Gotowe bibliografie tematyczne / Bipolar Mitotic Spindle - Mammalian Cells

Spis treści

Artykuły w czasopismach
Rozprawy doktorskie
Części książek

Gotowa bibliografia na temat „Bipolar Mitotic Spindle - Mammalian Cells”

Autor: Grafiati

Data publikacji: 7 września 2023

Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych

Wybierz rodzaj źródła:

Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Bipolar Mitotic Spindle - Mammalian Cells”.

Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.

Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.

Artykuły w czasopismach na temat "Bipolar Mitotic Spindle - Mammalian Cells"

Vaisberg, E. A., M. P. Koonce i J. R. McIntosh. "Cytoplasmic dynein plays a role in mammalian mitotic spindle formation." Journal of Cell Biology 123, nr 4 (15.11.1993): 849–58. http://dx.doi.org/10.1083/jcb.123.4.849.

Pełny tekst źródła

Streszczenie:

The formation and functioning of a mitotic spindle depends not only on the assembly/disassembly of microtubules but also on the action of motor enzymes. Cytoplasmic dynein has been localized to spindles, but whether or how it functions in mitotic processes is not yet known. We have cloned and expressed DNA fragments that encode the putative ATP-hydrolytic sites of the cytoplasmic dynein heavy chain from HeLa cells and from Dictyostelium. Monospecific antibodies have been raised to the resulting polypeptides, and these inhibit dynein motor activity in vitro. Their injection into mitotic mammalian cells blocks the formation of spindles in prophase or during recovery from nocodazole treatment at later stages of mitosis. Cells become arrested with unseparated centrosomes and form monopolar spindles. The injected antibodies have no detectable effect on chromosome attachment to a bipolar spindle or on motions during anaphase. These data suggest that cytoplasmic dynein plays a unique and important role in the initial events of bipolar spindle formation, while any later roles that it may play are redundant. Possible mechanisms of dynein's involvement in mitosis are discussed.

Style APA, Harvard, Vancouver, ISO itp.

Gayek, A. Sophia, i Ryoma Ohi. "Kinetochore-microtubule stability governs the metaphase requirement for Eg5". Molecular Biology of the Cell 25, nr 13 (lipiec 2014): 2051–60. http://dx.doi.org/10.1091/mbc.e14-03-0785.

Pełny tekst źródła

Streszczenie:

The mitotic spindle is a bipolar, microtubule (MT)-based cellular machine that segregates the duplicated genome into two daughter cells. The kinesin-5 Eg5 establishes the bipolar geometry of the mitotic spindle, but previous work in mammalian cells suggested that this motor is unimportant for the maintenance of spindle bipolarity. Although it is known that Kif15, a second mitotic kinesin, enforces spindle bipolarity in the absence of Eg5, how Kif15 functions in this capacity and/or whether other biochemical or physical properties of the spindle promote its bipolarity have been poorly studied. Here we report that not all human cell lines can efficiently maintain bipolarity without Eg5, despite their expressing Kif15. We show that the stability of chromosome-attached kinetochore-MTs (K-MTs) is important for bipolar spindle maintenance without Eg5. Cells that efficiently maintain bipolar spindles without Eg5 have more stable K-MTs than those that collapse without Eg5. Consistent with this observation, artificial destabilization of K-MTs promotes spindle collapse without Eg5, whereas stabilizing K-MTs improves bipolar spindle maintenance without Eg5. Our findings suggest that either rapid K-MT turnover pulls poles inward or slow K-MT turnover allows for greater resistance to inward-directed forces.

Style APA, Harvard, Vancouver, ISO itp.

Gillett, Emily S., Christopher W. Espelin i Peter K. Sorger. "Spindle checkpoint proteins and chromosome–microtubule attachment in budding yeast". Journal of Cell Biology 164, nr 4 (9.02.2004): 535–46. http://dx.doi.org/10.1083/jcb.200308100.

