no indication that the radiation response of cultured cells is affected by Johrei treatment.

APA, Harvard, Vancouver, ISO, and other styles

24

Radvanyi, L. G., G. B. Mills, and R. G. Miller. "Religation of the T cell receptor after primary activation of mature T cells inhibits proliferation and induces apoptotic cell death." Journal of Immunology 150, no. 12 (June 15, 1993): 5704–15. http://dx.doi.org/10.4049/jimmunol.150.12.5704.

Full text

Abstract:

Abstract The proliferative response of murine splenic T cells, initially activated by cross-linking the TCR complex with either antibodies, mitogenic lectin, or alloantigen was severely inhibited when the activated cells were recovered and given an additional activation signal by recross-linking the TCR complex, or by adding Ca2+ ionophore and phorbol ester. Under the same conditions, cross-linking other T cell surface determinants such as CD4, CD8, or class I MHC on preactivated T cells had no effect. Assessment of cell viability using vital dye exclusion together with the detection of DNA fragmentation revealed that the reduction of the proliferative responses was associated with an induction of apoptotic-like cell death in the activated T cell population and not due to a blockade of cell division. Accumulation of eosin stained (dead) cells did not occur immediately upon replating the activated cells, but began after a lag period during which at least two cell divisions occurred. In addition, perturbation of T cell proliferation after activation depended on how the cells were initially activated. Only T cells activated in the presence of additional cells found in spleen and lymph node were susceptible to inhibition; T cells activated after nylon wool purification were not susceptible. These results have potential implications for understanding self-tolerance and immunoregulation.

APA, Harvard, Vancouver, ISO, and other styles

25

Vidair, C. A., and W. C. Dewey. "Division-associated and division-independent hyperthermic cell death: Comparison with other cytotoxic agents." International Journal of Hyperthermia 7, no. 1 (January 1991): 51–60. http://dx.doi.org/10.3109/02656739109004976.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Takeuchi, Hiroaki, Teruko Nakazawa, Takeshi Okamoto, Mutsunori Shirai, Mitsuo Kimoto, Mitsuaki Nishioka, Sergio A. Con, Norihito Morimoto, and Tetsuro Sugiura. "Cell Elongation and Cell Death ofHelicobacter pyloriIs Modulated by the Disruption ofcdrA(Cell Division-Related Gene A)." Microbiology and Immunology 50, no. 7 (July 2006): 487–97. http://dx.doi.org/10.1111/j.1348-0421.2006.tb03819.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Loftus, Luke V., Sarah R. Amend, and Kenneth J. Pienta. "Interplay between Cell Death and Cell Proliferation Reveals New Strategies for Cancer Therapy." International Journal of Molecular Sciences 23, no. 9 (April 25, 2022): 4723. http://dx.doi.org/10.3390/ijms23094723.

Full text

Abstract:

Cell division and cell death are fundamental processes governing growth and development across the tree of life. This relationship represents an evolutionary link between cell cycle and cell death programs that is present in all cells. Cancer is characterized by aberrant regulation of both, leading to unchecked proliferation and replicative immortality. Conventional anti-cancer therapeutic strategies take advantage of the proliferative dependency of cancer yet, in doing so, are triggering apoptosis, a death pathway to which cancer is inherently resistant. A thorough understanding of how therapeutics kill cancer cells is needed to develop novel, more durable treatment strategies. While cancer evolves cell-intrinsic resistance to physiological cell death pathways, there are opportunities for cell cycle agnostic forms of cell death, for example, necroptosis or ferroptosis. Furthermore, cell cycle independent death programs are immunogenic, potentially licensing host immunity for additional antitumor activity. Identifying cell cycle independent vulnerabilities of cancer is critical for developing alternative strategies that can overcome therapeutic resistance.

