Academic literature on the topic 'Endomitose'
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Journal articles on the topic "Endomitose"
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Geddis, Amy E. "Shedding light on endomitosis." Blood 116, no. 13 (September 30, 2010): 2202–3. http://dx.doi.org/10.1182/blood-2010-07-293449.
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Jackson, Carl W. "Megakaryocyte endomitosis: A review." International Journal of Cell Cloning 8, no. 4 (1990): 224–26. http://dx.doi.org/10.1002/stem.5530080405.
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Zimmet, J. M., D. Ladd, C. W. Jackson, P. E. Stenberg, and K. Ravid. "A role for cyclin D3 in the endomitotic cell cycle." Molecular and Cellular Biology 17, no. 12 (December 1997): 7248–59. http://dx.doi.org/10.1128/mcb.17.12.7248.
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Platelets, essential for thrombosis and hemostasis, develop from polyploid megakaryocytes which undergo endomitosis. During this cell cycle, cells experience abrogated mitosis and reenter a phase of DNA synthesis, thus leading to endomitosis. In the search for regulators of the endomitotic cell cycle, we have identified cyclin D3 as an important regulatory factor. Of the D-type cyclins, cyclin D3 is present at high levels in megakaryocytes undergoing endomitosis and is markedly upregulated following exposure to the proliferation-, maturation-, and ploidy-promoting factor, Mpl ligand. Transgenic mice in which cyclin D3 is overexpressed in the platelet lineage display a striking increase in endomitosis, similar to changes seen following Mpl ligand administration to normal mice. Electron microscopy analysis revealed that unlike such treated mice, however, D3 transgenic mice show a poor development of demarcation membranes, from which platelets are believed to fragment, and no increase in platelets. Thus, while our model supports a key role for cyclin D3 in the endomitotic cell cycle, it also points to the unique role of Mpl ligand in priming megakaryocytes towards platelet fragmentation. The role of cyclin D3 in promoting endomitosis in other lineages programmed to abrogate mitosis will need further exploration.
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Pleines, Irina, and Bernhard Nieswandt. "RhoA/ROCK guides NMII on the way to MK polyploidy." Blood 128, no. 26 (December 29, 2016): 3025–26. http://dx.doi.org/10.1182/blood-2016-11-746685.
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A unique feature of megakaryocyte maturation is the switch from mitosis to replication of DNA without cell division, a process termed endomitosis. In this issue of Blood, Roy et al elegantly demonstrate that RhoA/ROCK signaling is critical for the differential activity and localization of nonmuscle myosin (NM) IIA and IIB isoforms at the megakaryocyte cleavage furrow, a key step in the induction of endomitosis.1
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Bermejo, Rodrigo, Nuria Vilaboa, and Carmela Calés. "Regulation of CDC6, Geminin, and CDT1 in Human Cells that Undergo Polyploidization." Molecular Biology of the Cell 13, no. 11 (November 2002): 3989–4000. http://dx.doi.org/10.1091/mbc.e02-04-0217.
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Endomitosis is the process by which mammalian megakaryocytes become polyploid during terminal differentiation. As in other endoreplicating cells, cyclin-cdk complexes are distinctly regulated, probably to overcome the strict mechanisms that prevent rereplication in most somatic cells. We have asked whether key factors involved in the assembly and licensing of replication origins are equally regulated during endomitosis. Cdc6, cdt1, and geminin expression was analyzed during differentiation of two human megakaryoblastic cell lines, HEL and K562, which respectively do and do not establish endoreplication cycles. Geminin was downregulated, whereas cdt1 levels were maintained upon differentiation of both cell lines, independently of whether cells entered extra S-phases. In contrast, cdc6 was present and remained nuclear only in differentiated endoreplicating cells. Interestingly, cdc6 protein expression was reestablished in K562 cells that underwent endomitosis after transient or stable cyclin E overexpression. The high levels of cyclin E reached in these cells appeared to influence the stabilization of cdc6 protein rather than its RNA transcription rate. Finally, cdc6 overexpression drove HEL cells into endoreplication cycles in the absence of differentiation stimuli. Our results show that both cdt1 and cdc6 are differentially regulated during megakaryocytic differentiation and suggest an active role of cdc6 in endomitosis.
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Langstein, Joachim, Jan Michel, and Herbert Schwarz. "CD137 Induces Proliferation and Endomitosis in Monocytes." Blood 94, no. 9 (November 1, 1999): 3161–68. http://dx.doi.org/10.1182/blood.v94.9.3161.