Pełny tekst źródła

Streszczenie:

Accurate chromosome segregation depends on precise regulation of mitosis by the spindle checkpoint. This checkpoint monitors the status of kinetochore–microtubule attachment and delays the metaphase to anaphase transition until all kinetochores have formed stable bipolar connections to the mitotic spindle. Components of the spindle checkpoint include the mitotic arrest defective (MAD) genes MAD1–3, and the budding uninhibited by benzimidazole (BUB) genes BUB1 and BUB3. In animal cells, all known spindle checkpoint proteins are recruited to kinetochores during normal mitoses. In contrast, we show that whereas Saccharomyces cerevisiae Bub1p and Bub3p are bound to kinetochores early in mitosis as part of the normal cell cycle, Mad1p and Mad2p are kinetochore bound only in the presence of spindle damage or kinetochore lesions that interfere with chromosome–microtubule attachment. Moreover, although Mad1p and Mad2p perform essential mitotic functions during every division cycle in mammalian cells, they are required in budding yeast only when mitosis goes awry. We propose that differences in the behavior of spindle checkpoint proteins in animal cells and budding yeast result primarily from evolutionary divergence in spindle assembly pathways.

Style APA, Harvard, Vancouver, ISO itp.

Orjalo, Arturo V., Alexei Arnaoutov, Zhouxin Shen, Yekaterina Boyarchuk, Samantha G. Zeitlin, Beatriz Fontoura, Steven Briggs, Mary Dasso i Douglass J. Forbes. "The Nup107-160 Nucleoporin Complex Is Required for Correct Bipolar Spindle Assembly". Molecular Biology of the Cell 17, nr 9 (wrzesień 2006): 3806–18. http://dx.doi.org/10.1091/mbc.e05-11-1061.

Pełny tekst źródła

Streszczenie:

The Nup107-160 complex is a critical subunit of the nuclear pore. This complex localizes to kinetochores in mitotic mammalian cells, where its function is unknown. To examine Nup107-160 complex recruitment to kinetochores, we stained human cells with antisera to four complex components. Each antibody stained not only kinetochores but also prometaphase spindle poles and proximal spindle fibers, mirroring the dual prometaphase localization of the spindle checkpoint proteins Mad1, Mad2, Bub3, and Cdc20. Indeed, expanded crescents of the Nup107-160 complex encircled unattached kinetochores, similar to the hyperaccumulation observed of dynamic outer kinetochore checkpoint proteins and motors at unattached kinetochores. In mitotic Xenopus egg extracts, the Nup107-160 complex localized throughout reconstituted spindles. When the Nup107-160 complex was depleted from extracts, the spindle checkpoint remained intact, but spindle assembly was rendered strikingly defective. Microtubule nucleation around sperm centrosomes seemed normal, but the microtubules quickly disassembled, leaving largely unattached sperm chromatin. Notably, Ran-GTP caused normal assembly of microtubule asters in depleted extracts, indicating that this defect was upstream of Ran or independent of it. We conclude that the Nup107-160 complex is dynamic in mitosis and that it promotes spindle assembly in a manner that is distinct from its functions at interphase nuclear pores.

Style APA, Harvard, Vancouver, ISO itp.

Lingle, W., J. Salisbury, S. Barrett, V. Negron i C. Whitehead. "The Role of the Centrosome in Development and Progression of Breast Cancer". Microscopy and Microanalysis 7, S2 (sierpień 2001): 582–83. http://dx.doi.org/10.1017/s1431927600028981.