APA, Harvard, Vancouver, ISO, and other styles

28

Loftus, Luke V., Sarah R. Amend, and Kenneth J. Pienta. "Interplay between Cell Death and Cell Proliferation Reveals New Strategies for Cancer Therapy." International Journal of Molecular Sciences 23, no. 9 (April 25, 2022): 4723. http://dx.doi.org/10.3390/ijms23094723.

Full text

Abstract:

Cell division and cell death are fundamental processes governing growth and development across the tree of life. This relationship represents an evolutionary link between cell cycle and cell death programs that is present in all cells. Cancer is characterized by aberrant regulation of both, leading to unchecked proliferation and replicative immortality. Conventional anti-cancer therapeutic strategies take advantage of the proliferative dependency of cancer yet, in doing so, are triggering apoptosis, a death pathway to which cancer is inherently resistant. A thorough understanding of how therapeutics kill cancer cells is needed to develop novel, more durable treatment strategies. While cancer evolves cell-intrinsic resistance to physiological cell death pathways, there are opportunities for cell cycle agnostic forms of cell death, for example, necroptosis or ferroptosis. Furthermore, cell cycle independent death programs are immunogenic, potentially licensing host immunity for additional antitumor activity. Identifying cell cycle independent vulnerabilities of cancer is critical for developing alternative strategies that can overcome therapeutic resistance.

APA, Harvard, Vancouver, ISO, and other styles

29

Handyside, Alan H., and Susan Hunter. "Cell division and death in the mouse blastocyst before implantation." Roux's Archives of Developmental Biology 195, no. 8 (October 1986): 519–26. http://dx.doi.org/10.1007/bf00375893.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Matoz-Fernandez, D. A., Kirsten Martens, Rastko Sknepnek, J. L. Barrat, and Silke Henkes. "Cell division and death inhibit glassy behaviour of confluent tissues." Soft Matter 13, no. 17 (2017): 3205–12. http://dx.doi.org/10.1039/c6sm02580c.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Heinzel, Susanne, Tran Binh Giang, Andrey Kan, Julia M. Marchingo, Bryan K. Lye, Lynn M. Corcoran, and Philip D. Hodgkin. "A Myc-dependent division timer complements a cell-death timer to regulate T cell and B cell responses." Nature Immunology 18, no. 1 (November 7, 2016): 96–103. http://dx.doi.org/10.1038/ni.3598.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Ye, Yixia, Antonella Tinari, Walter Malorni, Richard A. Lockshin, and Zahra Zakeri. "Activation of Cyclin-Dependent Kinase 5 Is a Consequence of Cell Death." Journal of Biomedicine and Biotechnology 2009 (2009): 1–11. http://dx.doi.org/10.1155/2009/805709.

Full text

Abstract:

Cyclin-dependent kinase 5 (Cdk5) is similar to other Cdks but is activated during cell differentiation and cell death rather than cell division. Since activation of Cdk5 has been reported in many situations leading to cell death, we attempted to determine if it was required for any form of cell death. We found that Cdk5 is activated during apoptotic deaths and that the activation can be detected even when the cells continue to secondary necrosis. This activation can occur in the absence of Bim, calpain, or neutral cathepsins. The kinase is typically activated by p25, derived from p35 by calpain-mediated cleavage, but inhibition of calpain does not affect cell death or the activation of Cdk5. Likewise, RNAi-forced suppression of the synthesis of Cdk5 does not affect the incidence or kinetics of cell death. We conclude that Cdk5 is activated as a consequence of metabolic changes that are common to many forms of cell death. Thus its activation suggests processes during cell death that will be interesting or important to understand, but activation of Cdk5 is not necessary for cells to die.

APA, Harvard, Vancouver, ISO, and other styles

33

Uchiumi, Yu, Hisashi Ohtsuki, and Akira Sasaki. "Evolution of self-limited cell division of symbionts." Proceedings of the Royal Society B: Biological Sciences 286, no. 1895 (January 30, 2019): 20182238. http://dx.doi.org/10.1098/rspb.2018.2238.