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Abstract Peripheral monocytes are short-lived and are replenished from hematopoietic stem cells whose proliferation is believed to be confined to the bone marrow. Human peripheral monocytes are assumed not to be able to proliferate. In this study we show that CD137 (ILA/4-1BB), a member of the tumor necrosis factor receptor family, induces a widespread and profound proliferation of human peripheral monocytes. Macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor are essential, but not sufficient for proliferation. Additional soluble autocrine factors induced by CD137 are required. Induction of proliferation is mediated via reverse signaling through a CD137 ligand, expressed constitutively by peripheral monocytes. The ability of CD137 to induce proliferation in human peripheral monocytes is not shared by any other known molecule.
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Langstein, Joachim, Jan Michel, and Herbert Schwarz. "CD137 Induces Proliferation and Endomitosis in Monocytes." Blood 94, no. 9 (November 1, 1999): 3161–68. http://dx.doi.org/10.1182/blood.v94.9.3161.421k31_3161_3168.
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Peripheral monocytes are short-lived and are replenished from hematopoietic stem cells whose proliferation is believed to be confined to the bone marrow. Human peripheral monocytes are assumed not to be able to proliferate. In this study we show that CD137 (ILA/4-1BB), a member of the tumor necrosis factor receptor family, induces a widespread and profound proliferation of human peripheral monocytes. Macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor are essential, but not sufficient for proliferation. Additional soluble autocrine factors induced by CD137 are required. Induction of proliferation is mediated via reverse signaling through a CD137 ligand, expressed constitutively by peripheral monocytes. The ability of CD137 to induce proliferation in human peripheral monocytes is not shared by any other known molecule.
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Carow, Catherine E., Norma E. Fox, and Kenneth Kaushansky. "Kinetics of endomitosis in primary murine megakaryocytes." Journal of Cellular Physiology 188, no. 3 (2001): 291–303. http://dx.doi.org/10.1002/jcp.1120.
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Therman, Eeva, Gloria E. Sarto, and Evelyn M. Kuhn. "The course of endomitosis in human cells." Cancer Genetics and Cytogenetics 19, no. 3-4 (January 1986): 301–10. http://dx.doi.org/10.1016/0165-4608(86)90059-2.
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Therman, Eeva, Carter Denniston, Usko Nieminen, Dolores A. Buchler, and Sakari Timonen. "X chromatin, endomitoses, and mitotic abnormalities in human cervical cancer." Cancer Genetics and Cytogenetics 16, no. 1 (March 1985): 1–11. http://dx.doi.org/10.1016/0165-4608(85)90072-x.
Full textDissertations / Theses on the topic "Endomitose"
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VITRAT, NATACHA. "Etude des endomitoses dans les megacaryocytes humains." Paris 7, 2000. http://www.theses.fr/2000PA077232.
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Au cours de leur differenciation, les megacaryocytes (mks) commutent leur systeme de proliferation par mitose vers un systeme de division atypique consistant en une duplication de l'adn sans division nucleaire et cytoplasmique. Ce processus, appele endomitose, aboutit a des cellules polyploides mononucleees. Mon travail de these visait a une meilleure comprehension de ce phenomene de polyploidisation. Nous avons demontre par un abord descriptif que les endomitoses dans les mks humains sont des divisions cellulaires incompletes avec absence des temps tardifs, y compris la cytocinese. Les fuseaux mitotiques observes dans les mks polyploides en metaphase sont multipolaires et presentent une organisation complexe (chaque aster pouvant participer a plusieurs sous-fuseaux) probablement a l'origine de la migration asymetrique des chromosomes a l'anaphase. Leur structure compacte suggere par ailleurs une anomalie dans l'elongation des microtubules conduisant a un eloignement insuffisant des poles (anaphase b). Les deux lots chromosomiques, trop rapproches en l'absence d'etirement de la cellule, se retrouveraient confines au sein d'un seul noyau lors de la reformation de l'enveloppe nucleaire en fin d'endomitose. Les mecanismes cellulaires et moleculaires responsables du processus de polyploidisation sont encore mal connus. Nous avons explore en priorite l'hypothese d'une deregulation dans l'expression de certains regulateurs du cycle cellulaire. Nous avons ainsi mis en evidence par un abord biochimique dans les mks polyploides : 1) la presence d'un complexe cdk1/cycline b1 fonctionnel, dont l'activite necessaire a l'accomplissement d'une vraie mitose corrobore le modele que nous proposons pour decrire les endomitoses. 2) une expression anormalement elevee de cycline d3 et de p21 dans les mks polyploides. D'apres des travaux preliminaires, la surexpression de p21 assurerait l'arret des endomitoses. 3) l'existence d'un point de controle metaphase/anaphase normal.
