Relevant bibliographies by topics / Mitotic delay

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Mitotic delay'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "Mitotic delay"

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Boronat, Susanna, and Judith L. Campbell. "Mitotic Cdc6 Stabilizes Anaphase-Promoting Complex Substrates by a Partially Cdc28-Independent Mechanism, and This Stabilization Is Suppressed by Deletion of Cdc55." Molecular and Cellular Biology 27, no. 3 (2006): 1158–71. http://dx.doi.org/10.1128/mcb.01745-05.

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ABSTRACT Ectopic expression of Cdc6p results in mitotic delay, and this has been attributed to Cdc6p-mediated inhibition of Cdc28 protein kinase and failure to activate the anaphase-promoting complex (APC). Here we show that endogenous Cdc6p delays a specific subset of mitotic events and that Cdc28 inhibition is not sufficient to account for it. The depletion of Cdc6p in G2/M cells reveals that Cdc6p is rate limiting for the degradation of the APC/Cdc20 substrates Pds1p and Clb2p. Conversely, the premature expression of Cdc6p delays the degradation of APC/Cdc20 substrates. Abolishing Cdc6p/Cdc
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Kang, Dongmin, James Chen, Jim Wong, and Guowei Fang. "The checkpoint protein Chfr is a ligase that ubiquitinates Plk1 and inhibits Cdc2 at the G2 to M transition." Journal of Cell Biology 156, no. 2 (2002): 249–60. http://dx.doi.org/10.1083/jcb.200108016.

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The checkpoint protein Chfr delays entry into mitosis, in the presence of mitotic stress (Scolnick, D.M., and T.D. Halazonetis. 2000. Nature. 406:430–435). We show here that Chfr is a ubiquitin ligase, both in vitro and in vivo. When transfected into HEK293T cells, Myc–Chfr promotes the formation of high molecular weight ubiquitin conjugates. The ring finger domain in Chfr is required for the ligase activity; this domain auto-ubiquitinates, and mutations of conserved residues in this domain abolish the ligase activity. Using Xenopus cell-free extracts, we demonstrated that Chfr delays the entr
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Zachos, George, Michael D. Rainey, and David A. F. Gillespie. "Chk1-Dependent S-M Checkpoint Delay in Vertebrate Cells Is Linked to Maintenance of Viable Replication Structures." Molecular and Cellular Biology 25, no. 2 (2005): 563–74. http://dx.doi.org/10.1128/mcb.25.2.563-574.2005.

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ABSTRACT We investigated mitotic delay during replication arrest (the S-M checkpoint) in DT40 B-lymphoma cells deficient in the Chk1 or Chk2 kinase. We show here that cells lacking Chk1, but not those lacking Chk2, enter mitosis with incompletely replicated DNA when DNA synthesis is blocked, but only after an initial delay. This initial delay persists when S-M checkpoint failure is induced in Chk2−/− cells with the Chk1 inhibitor UCN-01, indicating that it does not depend on Chk1 or Chk2 activity. Surprisingly, dephosphorylation of tyrosine 15 did not accompany Cdc2 activation during premature
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Gong, Delquin, and James E. Ferrell. "The Roles of Cyclin A2, B1, and B2 in Early and Late Mitotic Events." Molecular Biology of the Cell 21, no. 18 (2010): 3149–61. http://dx.doi.org/10.1091/mbc.e10-05-0393.

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Here we have used siRNAs and time-lapse epifluorescence microscopy to examine the roles of various candidate mitotic cyclins in chromatin condensation in HeLa cells. Knocking down cyclin A2 resulted in a substantial (∼7 h) delay in chromatin condensation and histone H3 phosphorylation, and expressing an siRNA-resistant form of cyclin A2 partially rescued chromatin condensation. There was no detectable delay in DNA replication in the cyclin A2 knockdowns, arguing that the delay in chromatin condensation is not secondary to a delay in S-phase completion. Cyclin A2 is required for the activation
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Jelluma, Nannette, Tobias B. Dansen, Tale Sliedrecht, Nicholas P. Kwiatkowski, and Geert J. P. L. Kops. "Release of Mps1 from kinetochores is crucial for timely anaphase onset." Journal of Cell Biology 191, no. 2 (2010): 281–90. http://dx.doi.org/10.1083/jcb.201003038.

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Mps1 kinase activity is required for proper chromosome segregation during mitosis through its involvements in microtubule–chromosome attachment error correction and the mitotic checkpoint. Mps1 dynamically exchanges on unattached kinetochores but is largely removed from kinetochores in metaphase. Here we show that Mps1 promotes its own turnover at kinetochores and that removal of Mps1 upon chromosome biorientation is a prerequisite for mitotic checkpoint silencing. Inhibition of Mps1 activity increases its half-time of recovery at unattached kinetochores and causes accumulation of Mps1 protein
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Markossian, Sarine, Subbulakshmi Suresh, Aysha H. Osmani, and Stephen A. Osmani. "Nup2 requires a highly divergent partner, NupA, to fulfill functions at nuclear pore complexes and the mitotic chromatin region." Molecular Biology of the Cell 26, no. 4 (2015): 605–21. http://dx.doi.org/10.1091/mbc.e14-09-1359.