Full text

Abstract:

In mutualism between unicellular hosts and their endosymbionts, symbiont's cell division is often synchronized with its host's, ensuring the permanent relationship between endosymbionts and their hosts. The evolution of synchronized cell division thus has been considered to be an essential step in the evolutionary transition from symbionts to organelles. However, if symbionts would accelerate their cell division without regard for the synchronization with the host, they would proliferate more efficiently. Thus, it is paradoxical that symbionts evolve to limit their own division for synchronized cell division. Here, we theoretically explore the condition for the evolution of self-limited cell division of symbionts, by assuming that symbionts control their division rate and that hosts control symbionts' death rate by intracellular digestion and nutrient supply. Our analysis shows that symbionts can evolve to limit their own cell division. Such evolution occurs if not only symbiont's but also host's benefit through symbiosis is large. Moreover, the coevolution of hosts and symbionts leads to either permanent symbiosis where symbionts proliferate to keep pace with their host, or the arms race between symbionts that behave as lytic parasites and hosts that resist them by rapid digestion.

APA, Harvard, Vancouver, ISO, and other styles

34

Renno, Toufic, Antoine Attinger, Sabrina Locatelli, Talitha Bakker, Sonia Vacheron, and H. Robson MacDonald. "Cutting Edge: Apoptosis of Superantigen-Activated T Cells Occurs Preferentially After a Discrete Number of Cell Divisions In Vivo." Journal of Immunology 162, no. 11 (June 1, 1999): 6312–15. http://dx.doi.org/10.4049/jimmunol.162.11.6312.

Full text

Abstract:

Abstract Staphylococcal enterotoxins are bacterial products that display superantigen activity in vitro as well as in vivo. For instance, staphylococcal enterotoxin B (SEB) polyclonally activates T cells that bear the Vβ8 gene segment of the TCR. SEB-activated T cells undergo a burst of proliferation that is followed by apoptosis. Using an in vivo adaptation of a fluorescent cell division monitoring technique, we show here that SEB-activated T cells divide asynchronously, and that apoptosis of superantigen-activated T cells is preferentially restricted to cells which have undergone a discrete number of cell divisions. Collectively, our data suggest that superantigen-activated T cells are programmed to undergo a fixed number of cell divisions before undergoing apoptosis. A delayed death program may provide a mechanistic compromise between effector functions and homeostasis of activated T cells.

APA, Harvard, Vancouver, ISO, and other styles

35

Stukalin, Evgeny B., Ivie Aifuwa, Jin Seob Kim, Denis Wirtz, and Sean X. Sun. "Age-dependent stochastic models for understanding population fluctuations in continuously cultured cells." Journal of The Royal Society Interface 10, no. 85 (August 6, 2013): 20130325. http://dx.doi.org/10.1098/rsif.2013.0325.

Full text

Abstract:

For symmetrically dividing cells, large variations in the cell cycle time are typical, even among clonal cells. The consequence of this variation is important in stem cell differentiation, tissue and organ size control, and cancer development, where cell division rates ultimately determine the cell population. We explore the connection between cell cycle time variation and population-level fluctuations using simple stochastic models. We find that standard population models with constant division and death rates fail to predict the level of population fluctuation. Instead, variations in the cell division time contribute to population fluctuations. An age-dependent birth and death model allows us to compute the mean squared fluctuation or the population dispersion as a function of time. This dispersion grows exponentially with time, but scales with the population. We also find a relationship between the dispersion and the cell cycle time distribution for synchronized cell populations. The model can easily be generalized to study populations involving cell differentiation and competitive growth situations.

APA, Harvard, Vancouver, ISO, and other styles

36

Khalkar, Prajakta, Nuria Díaz-Argelich, Juan Antonio Palop, Carmen Sanmartín, and Aristi Fernandes. "Novel Methylselenoesters Induce Programed Cell Death via Entosis in Pancreatic Cancer Cells." International Journal of Molecular Sciences 19, no. 10 (September 20, 2018): 2849. http://dx.doi.org/10.3390/ijms19102849.