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Perazza, Daniel. "Les hormones gibberellines et les gènes kaktus controlent les endoréplications dans les trichomes d'Arabidopsis thaliana." Université Joseph Fourier (Grenoble ; 1971-2015), 1997. http://www.theses.fr/1997GRE10058.
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Au terme d'une recherche de mutants affectes dans la reponse aux phytohormones gibberellines (ga) chez arabidopsis thaliana, une nouvelle fonction des ga dans la formation des trichomes et le controle des endoreplications a ete mise en evidence. Les trichomes foliaires sont des cellules epidermiques specialisees a trois branches qui demandent 4 endoreplications, ammenant l'adn nucleaire de 2c a 32c. Le developpement des trichomes est un modele pour l'etude de la specification et de la differenciation cellulaire chez les plantes. Chez le mutant gal-3, deficient dans la biosynthese des ga, les trichomes ne se developpent pas et les cellules epidermiques subissent moins d'endoreplications. Au contraire, le mutant spy-5, chez qui la reponse aux ga est activee, developpe des trichomes a branches surnumeraires ayant subi une endoreplication supplementaire (64c). La surexpression du facteur de transcription gl1 (de type myb) restaure la formation des trichomes et la polysomatie de l'epiderme chez le mutant gal-3, demontrant que les ga controlent ces processus via gl1. L'activation de gl1 est transcriptionnelle puisque le gene rapporteur gusa place sous le controle du promoteur pgl1 ne s'exprime qu'en presence de ga. Par contre, le facteur de transcription ttg, aussi implique dans l'initiation des trichomes, semble present chez les plantes gal-3. Les gibberellines controlent donc positivement l'initiation et la morphogenese des trichomes, ainsi que le niveau de polysomatie de l'epiderme via le gene gl1. De nouveaux mutants kaktus developpant des trichomes a branches surnumeraires ont ete isoles a partir d'une collection de graines d'arabidopsis traitees a l'ems. Le contenu en adn de ces trichomes mutants est de 64c, ce qui montre qu'ils ont subi une endoreplication supplementaire. La polysomatie des cellules foliaires des couches internes n'est pas alteree, ce qui indique que les genes kak sont specifiques des cellules epidermiques, voire des seuls trichomes. Les sept mutants kak etudies definissent au moins trois loci independants et deux d'entre eux ont ete cartographies. L'additivite de phenotype entre certaines mutations kak ainsi que l'additivite observee chez les doubles mutants kak,try indiquent l'existence d'au moins trois voies independantes d'inhibition d'une cinquieme endoreplication. Chacune de ces voies est dependante du gene gl3.
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Wiggins, Claire Susan. "Megakaryocyte endomitosis : the expression of glycoproteins Ib and IIIa in megakaryocyte differentiation and their role in endomitosis in correlation with cell cycle proteins." Thesis, Queen Mary, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405874.
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Gendre-Gilles, Laure. "Régulation de l'arrêt des endomitoses et de la différenciation mégacaryocytaire terminale : rôle de p19 INK4D et de MAL." Paris 7, 2009. http://www.theses.fr/2009PA077075.