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Chromatin and nuclear pore complexes (NPCs) undergo dramatic changes during mitosis, which in vertebrates and Aspergillus nidulans involves movement of Nup2 from NPCs to the chromatin region to fulfill unknown functions. This transition is shown to require the Cdk1 mitotic kinase and be promoted prematurely by ectopic expression of the NIMA kinase. Nup2 localizes with a copurifying partner termed NupA, a highly divergent yet essential NPC protein. NupA and Nup2 locate throughout the chromatin region during prophase but during anaphase move to surround segregating DNA. NupA function is shown to
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Szkotnicki, Lee, John M. Crutchley, Trevin R. Zyla, Elaine S. G. Bardes, and Daniel J. Lew. "The Checkpoint Kinase Hsl1p Is Activated by Elm1p-dependent Phosphorylation." Molecular Biology of the Cell 19, no. 11 (2008): 4675–86. http://dx.doi.org/10.1091/mbc.e08-06-0663.

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Saccharomyces cerevisiae cells growing in the outdoor environment must adapt to sudden changes in temperature and other variables. Many such changes trigger stress responses that delay bud emergence until the cells can adapt. In such circumstances, the morphogenesis checkpoint delays mitosis until a bud has been formed. Mitotic delay is due to the Wee1 family mitotic inhibitor Swe1p, whose degradation is linked to bud emergence by the checkpoint kinase Hsl1p. Hsl1p is concentrated at the mother-bud neck through association with septin filaments, and it was reported that Hsl1p activation involv
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Muraoka-Cook, Rebecca S., Laura S. Caskey, Melissa A. Sandahl, et al. "Heregulin-Dependent Delay in Mitotic Progression Requires HER4 and BRCA1." Molecular and Cellular Biology 26, no. 17 (2006): 6412–24. http://dx.doi.org/10.1128/mcb.01950-05.

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ABSTRACT HER4 expression in human breast cancers correlates with a positive prognosis. While heregulin inhibits the growth of HER4-positive breast cancer cells, it does so by undefined mechanisms. We demonstrate that heregulin-induced HER4 activity inhibits cell proliferation and delays G2/M progression of breast cancer cells. While investigating pathways of G2/M delay, we noted that heregulin increased the expression of BRCA1 in a HER4-dependent, HER2-independent manner. Induction of BRCA1 by HER4 occurred independently of the cell cycle. Moreover, BRCA1 expression was elevated in HER4-postiv
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Petsalaki, Eleni, and George Zachos. "Chk2 prevents mitotic exit when the majority of kinetochores are unattached." Journal of Cell Biology 205, no. 3 (2014): 339–56. http://dx.doi.org/10.1083/jcb.201310071.

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The spindle checkpoint delays exit from mitosis in cells with spindle defects. In this paper, we show that Chk2 is required to delay anaphase onset when microtubules are completely depolymerized but not in the presence of relatively few unattached kinetochores. Mitotic exit in Chk2-deficient cells correlates with reduced levels of Mps1 protein and increased Cdk1–tyrosine 15 inhibitory phosphorylation. Chk2 localizes to kinetochores and is also required for Aurora B–serine 331 phosphorylation in nocodazole or unperturbed early prometaphase. Serine 331 phosphorylation contributed to prometaphase
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Chippalkatti, Rohan, Boris Egger, and Beat Suter. "Mms19 promotes spindle microtubule assembly in Drosophila neural stem cells." PLOS Genetics 16, no. 11 (2020): e1008913. http://dx.doi.org/10.1371/journal.pgen.1008913.

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Mitotic divisions depend on the timely assembly and proper orientation of the mitotic spindle. Malfunctioning of these processes can considerably delay mitosis, thereby compromising tissue growth and homeostasis, and leading to chromosomal instability. Loss of functional Mms19 drastically affects the growth and development of mitotic tissues in Drosophila larvae and we now demonstrate that Mms19 is an important factor that promotes spindle and astral microtubule (MT) growth, and MT stability and bundling. Mms19 function is needed for the coordination of mitotic events and for the rapid progres
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Dissertations / Theses on the topic "Mitotic delay"

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LONGHIN, ELEONORA MARTA. "Particulate matter toxicity and health effects : in vitro assessment of the mechanisms of action." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29888.