Full text

Abstract:

Redox active selenium (Se) compounds have gained substantial attention in the last decade as potential cancer therapeutic agents. Several Se compounds have shown high selectivity and sensitivity against malignant cells. The cytotoxic effects are exerted by their biologically active metabolites, with methylselenol (CH3SeH) being one of the key executors. In search of novel CH3SeH precursors, we previously synthesized a series of methylselenoesters that were active (GI50 < 10 µM at 72 h) against a panel of cancer cell lines. Herein, we refined the mechanism of action of the two lead compounds with the additional synthesis of new analogs (ethyl, pentyl, and benzyl derivatives). A novel mechanism for the programmed cell death mechanism for Se-compounds was identified. Both methylseleninic acid and the novel CH3SeH precursors induced entosis by cell detachment through downregulation of cell division control protein 42 homolog (CDC42) and its downstream effector β1-integrin (CD29). To our knowledge, this is the first time that Se compounds have been reported to induce this type of cell death and is of importance in the characterization of the anticancerogenic properties of these compounds.

APA, Harvard, Vancouver, ISO, and other styles

37

Ashtari, Atefeh, Firoozeh Niazvand, and Layasadat Khorsandi. "Chemotherapy Drugs Based on Solid Lipid Nanoparticles for Breast Cancer Treatment." Medicina 56, no. 12 (December 13, 2020): 694. http://dx.doi.org/10.3390/medicina56120694.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Petrie, H. T., F. Livak, D. Burtrum, and S. Mazel. "T cell receptor gene recombination patterns and mechanisms: cell death, rescue, and T cell production." Journal of Experimental Medicine 182, no. 1 (July 1, 1995): 121–27. http://dx.doi.org/10.1084/jem.182.1.121.

Full text

Abstract:

The antigen-specific receptors of T and B lymphocytes are generated by somatic recombination between noncontiguous gene segments encoding the variable portions of these molecules. The semirandom nature of this process, while desirable for the generation of diversity, has been thought to exact a high price in terms of sterile (out-of-frame) products. Historically, the majority of T lymphocytes generated in mammals were thought to be useless, either because they generated such sterile rearrangements or because the receptors generated did not appropriately recognize self-molecules (i.e., positive and negative selection). In the studies described here, we characterize the onset of T cell receptor (TCR) alpha and beta chain gene rearrangements and quantitate their progression throughout T cell development. The results show that T cell production efficiency is enhanced through (a) rearrangement of TCR-beta chain genes early during T cell development, with selective expansion of those cells possessing in-frame rearrangements; (b) deletion of sterile rearrangements at the TCR-alpha chain locus through ordered (proximal to distal) sequential recombination; and (c) modification of nonselectable alpha/beta heterodimer specificities through generation and expression of new TCR-alpha chains. In addition, we demonstrate strict correlations between successful TCR-beta gene rearrangement, the onset of TCR-alpha gene rearrangement, rapid cell division, and programmed cell death, which together serve to maintain cell turnover and homeostasis during T cell development.

APA, Harvard, Vancouver, ISO, and other styles

39

Li, Q. J., T. M. Pazdera, and J. S. Minden. "Drosophila embryonic pattern repair: how embryos respond to cyclin E-induced ectopic division." Development 126, no. 10 (May 15, 1999): 2299–307. http://dx.doi.org/10.1242/dev.126.10.2299.