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La mégacaryopoïèse est le système de production et de régulation de la production des plaquettes et se divise en trois étapes: étape pendant laquelle les cellules font des mitoses, polyploïdisation par endomitose, libération des plaquettes par fragmentation du cytoplasme. Le travail de ma thèse a concerné la mégacaryopoïèse à travers l'étude de 2 protéines : MAL et p19INK4D (p19). MAL qui est le cofacteur transcriptionnel de SRF est aussi impliqué dans une translocation retrouvée dans les leucémies aiguës à mégacaryoblastes. Nous avons montré que son expression augmente avec la différenciation mégacaryocytaire et qu'en son absence, l'organisation du cytosquelette est fortement perturbée. Dans ces conditions, la migration et la formation des proplaquettes sont inhibées. Deux gènes présentent une expression fortement diminuée en l'absence de MAL dans les mégacaryocytes (MK), MMP-9 et MYL-9. Ces 2 gènes sont directement régulés par le complexe transcriptionnel MAL/SRF. Le défaut de migration que nous avons mis en évidence pourrait être lié à la diminution de MMP-9. Nous avons enfin montré qu'un défaut quantitatif de MYL-9 altère la formation des proplaquettes. Le seul inhibiteur du cycle cellulaire dont l'expression augmente linéairement avec la ploïdie est p19. Nous avons montré que cette protéine constitue un lien entre l'arrêt des endomitoses et la différenciation terminale des MK. Ces résultats ont été confirmés par l'étude des souris p79⁻⁄⁻A chez qui la ploïdie modale des MK est fortement augmentée. Enfin, l'expression de p19 est régulée par le facteur de transcription hématopoïétique AML-1, impliqué à différents niveaux de l'hématopoïèseMegakaryopoiesis is the System of platelet production divided in three steps: mitosis step, increase in ploidy level by endomitosis, platelet sheeding by cytoplasm fragmentation. My work focused on megakaryopoiesis through the study of two proteins: MAL and p19INK4D (p19). MAL is a transcriptional co-activator of SRF. In acute megakaryoblastic leukemia, thé MAL gene is translocated and fused with the gene encoding OTT. We showed that MAL expression increases during the megakaryocyte (MK) differentiation. MAL knockdown in MK progenitors reduced the percentage of cells forming filopodia, lamellipodia and stress fibers, and reduced proplatelet formation. MAL repression led to dysmorphic MK with disorganized demarcation membranes and alpha granules heterogeneously scattered in the cytoplasm. Gene expression profiling revealed a decrease in MMP9 and MYL9 expression after MAL inhibition. Chromatin immunoprecipitation in MK showed that the MAL/SRF complex directly regulates MYL9 and MMP9. MK migration was considerably decreased after MAL knock down, implicating MMP9 in migration. Finally, the use of a shRNA to decrease MYL9 expression showed that MYL9 was involved in proplatelet formation. P19 expression was increased during ploidization. We showed that p19 knockdown led to an increase in the mean ploidy of human MKs. This increase in ploidy was associated with a decrease in the more mature MKpopulation. Inversely, p19 overexpression resulted in a decrease in mean ploidy level. Confirming these results, bone marrow MKs from p19 KO mice exhibited an increase in mean ploidy level. Finally we showed that p19 is directly regulated by the hematopoietic transcription factor AML1
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Watanabe, Hiroshi. "Psychosine-triggered endomitosis is modulated by membrane sphingolipids through regulation of phosphoinositide 4,5-bisphosphate production at the cleavage furrow." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225518.
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Hsin-JouTseng and 曾馨柔. "The mechanism of endomitosis inhibited by PKA isoforms." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/88115520362452965535.
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碩士國立成功大學
藥理學研究所
101
Ployploidy, a cell containing more than two paired set of chromosome, can be observed in megakaryocytes, hepatocytes and muscular cells of human. The phenomenon of polyploidy, also known as endomitosis, is composed of interruption of cytokinesis and re-synthesis of DNA. The abnormality of endomitosis in megakarypoiesis can cause the platelet disorder. In megakarypoiesis, it is reported that cyclin B1 and CDK1 are correlated to interruption of cytokinesis. Cyclin D and cyclin E promote the entrance of S phase and DNA re-synthesis. It’s recently found that cAMP-PKA signaling can inhibit endomitosis through E2A-p21 axis. However, the alternation of those factors at different cell cycle stage in endomitotic cells and the specific mechanism of cAMP inhibition are not completely known. In this study, we observed alternation of cyclins and related factors in PMA-induced endomitosis with and without forskolin-mediated inhibition in HEL cells through Acurri C6 flow cytometry. The results showed that elevation of cAMP levels by forskolin indeed inhibits PMA-induced endomitosis, including the decrease of cell size and cell ploidy. In cytokinesis-related factors, we found number of cyclin B1-expressed-cells at G2/M phase has similar change under PMA treatment and PMA/forskolin co-treatment. However, cAMP can inhibit PMA-induced cyclin B1 expression in these cells at late stage. Furthermore, cdc2Y15 levels have no significantly difference between two groups. In factors related to S-phase entry, cyclin D3 levels are incresed after PMA treatment, but the increase can be inhibited by pre-treatment of cAMP. Moreover, cyclin E is significantly increased after PMA treatment, but forskolin had no effect on the expression induced by PMA. The results showed that cyclin D3 and p21 may be the determinant factors in forskolin-mediated inhibition. Recent studies revealed that cAMP inhibited endomitosis through PKA. To uncover the downstream PKA isoforms of cAMP, we reduced the expression of PKA isoforms with shRNA. The results showed that complete knockdown of PKAIIA can abolish the inhibition on PMA-induced endomitosis by forskolin. However, partial knockdown of PKAIIA can not reverse cAMP-mediated inhibition. Knockdown of PKAIA is not able to withstand the inhibitory effect of cAMP. Therefore, PKAIIA is the downstream factor of cAMP during the inhibition. Endomitosis is related to the production of functional platelet in human. Knowing the specific mechanisms and the downstream factors may contribute to the treatment strategy and drug design in the future.