Pełny tekst źródła

Streszczenie:

The centrosome is the major microtubule organizing center in most mammalian cells, and as such it determines the number, polarity, and spatial distribution of microtubules (MTs). Interphase MTs, together with actin and intermediate filaments, constitute the cell's cytoskeleton, which dynamically maintains cell polarity and tissue architecture. Interphase cells begin Gl of the cell cycle with one centrosome. During S phase, the centrosome duplicates concomitantly with DNA replication. Duplicated centrosomes usually remain in close proximity to one another until late G2, at which time they separate and then move during prophase to become the poles that organize the bipolar mitotic spindle. During the G2/M transition, interphase MTs depolymerize and a new population of highly dynamic mitotic MTs are nucleated at the spindle poles. The bipolar mitotic spindle apparatus constitutes the machinery that partitions and separates sister chromatids equally between two daughter cells.

Style APA, Harvard, Vancouver, ISO itp.

Guizzunti, Gianni, i Joachim Seemann. "Mitotic Golgi disassembly is required for bipolar spindle formation and mitotic progression". Proceedings of the National Academy of Sciences 113, nr 43 (10.10.2016): E6590—E6599. http://dx.doi.org/10.1073/pnas.1610844113.

Pełny tekst źródła

Streszczenie:

During mitosis, the mammalian Golgi vesiculates and, upon partitioning, reassembles in each daughter cell; however, it is not clear whether the disassembly process per se is important for partitioning or is merely an outcome of mitotic entry. Here, we show that Golgi vesiculation is required for progression to metaphase. To prevent Golgi disassembly, we expressed HRP linked to a Golgi-resident protein and acutely triggered the polymerization of 3,3′-diaminobenzidine (DAB) in the Golgi lumen. The DAB polymer does not affect interphase cell viability, but inhibits Golgi fragmentation by nocodazole and brefeldin A and also halts cells in early mitosis. The arrest is Golgi specific and does not occur when DAB is polymerized in the endosomes. Cells with a DAB polymer in the Golgi enter mitosis normally but arrest with an intact Golgi clustered at a monopolar spindle and an active spindle assembly checkpoint (SAC). Mitotic progression is restored upon centrosome depletion by the Polo-like kinase 4 inhibitor, centrinone, indicating that the link between the Golgi and the centrosomes must be dissolved to reach metaphase. These results demonstrate that Golgi disassembly is required for mitotic progression because failure to vesiculate the Golgi activates the canonical SAC. This requirement suggests that cells actively monitor Golgi integrity in mitosis.

Style APA, Harvard, Vancouver, ISO itp.

Yan, Kaowen, Li Li, Xiaojian Wang, Ruisha Hong, Ying Zhang, Hua Yang, Ming Lin i in. "The deubiquitinating enzyme complex BRISC is required for proper mitotic spindle assembly in mammalian cells". Journal of Cell Biology 210, nr 2 (20.07.2015): 209–24. http://dx.doi.org/10.1083/jcb.201503039.

Pełny tekst źródła

Streszczenie:

Deubiquitinating enzymes (DUBs) negatively regulate protein ubiquitination and play an important role in diverse physiological processes, including mitotic division. The BRCC36 isopeptidase complex (BRISC) is a DUB that is specific for lysine 63–linked ubiquitin hydrolysis; however, its biological function remains largely undefined. Here, we identify a critical role for BRISC in the control of mitotic spindle assembly in cultured mammalian cells. BRISC is a microtubule (MT)-associated protein complex that predominantly localizes to the minus ends of K-fibers and spindle poles and directly binds to MTs; importantly, BRISC promotes the assembly of functional bipolar spindle by deubiquitinating the essential spindle assembly factor nuclear mitotic apparatus (NuMA). The deubiquitination of NuMA regulates its interaction with dynein and importin-β, which are required for its function in spindle assembly. Collectively, these results uncover BRISC as an important regulator of the mitotic spindle assembly and cell division, and have important implications for the development of anticancer drugs targeting BRISC.

Style APA, Harvard, Vancouver, ISO itp.

Hauf, Silke, Richard W. Cole, Sabrina LaTerra, Christine Zimmer, Gisela Schnapp, Rainer Walter, Armin Heckel, Jacques van Meel, Conly L. Rieder i Jan-Michael Peters. "The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore–microtubule attachment and in maintaining the spindle assembly checkpoint". Journal of Cell Biology 161, nr 2 (21.04.2003): 281–94. http://dx.doi.org/10.1083/jcb.200208092.