Full text

Abstract:

The Drosophila melanogaster embryo ordinarily undergoes thirteen cycles of rapid syncytial division followed by three rounds of cellular division for most cells. Strict regulation of the number of divisions is believed to be essential for normal patterning and development. To determine how the embryo responds to hyperplastic growth, we have examined epidermal development in embryos that experience additional rounds of mitosis as the result of ectopic Cyclin E expression. We observed that the cell density in the epidermis nearly doubled within 1 hour of Cyclin E induction. The spacing and width of the ENGRAILED and wingless stripes was unchanged, but the cell density within the stripes was increased. By 4 hours after Cyclin E induction, the cell density had returned to almost normal values. The embryos developed, albeit more slowly, to produce viable larvae and adults. The excess cells were removed by apoptosis in a reaper-dependent fashion as evidenced by increased reaper expression. Embryos lacking cell death in the abdomen exhibited changes in ENGRAILED expression. In addition, germband retraction and dorsal closure were slower than normal. Ectopic Cyclin E expression in cell-death-deficient embryos exacerbated the germband retraction and ENGRAILED-expression defects.

APA, Harvard, Vancouver, ISO, and other styles

40

Puglisi, Fabio, Alessandro Marco Minisini, Giuseppe Aprile, Fabio Barbone, Palmina Cataldi, Daria Artico, Giuseppe Damante, Carlo Alberto Beltrami, and Carla Di Loreto. "Balance between Cell Division and Cell Death as Predictor of Survival in Patients with Non-Small-Cell Lung Cancer." Oncology 63, no. 1 (2002): 76–83. http://dx.doi.org/10.1159/000065724.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

McKinsey, Timothy A., Chun Li Zhang, and Eric N. Olson. "MEF2: a calcium-dependent regulator of cell division, differentiation and death." Trends in Biochemical Sciences 27, no. 1 (January 2002): 40–47. http://dx.doi.org/10.1016/s0968-0004(01)02031-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Wang, Haohua, Zhanjiang Yuan, Peijiang Liu, and Tianshou Zhou. "Division time-based amplifiers for stochastic gene expression." Molecular BioSystems 11, no. 9 (2015): 2417–28. http://dx.doi.org/10.1039/c5mb00391a.

Full text

Abstract:

While cell-to-cell variability is a phenotypic consequence of gene expression noise, sources of this noise may be complex – apart from intrinsic sources such as the random birth/death of mRNA and stochastic switching between promoter states, there are also extrinsic sources of noise such as cell division where division times are either constant or random.

APA, Harvard, Vancouver, ISO, and other styles

43

Ogawa, Atsushi, Kinji Kitamichi, Kyoko Toyofuku, and Choji Kawashima. "Quantitative Analysis of Cell Division and Cell Death in Seminal Root of Rye under Salt Stress." Plant Production Science 9, no. 1 (January 2006): 56–64. http://dx.doi.org/10.1626/pps.9.56.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Åkesson, Christina, Hanna Lindgren, Ronald W. Pero, Tomas Leanderson, and Fredrik Ivars. "An extract of Uncaria tomentosa inhibiting cell division and NF-κB activity without inducing cell death." International Immunopharmacology 3, no. 13-14 (December 2003): 1889–900. http://dx.doi.org/10.1016/j.intimp.2003.07.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Navarro Quiroz, Elkin, Roberto Navarro Quiroz, Mostapha Ahmad, Lorena Gomez Escorcia, Jose Villarreal, Cecilia Fernandez Ponce, and Gustavo Aroca Martinez. "Cell Signaling in Neuronal Stem Cells." Cells 7, no. 7 (July 14, 2018): 75. http://dx.doi.org/10.3390/cells7070075.

Full text

Abstract:

The defining characteristic of neural stem cells (NSCs) is their ability to multiply through symmetric divisions and proliferation, and differentiation by asymmetric divisions, thus giving rise to different types of cells of the central nervous system (CNS). A strict temporal space control of the NSC differentiation is necessary, because its alterations are associated with neurological dysfunctions and, in some cases, death. This work reviews the current state of the molecular mechanisms that regulate the transcription in NSCs, organized according to whether the origin of the stimulus that triggers the molecular cascade in the CNS is internal (intrinsic factors) or whether it is the result of the microenvironment that surrounds the CNS (extrinsic factors).