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Huang, Ding Yuan, and 黃鼎元. "Characterization of Disabled-2 in the control of endocytosis and endomitosis during megakaryocytopoiesis." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/98515637417123654288.
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碩士長庚大學
醫學生物技術暨檢驗學系
101
DAB2 is known as an adaptor protein, because it N terminal have PTB domain and C terminal have SH3 domain. This protein has two isoform p82, p59. This protein can regulate cell’s physiology function, including cell adhesion, gene transcription and differentiation of hematopoietic stem cell. Megakaryocyte is progenitor of platelet, and the megakaryocyte is differentiated by stem cell that stimulated by thrombopoietin (TPO) and activate specific transcription factor. In this differentiate pathway, these cells can produce protein by itself or endocytose from extracellular matrix, and their chromosome replication with no cytokinesis called endocytosis. In this study, we would like to find whether DAB2 participated in megakaryocyte differentiation. And focus on two tips. First, is DAB2 participated in fibrinogen endocytosis. Second, is DAB2 participated in endomitosis. Here, we show that used SD rat as our animal model and lentivirus-drived knockdown system to knockdown DAB2 in bone marrow. And we found that knockdown DAB2 decrease megakaryocyte number and the ability of fibrinogen endocytosis in mature megakaryocyte. However, the DAB2 protein knockdown also reduces the ability of endomitosis. These result indicate DAB2 participated in megakaryocyte differentiation and DAB2 also participated in fibrinogen endocytosis and endomitosis.
Book chapters on the topic "Endomitose"
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"Endomitosis." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 605. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_5306.
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Maynard Smith, John, and Eors Szathmary. "The origin of sex and the nature of species." In The Major Transitions in Evolution. Oxford University Press, 1997. http://dx.doi.org/10.1093/oso/9780198502944.003.0013.
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By sex in eukaryotes, we understand a more-or-less regular succession of meiosis and syngamy. A natural consequence of this is the alternation of haploid and diploid phases in the life cycle. Eukaryotic sex significantly differs from prokaryotic sex in two crucial respects: the cellular mechanisms are quite different, and the transfer of genetic material in prokaryotes is less frequent and more localized (Maynard Smith et al., 1991). However, there seems to be significant continuity in the molecular mechanisms: sex in either case requires recombination enzymes, many of which are active in repair of damaged DNA as well. Thus, it seems plausible that recombinational repair was a preadaptation for sexual recombination. We mention in passing that there is a theory that selection for the recombinational repair of doublestrand DNA damage is responsible for the current maintenance of eukaryotic sex (Bernstein et al., 1981, 1988), but there are severe theoretical as well as factual problems with this theory; we will mention some factual difficulties later. Although an alternation of haploid and diploid phases follows from sex, a clue to the origin problem may lie in the idea that this alternation existed before the evolution of sexual recombination proper. The first hint that this may have been so comes from the classic paper by Cleveland (1947), where he proposed that the haploid-diploid cycle may have started with a spontaneous diploidization by endomitosis: that is, without syngamy. His suggestions were based on original observations on primitive flagellates (hypermastigotes and polymastigotes). Among them, Barbulanympha has a regular endomitosis-meiosis cycle. Margulis & Sagan (1986) called renewed attention to Cleveland’s ideas. In particular, they argued that the alternation of ploidy phases could have a primarily ecological explanation: if the environment alternates in some important factors, this may drive a haploid-diploid cycle, provided the phases are adaptations to different environments. For example, diploids have a smaller relative surface area than haploids, which may confer higher metabolic efficiency. We shall come back to such ideas soon. We focus first on the possible cellular mechanisms connecting the two phases. It is important that some protists have a one-step rather than a two-step meiosis: after syngamy, the two homologous chromosomes become disjunct without premeiotic doubling.
Conference papers on the topic "Endomitose"
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Kosoff, Rachelle E., and Jonathan Chernoff. "Abstract A40: Megakaryocyte endomitosis requires Pak2 to regulate actin and microtubule networks." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-a40.
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