Pełny tekst źródła

Streszczenie:

The proper segregation of sister chromatids in mitosis depends on bipolar attachment of all chromosomes to the mitotic spindle. We have identified the small molecule Hesperadin as an inhibitor of chromosome alignment and segregation. Our data imply that Hesperadin causes this phenotype by inhibiting the function of the mitotic kinase Aurora B. Mammalian cells treated with Hesperadin enter anaphase in the presence of numerous monooriented chromosomes, many of which may have both sister kinetochores attached to one spindle pole (syntelic attachment). Hesperadin also causes cells arrested by taxol or monastrol to enter anaphase within <1 h, whereas cells in nocodazole stay arrested for 3–5 h. Together, our data suggest that Aurora B is required to generate unattached kinetochores on monooriented chromosomes, which in turn could promote bipolar attachment as well as maintain checkpoint signaling.

Style APA, Harvard, Vancouver, ISO itp.

Roig, Joan, Aaron Groen, Jennifer Caldwell i Joseph Avruch. "Active Nercc1 Protein Kinase Concentrates at Centrosomes Early in Mitosis and Is Necessary for Proper Spindle Assembly". Molecular Biology of the Cell 16, nr 10 (październik 2005): 4827–40. http://dx.doi.org/10.1091/mbc.e05-04-0315.

Pełny tekst źródła

Streszczenie:

The Nercc1 protein kinase autoactivates in vitro and is activated in vivo during mitosis. Autoactivation in vitro requires phosphorylation of the activation loop at threonine 210. Mitotic activation of Nercc1 in mammalian cells is accompanied by Thr210 phosphorylation and involves a small fraction of total Nercc1. Mammalian Nercc1 coimmunoprecipitates γ-tubulin and the activated Nercc1 polypeptides localize to the centrosomes and spindle poles during early mitosis, suggesting that active Nercc has important functions at the microtubular organizing center during cell division. To test this hypothesis, we characterized the Xenopus Nercc1 orthologue (XNercc). XNercc endogenous to meiotic egg extracts coprecipitates a multiprotein complex that contains γ-tubulin and several components of the γ-tubulin ring complex and localizes to the poles of spindles formed in vitro. Reciprocally, immunoprecipitates of the γ-tubulin ring complex polypeptide Xgrip109 contain XNercc. Immunodepletion of XNercc from egg extracts results in delayed spindle assembly, fewer bipolar spindles, and the appearance of aberrant microtubule structures, aberrations corrected by addition of purified recombinant XNercc. XNercc immunodepletion also slows aster assembly induced by Ran-GTP, producing Ran-asters of abnormal size and morphology. Thus, Nercc1 contributes to both the centrosomal and the chromatin/Ran pathways that collaborate in the organization of a bipolar spindle.

Style APA, Harvard, Vancouver, ISO itp.

Mountain, Vicki, Calvin Simerly, Louisa Howard, Asako Ando, Gerald Schatten i Duane A. Compton. "The Kinesin-Related Protein, Hset, Opposes the Activity of Eg5 and Cross-Links Microtubules in the Mammalian Mitotic Spindle". Journal of Cell Biology 147, nr 2 (18.10.1999): 351–66. http://dx.doi.org/10.1083/jcb.147.2.351.