APA, Harvard, Vancouver, ISO, and other styles

46

Islam, Mohammad, Satyaki Roy, Sajal Das, and Dipak Barua. "Multicellular Models Bridging Intracellular Signaling and Gene Transcription to Population Dynamics." Processes 6, no. 11 (November 4, 2018): 217. http://dx.doi.org/10.3390/pr6110217.

Full text

Abstract:

Cell signaling and gene transcription occur at faster time scales compared to cellular death, division, and evolution. Bridging these multiscale events in a model is computationally challenging. We introduce a framework for the systematic development of multiscale cell population models. Using message passing interface (MPI) parallelism, the framework creates a population model from a single-cell biochemical network model. It launches parallel simulations on a single-cell model and treats each stand-alone parallel process as a cell object. MPI mediates cell-to-cell and cell-to-environment communications in a server-client fashion. In the framework, model-specific higher level rules link the intracellular molecular events to cellular functions, such as death, division, or phenotype change. Cell death is implemented by terminating a parallel process, while cell division is carried out by creating a new process (daughter cell) from an existing one (mother cell). We first demonstrate these capabilities by creating two simple example models. In one model, we consider a relatively simple scenario where cells can evolve independently. In the other model, we consider interdependency among the cells, where cellular communication determines their collective behavior and evolution under a temporally evolving growth condition. We then demonstrate the framework’s capability by simulating a full-scale model of bacterial quorum sensing, where the dynamics of a population of bacterial cells is dictated by the intercellular communications in a time-evolving growth environment.

APA, Harvard, Vancouver, ISO, and other styles

47

Sherley, James L. "A Kinetic Stem Cell Counting Analysis of the Specific Effects of Cell Culture Medium Growth Factors on Adipose-Derived Mesenchymal Stem Cells." Life 13, no. 3 (February 23, 2023): 614. http://dx.doi.org/10.3390/life13030614.

Full text

Abstract:

A recently described kinetic stem cell (KSC) counting method was used to investigate the stem-cell-specific effects of commercial growth factor supplements used for expanding stem cells in adipose-tissue-derived mesenchymal cell preparations. The supplements were a proprietary growth factor product, a source of fetal bovine serum, two sources of pooled human sera, and two sources of human platelet lysate. KSC counting analyses were performed to monitor effects on the fraction and viability of stem cells in serial cultures with their respective supplements. Serial cultures supplemented with the proprietary growth factor product or fetal bovine serum showed a similar high degree of maintenance of stem cell fraction with passage. In contrast, cultures supplemented with human sera or human platelet lysate showed rapid declines in stem cell fraction. KSC counting was used to discover the cellular basis for the decreasing stem cell fractions. For human platelet lysate, it was attributable to lower rates of self-renewing symmetric stem cell divisions. For human sera, both low rates of symmetric division and high rates of stem cell death were responsible. These results demonstrate the power of the KSC counting method to provide previously inaccessible information for improving future tissue stem cell biomanufacturing.

APA, Harvard, Vancouver, ISO, and other styles

48

Sugimoto, Asako, Ayumi Kusano, Rebecca R. Hozak, W. Brent Derry, Jiangwen Zhu, and Joel H. Rothman. "Many Genomic Regions Are Required for Normal Embryonic Programmed Cell Death in Caenorhabditis elegans." Genetics 158, no. 1 (May 1, 2001): 237–52. http://dx.doi.org/10.1093/genetics/158.1.237.