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Urban airborne particulate matter (PM) is known to increase morbidity and mortality due to cardiopulmonary diseases related to inflammatory processes and genotoxic effects. The study of PM-induced toxicity represents a very important field in order to understand the clinical outcomes and define the most harmful components involved. Despite the researchers’ effort, there are still unresolved questions regarding the cell mechanisms inducing the different adverse effects. Moreover, which PM components are more significant in determining the biological responses is still a debated question, althou
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Hazra, Ditipriya. "Insights into the control of mRNA decay by YTH proteins during the transition from meiosis to mitosis in yeasts." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLX041.

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Aperçu du contrôle de la dégradation des ARNm par les protéines YTHpendant la transition de la méiose à la mitose chez les levures.Le cycle cellulaire est contrôlé par des processus complexes et interconnectés. Un gène est transcrit en ARNm qui est traduit en protéines mais de nombreux processus de régulation travaillent pour contrôler chaque étape de ce processus apparemment simple. Parmi ces points de contrôle, la régulation post-transcriptionnelle est importante, et la formation d'un complexe protéine-ARN peut diriger le destin cellulaire. Parmi ces protéines de liaison à l'ARN, les protéin
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Alakhras, Raghda Said H. "Study of the genotoxicity mechanisms of all-trans retinoic acid and its analogue EA-4." Thesis, 2011. http://nemertes.lis.upatras.gr/jspui/handle/10889/4762.

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Vitamin A and its metabolites retinal and retinoic acid are important molecules for the regulation of normal cellular growth, differentiation and other important functions. Retinoids are known to exert mutagenic as well as antimutagenic activity, although conflicting reports are known. All-trans retinoic acid (ATRA) is used in the treatment of many diseases such as acne, psoriasis and ichthyosis. It is also used in differentiated therapy of acute promyelocytic leukemia; however, it is frequently observed that relapses occur when ATRA is prescribed as maintenance therapy. Therefore, understandi
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Hung, Lin-Chieh, та 洪琳捷. "Cucurbitacin E (CuE) induce GADD45β mediated prolonged delay in mitosis by CDC2/Cyclin B complex disassociated in human brain malignant (GBM) cell lines". Thesis, 2016. http://ndltd.ncl.edu.tw/handle/whq338.

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碩士<br>長榮大學<br>醫學研究所<br>104<br>The Ministry of Health and Welfare, National Health Department, has recently identified malignant tumors as the leading cause of death in Taiwan. Glioblastoma multiforme (GBM) is the most common malignant brain cancer, which accounts for more than half of all brain tumors. GBM has a high mortality rate and is recurrent and resistant to chemotherapy. Common cancer therapies, including surgery, chemotherapy, and targeted therapy, induce many side effects on normal cells and tissues. Extracts of herbal or natural products have proved to be complementary medicine with
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Book chapters on the topic "Mitotic delay"

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McKenna, W. Gillies, and Ruth J. Muschel. "Radiation Induced G2 Delay and Mitotic Cyclin Expression." In The Cell Cycle. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_46.

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Avila-Vales, Eric, Abraham Canul-Pech, Gerardo E. García-Almeida, and Ángel G. C. Pérez. "Global Stability of a Delay Virus Dynamics Model with Mitotic Transmission and Cure Rate." In Studies in Systems, Decision and Control. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49896-2_4.

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Kaszkin, M., and V. Kinzel. "Role of Phospholipid Metabolites in the Cell Cycle Delay Caused by Epidermal Growth Factor at the Transition from G2-Phase to Mitosis in A431 Cells." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_105.

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Conference papers on the topic "Mitotic delay"

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Chagas, Carlos Ricardo, Ricardo Pinto, José Antônio Franco, Gabriela Del Prete Magalhães, and Natascha Carneiro Chagas. "PRIMARY ANGIOSARCOMA OF THE BREAST: A CASE REPORT." In Brazilian Breast Cancer Symposium 2022. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s2096.

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A 39-year-old woman presented to our mastology session with complaints of a right breast lump in 2014, which had grown very slowly and changed in color over the past year (purple). On physical examination, the breast was found in a 12-1 o’clock position, bruise-like, and soft-to-firm in consistency. On mammography, the lump presented diffuse-dense and ultrasonography showed an ill-defined mass and poor-delimited hyperechogenic infiltration in the upper inner portion of the right breast that measured about 7 cm in size. A core biopsy was performed on the suspicious lesion. The pathological resu
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Carney, Bruce, Victoria Caruso, and Lynne Cassimeris. "Abstract C32: Stathmin depletion from cells lacking p53 delays mitotic entry by increasing microtubule stability during interphase." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-c32.

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Harder, N., F. Mora-Bermudez, W. J. Godinez, J. Ellenberg, R. Eils, and K. Rohr. "DETERMINATION OF MITOTIC DELAYS IN 3D FLUORESCENCE MICROSCOPY IMAGES OF HUMAN CELLS USING AN ERROR-CORRECTING FINITE STATE MACHINE." In 2007 4th IEEE International Symposium on Biomedical Imaging: From Nano to Macro. IEEE, 2007. http://dx.doi.org/10.1109/isbi.2007.357034.

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