Pełny tekst źródła

Streszczenie:

We have prepared antibodies specific for HSET, the human homologue of the KAR3 family of minus end-directed motors. Immuno-EM with these antibodies indicates that HSET frequently localizes between microtubules within the mammalian metaphase spindle consistent with a microtubule cross-linking function. Microinjection experiments show that HSET activity is essential for meiotic spindle organization in murine oocytes and taxol-induced aster assembly in cultured cells. However, inhibition of HSET did not affect mitotic spindle architecture or function in cultured cells, indicating that centrosomes mask the role of HSET during mitosis. We also show that (acentrosomal) microtubule asters fail to assemble in vitro without HSET activity, but simultaneous inhibition of HSET and Eg5, a plus end-directed motor, redresses the balance of forces acting on microtubules and restores aster organization. In vivo, centrosomes fail to separate and monopolar spindles assemble without Eg5 activity. Simultaneous inhibition of HSET and Eg5 restores centrosome separation and, in some cases, bipolar spindle formation. Thus, through microtubule cross-linking and oppositely oriented motor activity, HSET and Eg5 participate in spindle assembly and promote spindle bipolarity, although the activity of HSET is not essential for spindle assembly and function in cultured cells because of centrosomes.

Style APA, Harvard, Vancouver, ISO itp.

Więcej źródeł

Rozprawy doktorskie na temat "Bipolar Mitotic Spindle - Mammalian Cells"

Kato, Takayuki. "Localization of a mammalian homolog of diaphanous, mDia1, to the mitotic spindle in HeLa cells". Kyoto University, 2001. http://hdl.handle.net/2433/150544.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

Tulu, Ustun Serdar. "Contribution of non-centrosomal microtubules to mitotic spindle assembly in mammalian cells". 2007. https://scholarworks.umass.edu/dissertations/AAI3275811.

Pełny tekst źródła

Streszczenie:

In mammalian cells, the formation of a bipolar spindle is an essential process as any mistake in the segregation of chromosomes can result in aneuploidy, an outcome that can be detrimental to the organism. Microtubules are the key structures required for the success of this operation, as they are the main constituents of mammalian bipolar spindles. Centrosomes also play an important role, being the primary source of microtubules. Although centrosomes are dispensable for the formation of bipolar spindles, the fidelity of this process decreases when they are experimentally removed. One way to explain how a bipolar spindle assembles has been the ‘search and capture’ model. According to this model, microtubules emanating from centrosomes search the cytoplasm for kinetochores, which capture microtubules laterally. Once captured, the chromosomes move towards the spindle equator, ultimately resulting in a bipolar spindle. In the research presented here, our aim is to understand the role of microtubule sources other than centrosomes in centrosome-containing mammalian cells. We use different techniques and manipulations to bypass the presence of the centrosomes in order to identify the origin of these sources and their importance. We mainly use LLCPK1, pig kidney epithelial, cells stably expressing GFP tagged proteins, such as alpha-tubulin, to follow microtubules and their associated proteins in live cells. Two main sources of microtubules other than centrosomes have been documented: peripheral microtubules and kinetochores. Peripheral, non-centrosome-associated microtubules were originally thought to disassemble at the beginning of mitosis. However, we found that they form bundles and contribute to the forming spindle. Our model for spindle assembly, which incorporates these peripheral microtubules, and the ‘search and capture’ model are not mutually exclusive; instead, they compliment each other in the formation of bipolar spindles. Lastly, we develop a spindle assembly assay in which centrosomes and kinetochores can be observed separately in mammalian cells. The data documented here demonstrate that kinetochores also contribute to the formation of bipolar spindles by nucleating and organizing microtubules. In addition, TPX2, a microtubule associated protein, is revealed as one of the requirements for microtubule formation and organization at the kinetochores.

Style APA, Harvard, Vancouver, ISO itp.

Części książek na temat "Bipolar Mitotic Spindle - Mammalian Cells"

Decarreau, Justin, Jonathan Driver, Charles Asbury i Linda Wordeman. "Rapid Measurement of Mitotic Spindle Orientation in Cultured Mammalian Cells". W Methods in Molecular Biology, 31–40. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0329-0_2.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

Oferujemy zniżki na wszystkie plany premium dla autorów, których prace zostały uwzględnione w tematycznych zestawieniach literatury. Skontaktuj się z nami, aby uzyskać unikalny kod promocyjny!