Full text

Abstract:

Abstract To identify genes involved in programmed cell death (PCD) in Caenorhabditis elegans, we screened a comprehensive set of chromosomal deficiencies for alterations in the pattern of PCD throughout embryonic development. From a set of 58 deficiencies, which collectively remove ∼74% of the genome, four distinct classes were identified. In class I (20 deficiencies), no significant deviation from wild type in the temporal pattern of cell corpses was observed, indicating that much of the genome does not contain zygotic genes that perform conspicuous roles in embryonic PCD. The class II deficiencies (16 deficiencies defining at least 11 distinct genomic regions) led to no or fewer-than-normal cell corpses. Some of these cause premature cell division arrest, probably explaining the diminution in cell corpse number; however, others have little effect on cell proliferation, indicating that the reduced cell corpse number is not a direct result of premature embryonic arrest. In class III (18 deficiencies defining at least 16 unique regions), an excess of cell corpses was observed. The developmental stage at which the extra corpses were observed varied among the class III deficiencies, suggesting the existence of genes that perform temporal-specific functions in PCD. The four deficiencies in class IV (defining at least three unique regions), showed unusually large corpses that were, in some cases, attributable to extremely premature arrest in cell division without a concomitant block in PCD. Deficiencies in this last class suggest that the cell death program does not require normal embryonic cell proliferation to be activated and suggest that while some genes required for cell division might also be required for cell death, others are not. Most of the regions identified by these deficiencies do not contain previously identified zygotic cell death genes. There are, therefore, a substantial number of as yet unidentified genes required for normal PCD in C. elegans.

APA, Harvard, Vancouver, ISO, and other styles

49

Warren, Hilary S., and Beverley F. Kinnear. "Quantitative Analysis of the Effect of CD16 Ligation on Human NK Cell Proliferation." Journal of Immunology 162, no. 2 (January 15, 1999): 735–42. http://dx.doi.org/10.4049/jimmunol.162.2.735.

Full text

Abstract:

Abstract CD16 (FcγRIIIA), the low affinity receptor for IgG, is expressed on the majority of human peripheral blood NK cells. Ligation of CD16 with mAb or immune complexes activates NK cell cytotoxicity and cytokine secretion, and stimulates death of activated NK cells by apoptosis. This study uses NK cells labeled with the stable intracytoplasmic fluorescent dye 5- and 6-carboxyfluorescein diacetate succinimidyl ester to provide quantitative data on the effect of CD16 ligation on NK cell division and NK cell survival. When NK cells are cultured with rIL-2 and CD16 is ligated, NK cell division is stimulated, but there also is a substantial loss of NK progenitor cells. When NK cell proliferation is stimulated by coculture with γ-irradiated MM-170 malignant melanoma cells and rIL-2, CD16 ligation enhances entry of NK cells into division. In some cases, CD16 ligation is essential for NK cell proliferation stimulated by MM-170 cells. In these cultures, there is no loss of NK progenitor cells. This study demonstrates that CD16 is an activation receptor for NK cell proliferation, and suggests that cellular costimulation alters the balance between NK cell death and NK cell proliferation stimulated by CD16 ligation.

APA, Harvard, Vancouver, ISO, and other styles

50

Altieri, Dario C. "Survivin and IAP proteins in cell-death mechanisms." Biochemical Journal 430, no. 2 (August 13, 2010): 199–205. http://dx.doi.org/10.1042/bj20100814.

Full text

Abstract:

From the realization that cell number homoeostasis is fundamental to the biology of all metazoans, and that deregulation of this process leads to human diseases, enormous interest has been devoted over the last two decades to map the requirements of cell death and cell survival. This effort has led to tangible progress, and we can now chart with reasonable accuracy complex signalling circuitries controlling cell-fate decisions. Some of this knowledge has translated into novel therapeutics, and the outcome of these strategies, especially in cancer, is eagerly awaited. However, the function of cell-death modifiers have considerably broadened over the last few years, and these molecules are increasingly recognized as arbiters of cellular homoeostasis, from cell division, to intracellular signalling to cellular adaptation. This panoply of functions is best exemplified by members of the IAP (inhibitor of apoptosis) gene family, molecules originally narrowly defined as endogenous caspase inhibitors, but now firmly positioned at the crossroads of multiple normal and transformed cellular responses.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Cell division and cell death'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles