subject:(cell cycle)

University of Georgia

1. Burbage, Christopher Dieter. Picocyanobacterial cellular physiology and trophic interaction with a heterotrophic nanoflagellate.

Degree: PhD, Marine Sciences, 2007, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/burbage_christopher_d_200712_phd

► Prochlorococcus and Synechococcus are two closely related picocyanobacteria that together are responsible for a large proportion of the total primary production in open ocean environments.… (more)

▼ Prochlorococcus and Synechococcus are two closely related picocyanobacteria that together are responsible for a large proportion of the total primary production in open ocean environments. Relatively little is known about the growth rates and trophic interactions of these organisms in the field. This dissertation focuses on characterizing the growth physiology of representative strains of Prochlorococcus (MIT9312) and Synechococcus (WH8103), and exploring the potential role of these organisms as prey for a model heterotrophic nanoflagellate (Paraphysomonas imperforata). Two proposed approaches for assessing picocyanobacterial growth rates in the field would use either cellular RNA content or population DNA distributions as the basis for estimating growth rate. In this study I show that biomass-normalized RNA content is linearly related to growth rate in Synechococcus WH8103. Re-analysis of previously published data suggests that many (though not all) other Synechococcus strains behave similarly, and therefore that cellular RNA may represent a reasonable approach for estimating in situ growth rates in natural Synechococcus populations. However, the non-linear relationship observed here (and in previous studies) for Prochlorococcus indicates that application of the approach may be problematic in this case. The cell cycle study in this dissertation is the first to systematically characterize the relationship between growth rate and cell cycle behavior in Prochlorococcus. I show that Prochlorococcus and Synechococcus display a notable degree of similarity with respect to this behavior. The combined duration of the replication and post-replication phases varied with growth rate in both species, suggesting that typical strategies for calculating growth rates from DNA data may need to be modified. Furthermore, I found that cell mass at the start of DNA replication decreased with increasing growth rate, indicating that the initiation of chromosome replication may not be a simple function of cell biomass, as previously suggested. Regarding picocyanobacteria as potential prey items for heterotrophic flagellates, I found that P. imperforata could graze and grow upon both these strains, but that Synechococcus was the preferred prey. This preference was flexible, however, and could be modulated by the ratio of prey types and/or the overall concentration of available prey. Advisors/Committee Members: Brian J. Binder.

Subjects/Keywords: cell cycle

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APA (6^th Edition):

Burbage, C. D. (2007). Picocyanobacterial cellular physiology and trophic interaction with a heterotrophic nanoflagellate. (Doctoral Dissertation). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/burbage_christopher_d_200712_phd

Chicago Manual of Style (16^th Edition):

Burbage, Christopher Dieter. “Picocyanobacterial cellular physiology and trophic interaction with a heterotrophic nanoflagellate.” 2007. Doctoral Dissertation, University of Georgia. Accessed January 22, 2020. http://purl.galileo.usg.edu/uga_etd/burbage_christopher_d_200712_phd.

MLA Handbook (7^th Edition):

Burbage, Christopher Dieter. “Picocyanobacterial cellular physiology and trophic interaction with a heterotrophic nanoflagellate.” 2007. Web. 22 Jan 2020.

Vancouver:

Burbage CD. Picocyanobacterial cellular physiology and trophic interaction with a heterotrophic nanoflagellate. [Internet] [Doctoral dissertation]. University of Georgia; 2007. [cited 2020 Jan 22]. Available from: http://purl.galileo.usg.edu/uga_etd/burbage_christopher_d_200712_phd.

Council of Science Editors:

Burbage CD. Picocyanobacterial cellular physiology and trophic interaction with a heterotrophic nanoflagellate. [Doctoral Dissertation]. University of Georgia; 2007. Available from: http://purl.galileo.usg.edu/uga_etd/burbage_christopher_d_200712_phd

University of Manitoba

2. Baxter, Shannon A. Mechanisms of PROX1 mediated regulation of the lymphatic endothelial cell cycle.

Degree: Biochemistry and Medical Genetics, 2010, University of Manitoba

URL: http://hdl.handle.net/1993/14917

► The homeobox transcription factor PROX1 is the mammalian ortholog of the Drosophila gene Prospero. Expression of PROX1 in a subset of venous endothelial cells changes… (more)

▼ The homeobox transcription factor PROX1 is the mammalian ortholog of the Drosophila gene Prospero. Expression of PROX1 in a subset of venous endothelial cells changes their fate to lymphatic endothelial cells (LEC). PROX1 is required for lymphatic development as Prox1 null mice lack all lymphatic vasculature. PROX1 has been shown to have cell-type dependent roles in regulating the cell cycle. We hypothesize that PROX1 functions as a key cell cycle regulator in LECs and promotes their cell cycle progression. In this study, immunocytochemistry, western blotting and luciferase assays were used to characterize PROX1 mediated activation of the mouse Ccne1 promoter. Following deletion of the Prospero 1 domain (PD1∆), the resulting PROX1 protein is localized to both the nucleus and the cytoplasm. We have determined that PROX1 requires both E2F binding sites located in the Ccne1 promoter to activate transcription of the gene. We observed that siRNA knockdown of Prox1 reduced CYCLIN E1 protein levels as well as decreased cellular proliferation in LECs. In contrast, overexpression of a version of PROX1 in which the homeodomain and Prospero domain 2 (HDPD2Δ) were deleted increased CYCLIN E1 protein levels in human umbilical vein endothelial cells (HUVEC), but resulted in the arrest of cells in the G1 phase. We have also established that PROX1 is phosphorylated in primary human LECs. We have shown a role for the PD1 domain in mediating PROX1 subcellular localization and we have observed that the expression of the HDPD2Δ version of PROX1 blocks proliferation in HUVECs. We are the first to demonstrate a role for PROX1 as a transcriptional co-activator and to establish that PROX1 is phosphorylated in LECs. Advisors/Committee Members: Wigle, Jeffrey (Biochemistry and Medical Genetics) (supervisor), Eisenstat, David (Biochemistry and Medical Genetics) Gibson, Spencer (Biochemistry and Medical Genetics) Mowat, Micheal (Biochemistry and Medical Genetics) Dixon, Ian (Physiology) (examiningcommittee).

Subjects/Keywords: Lymphatic endothelial cell; Cell cycle

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APA (6^th Edition):

Baxter, S. A. (2010). Mechanisms of PROX1 mediated regulation of the lymphatic endothelial cell cycle. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/14917

Chicago Manual of Style (16^th Edition):

Baxter, Shannon A. “Mechanisms of PROX1 mediated regulation of the lymphatic endothelial cell cycle.” 2010. Masters Thesis, University of Manitoba. Accessed January 22, 2020. http://hdl.handle.net/1993/14917.

MLA Handbook (7^th Edition):

Baxter, Shannon A. “Mechanisms of PROX1 mediated regulation of the lymphatic endothelial cell cycle.” 2010. Web. 22 Jan 2020.

Vancouver:

Baxter SA. Mechanisms of PROX1 mediated regulation of the lymphatic endothelial cell cycle. [Internet] [Masters thesis]. University of Manitoba; 2010. [cited 2020 Jan 22]. Available from: http://hdl.handle.net/1993/14917.

Council of Science Editors:

Baxter SA. Mechanisms of PROX1 mediated regulation of the lymphatic endothelial cell cycle. [Masters Thesis]. University of Manitoba; 2010. Available from: http://hdl.handle.net/1993/14917

Hong Kong University of Science and Technology

3. Tang, Rui LIFS. Anti-apoptotic functions of BCL-W, MCL-1, and A1 in mitotic cell death.

Degree: 2016, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-100402 ; https://doi.org/10.14711/thesis-b1626285 ; http://repository.ust.hk/ir/bitstream/1783.1-100402/1/th_redirect.html

► Anti-microtubule agents activate the spindle-assembly checkpoint by perturbing spindle formation and trapping cells in mitosis. Whether cells undergo mitotic cell death subsequently is an important… (more)

Subjects/Keywords: Cell cycle ; Mitosis ; Cell death

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APA (6^th Edition):

Tang, R. L. (2016). Anti-apoptotic functions of BCL-W, MCL-1, and A1 in mitotic cell death. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-100402 ; https://doi.org/10.14711/thesis-b1626285 ; http://repository.ust.hk/ir/bitstream/1783.1-100402/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tang, Rui LIFS. “Anti-apoptotic functions of BCL-W, MCL-1, and A1 in mitotic cell death.” 2016. Thesis, Hong Kong University of Science and Technology. Accessed January 22, 2020. http://repository.ust.hk/ir/Record/1783.1-100402 ; https://doi.org/10.14711/thesis-b1626285 ; http://repository.ust.hk/ir/bitstream/1783.1-100402/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tang, Rui LIFS. “Anti-apoptotic functions of BCL-W, MCL-1, and A1 in mitotic cell death.” 2016. Web. 22 Jan 2020.

Vancouver:

Tang RL. Anti-apoptotic functions of BCL-W, MCL-1, and A1 in mitotic cell death. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2016. [cited 2020 Jan 22]. Available from: http://repository.ust.hk/ir/Record/1783.1-100402 ; https://doi.org/10.14711/thesis-b1626285 ; http://repository.ust.hk/ir/bitstream/1783.1-100402/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tang RL. Anti-apoptotic functions of BCL-W, MCL-1, and A1 in mitotic cell death. [Thesis]. Hong Kong University of Science and Technology; 2016. Available from: http://repository.ust.hk/ir/Record/1783.1-100402 ; https://doi.org/10.14711/thesis-b1626285 ; http://repository.ust.hk/ir/bitstream/1783.1-100402/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Hong Kong

4. Ruan, Yafei. Investigating the regulation of UHRF1 in cell cycle.

Degree: Master of Medical Sciences, 2015, University of Hong Kong

URL: Ruan, Y. [阮雅菲]. (2015). Investigating the regulation of UHRF1 in cell cycle. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659412 ; http://hdl.handle.net/10722/221484

►

UHRF1 is a multi-domain protein with multiple functions in mammalian cells including maintenance of DNA methylation, histone modification, DNA damage et al. UHRF1 itself also… (more)

Subjects/Keywords: Cell cycle; Ubiquitin

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APA (6^th Edition):

Ruan, Y. (2015). Investigating the regulation of UHRF1 in cell cycle. (Masters Thesis). University of Hong Kong. Retrieved from Ruan, Y. [阮雅菲]. (2015). Investigating the regulation of UHRF1 in cell cycle. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659412 ; http://hdl.handle.net/10722/221484

Chicago Manual of Style (16^th Edition):

Ruan, Yafei. “Investigating the regulation of UHRF1 in cell cycle.” 2015. Masters Thesis, University of Hong Kong. Accessed January 22, 2020. Ruan, Y. [阮雅菲]. (2015). Investigating the regulation of UHRF1 in cell cycle. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659412 ; http://hdl.handle.net/10722/221484.

MLA Handbook (7^th Edition):

Ruan, Yafei. “Investigating the regulation of UHRF1 in cell cycle.” 2015. Web. 22 Jan 2020.

Vancouver:

Ruan Y. Investigating the regulation of UHRF1 in cell cycle. [Internet] [Masters thesis]. University of Hong Kong; 2015. [cited 2020 Jan 22]. Available from: Ruan, Y. [阮雅菲]. (2015). Investigating the regulation of UHRF1 in cell cycle. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659412 ; http://hdl.handle.net/10722/221484.

Council of Science Editors:

Ruan Y. Investigating the regulation of UHRF1 in cell cycle. [Masters Thesis]. University of Hong Kong; 2015. Available from: Ruan, Y. [阮雅菲]. (2015). Investigating the regulation of UHRF1 in cell cycle. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659412 ; http://hdl.handle.net/10722/221484

University of Hong Kong

5. Xie, Si. Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation.

Degree: PhD, 2015, University of Hong Kong

URL: Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643

► Faithful transmission of genetic information from parent cells to daughter cells is crucial for the survival of all eukaryotic organisms. To achieve high fidelity of… (more)

▼ Faithful transmission of genetic information from parent cells to daughter cells is crucial for the survival of all eukaryotic organisms. To achieve high fidelity of inheritance, cells need to resist constant insults on genome from both environmental and endogenous sources which may lead to loss of genome integrity. Eukaryotic cells have evolved the surveillance mechanisms termed checkpoints for DNA damage detection and response. The S-phase checkpoint is activated by DNA damages during the replication process. Although the cascade of the S-phase checkpoint activation has been revealed to a great extent, the molecular basis of its intricate protein interaction network is not well understood. My studies focus on the interaction network of the replication fork protection complex (FPC) including Tipin and Timeless, which preserves the replication fork structure and facilitates the sufficient phosphorylation of Chk1 in the S-phase checkpoint activation. In Chapter 2, X-ray crystallography and biochemical binding assays were employed to define the complete RPA32 recognition mode shared by multiple RPA32-interacting proteins, which represents the molecular mechanism of Tipin recruitment by RPA32. Tipin has been considered as a constitutive binding partner of Timeless. In Chapter 3, my study focused on Timeless and has for the first time identified the physical interaction between Timeless and PARP-1. The crystal structures were determined for the Timeless PARP-1-binding domain in free form and in complex with PARP-1 catalytic domain which is the first reported PARP-1 crystal structure in complex with any of its interacting proteins. In vitro PARP-1 auto-modification assay indicates that the association of Timeless does not interfere with PARP-1 enzymatic activity. Interestingly, Timeless specifically interacts with PARP-1, but not PARP-2 or PARP-3. The PARP-1 and Timeless interaction raises the possibility that PARP-1 functions together with Timeless in the S-phase checkpoint pathway, while the preliminary data also supports that Timeless functions in homologous recombination for DSB repair which has not been demonstrated before. The second part of my work presented in Chapter 4 focuses on human UHRF1. UHRF1 has been extensively characterized for its function in histone methylation and DNA methylation maintenance, while the molecular mechanism of histone H3 recognition by UHRF1 remains elusive. The crystal structure of UHRF1 PHD finger in complex with histone H3 N-terminal tail is presented, demonstrating that PHD finger of UHRF1 recognizes the N-terminus of histone H3 containing unmodified R2 and K4. Structural analysis together with biochemical assays indicated that UHRF1 PHD finger and the adjacent dTudor domain act as one functional unit to specifically recognize the H3K9me3 mark. Based on these observations, a novel model is proposed demonstrating that histone methylation and DNA methylation reinforce each other through UHRF1, which is supported by experimental evidence from other groups in later…

Subjects/Keywords: Cell cycle; DNA replication

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APA (6^th Edition):

Xie, S. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Doctoral Dissertation). University of Hong Kong. Retrieved from Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643

Chicago Manual of Style (16^th Edition):

Xie, Si. “Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation.” 2015. Doctoral Dissertation, University of Hong Kong. Accessed January 22, 2020. Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643.

MLA Handbook (7^th Edition):

Xie, Si. “Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation.” 2015. Web. 22 Jan 2020.

Vancouver:

Xie S. Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2020 Jan 22]. Available from: Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643.

Council of Science Editors:

Xie S. Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: Xie, S. [谢思]. (2015). Structural and biochemical study of replication fork protection complex in S-phase checkpoint activation. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576755 ; http://dx.doi.org/10.5353/th_b5576755 ; http://hdl.handle.net/10722/228643

University of Louisville

6. Stallons, Lindsey Jay, 1983-. DNA polymerase iota promotes G2/M checkpoint activation and genetic stability after UV-induced DNA damage.

Degree: PhD, 2011, University of Louisville

URL: 10.18297/etd/1369 ; https://ir.library.louisville.edu/etd/1369

► Unrepaired DNA damage poses a serious threat to the genetic stability of a replicating cell. One mechanism of tolerating this damage is translesion DNA synthesis… (more)

▼ Unrepaired DNA damage poses a serious threat to the genetic stability of a replicating cell. One mechanism of tolerating this damage is translesion DNA synthesis (TLS), in which an accessory polymerase synthesizes DNA directly across from a damaged template. TLS is carried out by polymerase ? (Pol ?), 1, K, and REV1 in the Y-family and Pol ? in the B-family. Pol ? has the well-characterized ability to perform accurate bypass of the most common UV-induced DNA lesion; loss of Pol ? results in hypermutability and severely increased risk of skin cancer. The high mutation frequency in Pol ?-deficient cells has been attributed to the mutagenic TLS activity of Pol ?. Deletion of Pol ? in the Pol ?-deficient background results in greatly reduced UV-induced mutation frequencies, but unexpectedly the double knockout mice develop cancer faster than mice deficient in Pol ? alone. This unexpected finding suggests that Pol may have a cellular role outside of TLS, which we investigated using a gene expression approach. Pol ? -proficient and -deficient cells showed markedly different mRNA and microRNA expression changes after UV treatment. Bioinformatics analysis revealed that the G2/M checkpoint was the main point of divergence in the transcriptional response. Western blotting showed that G2/M markers were increased and G1/S markers were decreased 24 hours after UV treatment in Pol ?-proficient cells, indicating an active checkpoint. Loss of Pol ? reversed these trends. FACS analysis of cell cycle kinetics showed a time-dependent increase in the number of aneuploid Pol ?-deficient cells after UV treatment; this degree of genetic instability was not seen in Pol ?-proficient cells. We also examined the effects of Pol ? on UV carcinogenesis in isogenic mice lacking Xpa, a gene central to the repair of UV-induced DNA damage. Loss of Pol ? caused a trend towards reduced tumor latency (p=0.057), while Pol ?-deficiency caused a highly significant reduction in tumor latency (p < 0.01). These results indicate that Pol ? plays a role in G2/M checkpoint regulation and suppressing UV carcinogenesis. At the cost of frequent point mutations, Pol ? could help cells avoid death by resolving stalled replication forks and preventing double strand breaks. Advisors/Committee Members: States, J. Christopher.

Subjects/Keywords: Mutagenesis; Cell cycle; Polymerase iota

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APA (6^th Edition):

Stallons, Lindsey Jay, 1. (2011). DNA polymerase iota promotes G2/M checkpoint activation and genetic stability after UV-induced DNA damage. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/1369 ; https://ir.library.louisville.edu/etd/1369

Chicago Manual of Style (16^th Edition):

Stallons, Lindsey Jay, 1983-. “DNA polymerase iota promotes G2/M checkpoint activation and genetic stability after UV-induced DNA damage.” 2011. Doctoral Dissertation, University of Louisville. Accessed January 22, 2020. 10.18297/etd/1369 ; https://ir.library.louisville.edu/etd/1369.

MLA Handbook (7^th Edition):

Stallons, Lindsey Jay, 1983-. “DNA polymerase iota promotes G2/M checkpoint activation and genetic stability after UV-induced DNA damage.” 2011. Web. 22 Jan 2020.

Vancouver:

Stallons, Lindsey Jay 1. DNA polymerase iota promotes G2/M checkpoint activation and genetic stability after UV-induced DNA damage. [Internet] [Doctoral dissertation]. University of Louisville; 2011. [cited 2020 Jan 22]. Available from: 10.18297/etd/1369 ; https://ir.library.louisville.edu/etd/1369.

Council of Science Editors:

Stallons, Lindsey Jay 1. DNA polymerase iota promotes G2/M checkpoint activation and genetic stability after UV-induced DNA damage. [Doctoral Dissertation]. University of Louisville; 2011. Available from: 10.18297/etd/1369 ; https://ir.library.louisville.edu/etd/1369

University of New Mexico

7. Quintana, Anita. Changes in c-Myb activity during proliferation.

Degree: Biomedical Sciences Graduate Program, 2010, University of New Mexico

URL: https://digitalrepository.unm.edu/biom_etds/20

► c-myb encodes a transcription factor and is the cellular parent of the v-myb oncogene, which causes acute myeloid leukemia in chickens and mice. Truncation or… (more)

Subjects/Keywords: c-myb; cell cycle

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APA (6^th Edition):

Quintana, A. (2010). Changes in c-Myb activity during proliferation. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/20

Chicago Manual of Style (16^th Edition):

Quintana, Anita. “Changes in c-Myb activity during proliferation.” 2010. Doctoral Dissertation, University of New Mexico. Accessed January 22, 2020. https://digitalrepository.unm.edu/biom_etds/20.

MLA Handbook (7^th Edition):

Quintana, Anita. “Changes in c-Myb activity during proliferation.” 2010. Web. 22 Jan 2020.

Vancouver:

Quintana A. Changes in c-Myb activity during proliferation. [Internet] [Doctoral dissertation]. University of New Mexico; 2010. [cited 2020 Jan 22]. Available from: https://digitalrepository.unm.edu/biom_etds/20.

Council of Science Editors:

Quintana A. Changes in c-Myb activity during proliferation. [Doctoral Dissertation]. University of New Mexico; 2010. Available from: https://digitalrepository.unm.edu/biom_etds/20

8. Takatsuka, Hirotomo. Studies on functional roles of CDK-activating kinases in Arabidopsis development : シロイヌナズナの発生におけるCDK活性化キナーゼの機能に関する研究; シロイヌナズナノハッセイニオケル CDK カッセイカキナーゼノキノウニカンスルケンキュウ.

Degree: Nara Institute of Science and Technology / 奈良先端科学技術大学院大学

URL: http://hdl.handle.net/10061/5706

Subjects/Keywords: cell cycle

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APA (6^th Edition):

Takatsuka, H. (n.d.). Studies on functional roles of CDK-activating kinases in Arabidopsis development : シロイヌナズナの発生におけるCDK活性化キナーゼの機能に関する研究; シロイヌナズナノハッセイニオケル CDK カッセイカキナーゼノキノウニカンスルケンキュウ. (Thesis). Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Retrieved from http://hdl.handle.net/10061/5706

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Takatsuka, Hirotomo. “Studies on functional roles of CDK-activating kinases in Arabidopsis development : シロイヌナズナの発生におけるCDK活性化キナーゼの機能に関する研究; シロイヌナズナノハッセイニオケル CDK カッセイカキナーゼノキノウニカンスルケンキュウ.” Thesis, Nara Institute of Science and Technology / 奈良先端科学技術大学院大学. Accessed January 22, 2020. http://hdl.handle.net/10061/5706.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Takatsuka, Hirotomo. “Studies on functional roles of CDK-activating kinases in Arabidopsis development : シロイヌナズナの発生におけるCDK活性化キナーゼの機能に関する研究; シロイヌナズナノハッセイニオケル CDK カッセイカキナーゼノキノウニカンスルケンキュウ.” Web. 22 Jan 2020.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Takatsuka H. Studies on functional roles of CDK-activating kinases in Arabidopsis development : シロイヌナズナの発生におけるCDK活性化キナーゼの機能に関する研究; シロイヌナズナノハッセイニオケル CDK カッセイカキナーゼノキノウニカンスルケンキュウ. [Internet] [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; [cited 2020 Jan 22]. Available from: http://hdl.handle.net/10061/5706.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Takatsuka H. Studies on functional roles of CDK-activating kinases in Arabidopsis development : シロイヌナズナの発生におけるCDK活性化キナーゼの機能に関する研究; シロイヌナズナノハッセイニオケル CDK カッセイカキナーゼノキノウニカンスルケンキュウ. [Thesis]. Nara Institute of Science and Technology / 奈良先端科学技術大学院大学; Available from: http://hdl.handle.net/10061/5706

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Case Western Reserve University

9. Wang, Li. CELL CYCLE REGULATION IN THE POST-MITOTIC NEURONAL CELLS.

Degree: PhD, Genetics, 2007, Case Western Reserve University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=case1184254319

► A normal cell cycle is essential for cell proliferation in embryonic development. Once the appropriate numbers of cells are generated, however, there are various populations,… (more)

Subjects/Keywords: Cell cycle regulation; E2F1; Cdk5

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APA (6^th Edition):

Wang, L. (2007). CELL CYCLE REGULATION IN THE POST-MITOTIC NEURONAL CELLS. (Doctoral Dissertation). Case Western Reserve University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=case1184254319

Chicago Manual of Style (16^th Edition):

Wang, Li. “CELL CYCLE REGULATION IN THE POST-MITOTIC NEURONAL CELLS.” 2007. Doctoral Dissertation, Case Western Reserve University. Accessed January 22, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1184254319.

MLA Handbook (7^th Edition):

Wang, Li. “CELL CYCLE REGULATION IN THE POST-MITOTIC NEURONAL CELLS.” 2007. Web. 22 Jan 2020.

Vancouver:

Wang L. CELL CYCLE REGULATION IN THE POST-MITOTIC NEURONAL CELLS. [Internet] [Doctoral dissertation]. Case Western Reserve University; 2007. [cited 2020 Jan 22]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1184254319.

Council of Science Editors:

Wang L. CELL CYCLE REGULATION IN THE POST-MITOTIC NEURONAL CELLS. [Doctoral Dissertation]. Case Western Reserve University; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1184254319

Penn State University

10. MIN, JUNGSOO. Mechanisms of IGF-1 regulation of S and G2/M cell cycle phases in oligodendrocyte progenitor (OP) cells.

Degree: PhD, Molecular Medicine, 2009, Penn State University

URL: https://etda.libraries.psu.edu/catalog/10077

► Oligodendrocytes are macroglial cells in the central nervous system (CNS), which myelinate and provide electric insulation for the axons of nerve cells. Oligodendrocyte progenitor (OP)… (more)

▼ Oligodendrocytes are macroglial cells in the central nervous system (CNS), which myelinate and provide electric insulation for the axons of nerve cells. Oligodendrocyte progenitor (OP) cells generated in the developing neural tube differentiate into oligodendrocytes capable of producing myelin. OP cells undergo extensive proliferation before they become post-mitotic, mature oligodendrocytes. Intrinsic and extrinsic factors influence OP cells to decide whether to continue cell cycle progression or exit the cell cycle and terminally differentiate. Growth factors are extrinsic signals involved in developmental regulation of OPs. Some growth factors act independently and other growth factors act coordinately to exert maximal effects. Previously, our laboratory reported that insulin like growth factor-1 (IGF-1), which itself is a weak mitogen in oligodendrocyte lineage cells, synergizes with fibroblast growth factor-2 (FGF-2) for G1 cell cycle progression and S phase entry, in part, by inducing cyclin D1 and enhancing activity of cdk2. Here, we report that the combination of IGF-1 with FGF-2 accelerates S phase and promotes S phase progression. Particularly, IGF-1/FGF-2 enhances mRNA and protein expression of cyclin A and cdk2, the predominant regulators of S phase. Further, the growth factor combination increases effective complex formation in IGF-1/FGF-2 resulting in enhanced cdk2 activity. We further studied the signaling mechanism by which IGF-1 and FGF-2 synergize to exert their coordinated effects on cell cycle progression, specifically in S phase. Using specific inhibitors for MAP kinase and PI3 kinase, we determined that both pathways are necessary for expression of S phase proteins and mRNA and for phosphorylation of retinoblastoma protein (pRb), a target of cdk2. However, the effects of each pathway on S phase targets were distinct. We also demonstrate that IGF-1 plays a critical role in G2/M progression. OP cells exposed to FGF-2 alone fail to progress through G2/M. In contrast, the combination of IGF-1 with FGF-2 promotes progression through G2/M. Protein expression of cyclin B and cdk1 increases and cyclin B/cdk1 complex formation increases with concomitant increase in cdk1 kinase activity in the combination growth factor treatment. Nuclear localization of cyclin B and cdk1, one parameter for active cdk1, was enhanced in IGF-1/FGF-2 treated cells as well as the relative amount of cdc25C, an activator of cdk1. Using mechanism to arrest cells in S phase or with cells treated with FGF-2 alone into S phase, we demonstrated that IGF-1 by itself promotes G2/M progression. Overall, we have determined that IGF-1 plays an important role in cell cycle progression of OP cells, and furthermore, it is an essential factor for G2/M progression.

Subjects/Keywords: IGF-1; oligodendrocyte; cell cycle

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

MIN, J. (2009). Mechanisms of IGF-1 regulation of S and G2/M cell cycle phases in oligodendrocyte progenitor (OP) cells. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/10077

Chicago Manual of Style (16^th Edition):

MIN, JUNGSOO. “Mechanisms of IGF-1 regulation of S and G2/M cell cycle phases in oligodendrocyte progenitor (OP) cells.” 2009. Doctoral Dissertation, Penn State University. Accessed January 22, 2020. https://etda.libraries.psu.edu/catalog/10077.

MLA Handbook (7^th Edition):

MIN, JUNGSOO. “Mechanisms of IGF-1 regulation of S and G2/M cell cycle phases in oligodendrocyte progenitor (OP) cells.” 2009. Web. 22 Jan 2020.

Vancouver:

MIN J. Mechanisms of IGF-1 regulation of S and G2/M cell cycle phases in oligodendrocyte progenitor (OP) cells. [Internet] [Doctoral dissertation]. Penn State University; 2009. [cited 2020 Jan 22]. Available from: https://etda.libraries.psu.edu/catalog/10077.

Council of Science Editors:

MIN J. Mechanisms of IGF-1 regulation of S and G2/M cell cycle phases in oligodendrocyte progenitor (OP) cells. [Doctoral Dissertation]. Penn State University; 2009. Available from: https://etda.libraries.psu.edu/catalog/10077

Oregon State University

11. Worthington, David H. Hydroxyurea : physiological effects on Tetrahymena pyriformis and use in cell cycle analysis.

Degree: PhD, Genetics, 1973, Oregon State University

URL: http://hdl.handle.net/1957/44777

► Hydroxyurea (10mM) blocks the exponential growth of Tetrahymena pyriformis (GL-I) populations by arresting progress through the cell cycle once the cells enter S-phase. Autoradiographic analysis… (more)

▼ Hydroxyurea (10mM) blocks the exponential growth of Tetrahymena pyriformis (GL-I) populations by arresting progress through the cell cycle once the cells enter S-phase. Autoradiographic analysis reveals that HU reduces the uptake of tritiated thymidine (³H-TdR) into macronuclear DNA in S-phase cells to about 1/5 of that in untreated S-phase cells. These slowly synthesizing cells do not divide (even after 10 days) until the HU is removed. The HU-blocked cells are also rescued from S-phase arrest by adding 0. 5mM each of all four DNAprecursor deoxyribonucleosides (XdRs) thus indicating the primary effect of HU is the inhibition of the reduction of ribonucleosides. When the HU-block is removed by either washing the HU from the medium or by rescue with XdRs an excessive delay in recovering the capacity to divide is specifically induced in cells which were in S-phase at time of addition of HU. This delay may be due to the time needed to repair damage to the DNA which was induced specifically during S-phase. Fluoromicroscopic examination of euchrysine-stained cells exposed for a minimum of two hours starting in S-phase show a radical morphological change in the macronucleus. This phenomenon, termed the "halo effect," is characterized by the formation of apparently membrane-associated chromatin aggregates surrounding a constricted chromatin mass. Halo-induction by HU is S-phase specific and upon removal of the HU-block the halo remains until the first recovery division. The halo effect is interpreted as being a morphological indication of the cell's repair response to the damaging effects of HU upon macronuclear DNA. Observations of division of individual cells in microdrops, plus autoradiographic studies using ³H-TdR and standard cell cycle analysis techniques, reveal that HU blocks all cells in the initial 92% of S-phase but does not affect cells in the remaining 8 % of S-phase or in G₂ and division. Thus the fraction of the population of cells that is in G₂ can be approximately determined (within 6 minutes) by the fraction of the population able to divide in the presence of HU. This fraction can be related to the approximate duration of G₂ after mathematically compensating for the age gradient. Thus G₂ analysis of T. pyriformis (GL-I) is accomplished easily, quickly, and inexpensively with the use of HU. The possibilities of utilizing Sphase specific recovery delay and halo induction for simple means of determining the durations of G₁ and S-phase respectively are also discussed. The addition of all four XdRs (0. 5mM) to exponentially growing cells in rich organic complete medium without HU results in the generation time of these cells being decreased by 20%. Cell cycle analysis with phosphorus-33 (³³P) and experiments involving cell phase sensitivity to the presence of excess XdRs show that the excess XdRs are taken up and incorporated or pooled entirely during the initial 50% of S-phase. This acceleration of early S-phase completely accounts for the abbreviated generation… Advisors/Committee Members: Nachtwey, D. S. (advisor).

Subjects/Keywords: Cell cycle

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APA (6^th Edition):

Worthington, D. H. (1973). Hydroxyurea : physiological effects on Tetrahymena pyriformis and use in cell cycle analysis. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/44777

Chicago Manual of Style (16^th Edition):

Worthington, David H. “Hydroxyurea : physiological effects on Tetrahymena pyriformis and use in cell cycle analysis.” 1973. Doctoral Dissertation, Oregon State University. Accessed January 22, 2020. http://hdl.handle.net/1957/44777.

MLA Handbook (7^th Edition):

Worthington, David H. “Hydroxyurea : physiological effects on Tetrahymena pyriformis and use in cell cycle analysis.” 1973. Web. 22 Jan 2020.

Vancouver:

Worthington DH. Hydroxyurea : physiological effects on Tetrahymena pyriformis and use in cell cycle analysis. [Internet] [Doctoral dissertation]. Oregon State University; 1973. [cited 2020 Jan 22]. Available from: http://hdl.handle.net/1957/44777.

Council of Science Editors:

Worthington DH. Hydroxyurea : physiological effects on Tetrahymena pyriformis and use in cell cycle analysis. [Doctoral Dissertation]. Oregon State University; 1973. Available from: http://hdl.handle.net/1957/44777

Vanderbilt University

12. Talley, Jennell Marie. Exploring the assembly and function of the telomerase accessory proteins Est1 and Est3 in Saccharomyces cerevisiae.

Degree: PhD, Biological Sciences, 2011, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-07182011-134847/ ;

► The work presented in this dissertation focuses on a how the telomerase complex assembles both in vivo and in vitro and begins to explore how… (more)

Subjects/Keywords: proteasome; TERT; cell cycle; Telomere

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APA (6^th Edition):

Talley, J. M. (2011). Exploring the assembly and function of the telomerase accessory proteins Est1 and Est3 in Saccharomyces cerevisiae. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-07182011-134847/ ;

Chicago Manual of Style (16^th Edition):

Talley, Jennell Marie. “Exploring the assembly and function of the telomerase accessory proteins Est1 and Est3 in Saccharomyces cerevisiae.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed January 22, 2020. http://etd.library.vanderbilt.edu/available/etd-07182011-134847/ ;.

MLA Handbook (7^th Edition):

Talley, Jennell Marie. “Exploring the assembly and function of the telomerase accessory proteins Est1 and Est3 in Saccharomyces cerevisiae.” 2011. Web. 22 Jan 2020.

Vancouver:

Talley JM. Exploring the assembly and function of the telomerase accessory proteins Est1 and Est3 in Saccharomyces cerevisiae. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2020 Jan 22]. Available from: http://etd.library.vanderbilt.edu/available/etd-07182011-134847/ ;.

Council of Science Editors:

Talley JM. Exploring the assembly and function of the telomerase accessory proteins Est1 and Est3 in Saccharomyces cerevisiae. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://etd.library.vanderbilt.edu/available/etd-07182011-134847/ ;

Harvard University

13. Ho, Po-Yi. Models of microbial cell cycles.

Degree: PhD, 2019, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42029521

►

Cell division is a fundamental process of life, yet how the timing of cell division is regulated in microorganisms remain unclear. In this dissertation, I… (more)

Subjects/Keywords: Models; microbial cell cycle

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APA (6^th Edition):

Ho, P. (2019). Models of microbial cell cycles. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:42029521

Chicago Manual of Style (16^th Edition):

Ho, Po-Yi. “Models of microbial cell cycles.” 2019. Doctoral Dissertation, Harvard University. Accessed January 22, 2020. http://nrs.harvard.edu/urn-3:HUL.InstRepos:42029521.

MLA Handbook (7^th Edition):

Ho, Po-Yi. “Models of microbial cell cycles.” 2019. Web. 22 Jan 2020.

Vancouver:

Ho P. Models of microbial cell cycles. [Internet] [Doctoral dissertation]. Harvard University; 2019. [cited 2020 Jan 22]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42029521.

Council of Science Editors:

Ho P. Models of microbial cell cycles. [Doctoral Dissertation]. Harvard University; 2019. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42029521

University of Texas Southwestern Medical Center

14. Chaudhary, Jaideep. Function And Recruitment Of Centromeric Heterochromatin Protein 1.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/846

► During early mitosis, the sister chromatids are held together by Cohesin, a protein complex composed of Smc3, Smc1, Scc1/Rad21 and Scc3. Cohesin is first released… (more)

Subjects/Keywords: Cell Cycle Proteins; Mitosis; Heterochromatin

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APA (6^th Edition):

Chaudhary, J. (2011). Function And Recruitment Of Centromeric Heterochromatin Protein 1. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/846

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chaudhary, Jaideep. “Function And Recruitment Of Centromeric Heterochromatin Protein 1.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed January 22, 2020. http://hdl.handle.net/2152.5/846.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chaudhary, Jaideep. “Function And Recruitment Of Centromeric Heterochromatin Protein 1.” 2011. Web. 22 Jan 2020.

Vancouver:

Chaudhary J. Function And Recruitment Of Centromeric Heterochromatin Protein 1. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2020 Jan 22]. Available from: http://hdl.handle.net/2152.5/846.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chaudhary J. Function And Recruitment Of Centromeric Heterochromatin Protein 1. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/846

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Texas Southwestern Medical Center

15. Cai, Ling. Insights into the Metabolic Regulation of Growth and Proliferation in Saccharomyces Cerevisiae.

Degree: 2013, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/2715

► Cells needs to gauge their capacity to grow based on nutrient availability, and adopt different metabolic strategies for optimal growth and survival. We have investigated… (more)

▼ Cells needs to gauge their capacity to grow based on nutrient availability, and adopt different metabolic strategies for optimal growth and survival. We have investigated the molecular mechanism of how growth decisions are made based on metabolic status and how metabolic enzymes are regulated by nutrient availability. In the first part of this study, we report that acetyl-CoA is the downstream metabolite of carbon sources that represents a critical metabolic signal for growth and proliferation. Upon entry into growth, intracellular acetyl-CoA levels increase substantially and consequently induce the Gcn5p/SAGA-catalyzed acetylation of histones at genes important vi for growth, thereby enabling their rapid transcription and commitment to growth. Acetyl-CoA functions as a carbon-source rheostat that signals the initiation of the cellular growth program by promoting the acetylation of histones specifically at growth genes. In the second part of the study, we report the dynamic modification of ribosome biogenesis transcription factor Ifh1p regulated by different metabolic cues. Ribosome biogenesis requires an enormous commitment of energy and resources in growing cells. We show that Ifh1p is dynamically acetylated and phosphorylated as a function of the growth state of cells. Ifh1p is acetylated at numerous sites in its N-terminal region by Gcn5p and deacetylated by NAD+-dependent deacetylases of the sirtuin family. Acetylation of Ifh1p is responsive to intracellular acetyl-CoA levels and serves to regulate the stability of Ifh1p. The phosphorylation of Ifh1p is mediated by Protein Kinase A and is dependent on TORC1 signaling. Instead of modulating overall rates of RP gene transcription or growth, these nutrient-responsive modifications of Ifh1p play a more prominent role in the regulation of cellular replicative lifespan. Finally, we report the different roles of acetyl-CoA synthetases Acs1p and Acs2p in yeast metabolism. While Acs2p is important for rapid growth in glucose medium, Acs1p has unique roles in more challenging growth conditions. It is important for yeast metabolic cycling and is recruited to foci structure near mitochondria that might be involved in shuttling acetyl-CoA into the mitochondria during hypoxia. Advisors/Committee Members: Liu, Yi, DeBerardinis, Ralph J., Li, Bing, Ross, Elliott M..

Subjects/Keywords: Saccharomyces cerevisiae; Cell Cycle; Mitosis

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APA (6^th Edition):

Cai, L. (2013). Insights into the Metabolic Regulation of Growth and Proliferation in Saccharomyces Cerevisiae. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/2715

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Cai, Ling. “Insights into the Metabolic Regulation of Growth and Proliferation in Saccharomyces Cerevisiae.” 2013. Thesis, University of Texas Southwestern Medical Center. Accessed January 22, 2020. http://hdl.handle.net/2152.5/2715.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Cai, Ling. “Insights into the Metabolic Regulation of Growth and Proliferation in Saccharomyces Cerevisiae.” 2013. Web. 22 Jan 2020.

Vancouver:

Cai L. Insights into the Metabolic Regulation of Growth and Proliferation in Saccharomyces Cerevisiae. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2013. [cited 2020 Jan 22]. Available from: http://hdl.handle.net/2152.5/2715.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Cai L. Insights into the Metabolic Regulation of Growth and Proliferation in Saccharomyces Cerevisiae. [Thesis]. University of Texas Southwestern Medical Center; 2013. Available from: http://hdl.handle.net/2152.5/2715

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Sydney

16. Dokumcu, Kagan Ali. Non-encoded Mechanisms of Stress Adaptation in Cancer .

Degree: 2019, University of Sydney

URL: http://hdl.handle.net/2123/20959

► Tumour resistance attributed to clonal evolution of neoplastic cells, poses a major challenge for treatment of cancer. Clonality of neoplastic cells is mainly considered to… (more)

Subjects/Keywords: Cancer; Autophagy; Cell Cycle; MicroRNA

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APA (6^th Edition):

Dokumcu, K. A. (2019). Non-encoded Mechanisms of Stress Adaptation in Cancer . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/20959

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dokumcu, Kagan Ali. “Non-encoded Mechanisms of Stress Adaptation in Cancer .” 2019. Thesis, University of Sydney. Accessed January 22, 2020. http://hdl.handle.net/2123/20959.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dokumcu, Kagan Ali. “Non-encoded Mechanisms of Stress Adaptation in Cancer .” 2019. Web. 22 Jan 2020.

Vancouver:

Dokumcu KA. Non-encoded Mechanisms of Stress Adaptation in Cancer . [Internet] [Thesis]. University of Sydney; 2019. [cited 2020 Jan 22]. Available from: http://hdl.handle.net/2123/20959.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dokumcu KA. Non-encoded Mechanisms of Stress Adaptation in Cancer . [Thesis]. University of Sydney; 2019. Available from: http://hdl.handle.net/2123/20959

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

17. Zhao, Yichen LIFS. Functional study of GAS2L1 in mitosis.

Degree: 2015, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-92284 ; https://doi.org/10.14711/thesis-b1514805 ; http://repository.ust.hk/ir/bitstream/1783.1-92284/1/th_redirect.html

► Mitosis, as a very important process during the cell cycle, decides chromosome duplication, organelle separation and cell division. During mitosis, metaphase is middle of whole… (more)

Subjects/Keywords: Mitosis ; Cell cycle ; Carrier proteins

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APA (6^th Edition):

Zhao, Y. L. (2015). Functional study of GAS2L1 in mitosis. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-92284 ; https://doi.org/10.14711/thesis-b1514805 ; http://repository.ust.hk/ir/bitstream/1783.1-92284/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhao, Yichen LIFS. “Functional study of GAS2L1 in mitosis.” 2015. Thesis, Hong Kong University of Science and Technology. Accessed January 22, 2020. http://repository.ust.hk/ir/Record/1783.1-92284 ; https://doi.org/10.14711/thesis-b1514805 ; http://repository.ust.hk/ir/bitstream/1783.1-92284/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhao, Yichen LIFS. “Functional study of GAS2L1 in mitosis.” 2015. Web. 22 Jan 2020.

Vancouver:

Zhao YL. Functional study of GAS2L1 in mitosis. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2015. [cited 2020 Jan 22]. Available from: http://repository.ust.hk/ir/Record/1783.1-92284 ; https://doi.org/10.14711/thesis-b1514805 ; http://repository.ust.hk/ir/bitstream/1783.1-92284/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhao YL. Functional study of GAS2L1 in mitosis. [Thesis]. Hong Kong University of Science and Technology; 2015. Available from: http://repository.ust.hk/ir/Record/1783.1-92284 ; https://doi.org/10.14711/thesis-b1514805 ; http://repository.ust.hk/ir/bitstream/1783.1-92284/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

18. Qin, Yan LIFS. The role of hNOC3 in human DNA replication.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html

► Noc3p (nucleolar complex-associated protein) is highly conserved in eukaryotes, and it plays a critical role in the initiation of DNA replication in budding yeast. Noc3p… (more)

Subjects/Keywords: DNA replication ; Cell cycle

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APA (6^th Edition):

Qin, Y. L. (2013). The role of hNOC3 in human DNA replication. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Qin, Yan LIFS. “The role of hNOC3 in human DNA replication.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed January 22, 2020. http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Qin, Yan LIFS. “The role of hNOC3 in human DNA replication.” 2013. Web. 22 Jan 2020.

Vancouver:

Qin YL. The role of hNOC3 in human DNA replication. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2020 Jan 22]. Available from: http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Qin YL. The role of hNOC3 in human DNA replication. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-94452 ; https://doi.org/10.14711/thesis-b1266302 ; http://repository.ust.hk/ir/bitstream/1783.1-94452/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

19. Xu, Kaichun LIFS. Molecular regulation of mitotic slippage.

Degree: 2016, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-99847 ; https://doi.org/10.14711/thesis-b1626381 ; http://repository.ust.hk/ir/bitstream/1783.1-99847/1/th_redirect.html

► Antimicrotubule drugs are effective chemotherapeutic agents because they can disrupt normal mitotic spindle and activate the spindle-assembly checkpoint (SAC) to arrest cells in mitosis, thereby… (more)

Subjects/Keywords: Cell cycle ; Regulation ; Mitosis

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APA (6^th Edition):

Xu, K. L. (2016). Molecular regulation of mitotic slippage. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-99847 ; https://doi.org/10.14711/thesis-b1626381 ; http://repository.ust.hk/ir/bitstream/1783.1-99847/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Xu, Kaichun LIFS. “Molecular regulation of mitotic slippage.” 2016. Thesis, Hong Kong University of Science and Technology. Accessed January 22, 2020. http://repository.ust.hk/ir/Record/1783.1-99847 ; https://doi.org/10.14711/thesis-b1626381 ; http://repository.ust.hk/ir/bitstream/1783.1-99847/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Xu, Kaichun LIFS. “Molecular regulation of mitotic slippage.” 2016. Web. 22 Jan 2020.

Vancouver:

Xu KL. Molecular regulation of mitotic slippage. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2016. [cited 2020 Jan 22]. Available from: http://repository.ust.hk/ir/Record/1783.1-99847 ; https://doi.org/10.14711/thesis-b1626381 ; http://repository.ust.hk/ir/bitstream/1783.1-99847/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Xu KL. Molecular regulation of mitotic slippage. [Thesis]. Hong Kong University of Science and Technology; 2016. Available from: http://repository.ust.hk/ir/Record/1783.1-99847 ; https://doi.org/10.14711/thesis-b1626381 ; http://repository.ust.hk/ir/bitstream/1783.1-99847/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Hong Kong

20. Zheng, Fan. Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization.

Degree: PhD, 2015, University of Hong Kong

URL: Zheng, F. [郑{273c46}]. (2015). Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576784 ; http://hdl.handle.net/10722/221095

► Microtubules are involved in a wide range of cellular functions including the establishment of cell polarity, organelle trafficking and positioning, and mitotic chromosome segregation. To… (more)

▼ Microtubules are involved in a wide range of cellular functions including the establishment of cell polarity, organelle trafficking and positioning, and mitotic chromosome segregation. To accomplish such diverse functions during the cell cycle, microtubules must be organized and dynamically regulated by a large number of microtubule-associated proteins (MAPs) in space and time. Despite identification of many MAPs, the functions of these MAPs remain to be further explored and defined. In this study, I investigate the roles of several key MAPs in mitotic spindle assembly and in microtubule depolymerization during interphase, using the fission yeast Schizosaccharomyces pombe as a model organism. Fission yeast has a well-defined microtubule array and is genetically tractable. Importantly, most MAPs in fission yeast are evolutionarily conserved. All these features make fission yeast an excellent organism for microtubule studies. During mitosis, microtubules form a bipolar spindle for regulating chromosome segregation. In bipolar spindle formation, the kinesin-5 motor protein cut7p has been shown to be an essential player. However, studies in multiple model organisms also suggest that kinesin-independent mechanisms are required to ensure the efficiency of bipolar spindle assembly. One of the components involved in the kinesin-independent mechanism could be the evolutionarily conserved complex comprising alp7p (TACC in human) and alp14p (ch-TOG in human) as depletion of alp7p or alp14p causes defects in bipolar spindle formation. The function of the alp7p-alp14p complex in spindle assembly depends on their localization to the SPB (the centrosome in human cells). However, it remains unknown how the alp7p-alp14p complex is targeted to the SPB/centrosome. In the first part of this thesis (chapter 3), I demonstrate that the alp7p-alp14p complex is recruited to the SPB by the new SPB protein csi1p through the interaction between alp7p and csi1p. Domain mapping further revealed that the csi1p-interacting region in alp7p lies within the conserved TACC domain, and the carboxyl-terminal domain of csi1p is responsible for its interaction with alp7p. Compromised interaction between csi1p and alp7p impairs the SPBs localization of alp7p during mitosis, thus leading to bipolar spindle formation defects and consequently anaphase B lagging chromosomes. Hence, this study establishes that csi1p serves as a linking molecule tethering the microtubule-stabilizing factors alp7p and alp14p to the SPB to promote bipolar spindle assembly. In the second part of this thesis (chapter 4), I address the role of a new MAP in microtubule depolymerization in interphase. Two types of MAPs work synergistically to regulate microtubule dynamics. These MAPs function either to stabilize microtubules or to destabilize microtubules. Thus far few microtubule-destabilizing proteins have been identified and characterized. Here, I presented a new microtubule-destabilizing protein mcp1p. Mcp1p is mobile in the cell and localizes along microtubules, particularly…

Subjects/Keywords: Spindle (Cell division); Cell cycle; Microtubules

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zheng, F. (2015). Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization. (Doctoral Dissertation). University of Hong Kong. Retrieved from Zheng, F. [郑{273c46}]. (2015). Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576784 ; http://hdl.handle.net/10722/221095

Chicago Manual of Style (16^th Edition):

Zheng, Fan. “Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization.” 2015. Doctoral Dissertation, University of Hong Kong. Accessed January 22, 2020. Zheng, F. [郑{273c46}]. (2015). Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576784 ; http://hdl.handle.net/10722/221095.

MLA Handbook (7^th Edition):

Zheng, Fan. “Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization.” 2015. Web. 22 Jan 2020.

Vancouver:

Zheng F. Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization. [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2020 Jan 22]. Available from: Zheng, F. [郑{273c46}]. (2015). Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576784 ; http://hdl.handle.net/10722/221095.

Council of Science Editors:

Zheng F. Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization. [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: Zheng, F. [郑{273c46}]. (2015). Molecular mechanisms regulating bipolar spindle formation and microtubule depolymerization. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5576784 ; http://hdl.handle.net/10722/221095

University of Notre Dame

21. Randy Jeffrey. Effects of the Anti-Androgen Bicalutamide on Prostate Cancer Cells</h1>.

Degree: PhD, Biological Sciences, 2012, University of Notre Dame

URL: https://curate.nd.edu/show/qf85n873c5q

► The use of anti-androgen therapy for the treatment of invasive and metastatic prostate cancer is common practice. However, after an initial response, the tumor… (more)

Subjects/Keywords: cell death; prostate cancer; cell cycle; bicalutamide

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jeffrey, R. (2012). Effects of the Anti-Androgen Bicalutamide on Prostate Cancer Cells</h1>. (Doctoral Dissertation). University of Notre Dame. Retrieved from https://curate.nd.edu/show/qf85n873c5q

Chicago Manual of Style (16^th Edition):

Jeffrey, Randy. “Effects of the Anti-Androgen Bicalutamide on Prostate Cancer Cells</h1>.” 2012. Doctoral Dissertation, University of Notre Dame. Accessed January 22, 2020. https://curate.nd.edu/show/qf85n873c5q.

MLA Handbook (7^th Edition):

Jeffrey, Randy. “Effects of the Anti-Androgen Bicalutamide on Prostate Cancer Cells</h1>.” 2012. Web. 22 Jan 2020.

Vancouver:

Jeffrey R. Effects of the Anti-Androgen Bicalutamide on Prostate Cancer Cells</h1>. [Internet] [Doctoral dissertation]. University of Notre Dame; 2012. [cited 2020 Jan 22]. Available from: https://curate.nd.edu/show/qf85n873c5q.

Council of Science Editors:

Jeffrey R. Effects of the Anti-Androgen Bicalutamide on Prostate Cancer Cells</h1>. [Doctoral Dissertation]. University of Notre Dame; 2012. Available from: https://curate.nd.edu/show/qf85n873c5q

Washington University in St. Louis

22. Arjes, Heidi Ann. Failsafe Mechanisms Coordinate Cell Division and the Initiation of DNA Replication in Bacteria.

Degree: PhD, Biology and Biomedical Sciences: Molecular Genetics and Genomics, 2014, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/etd/1280

► During the cell cycle, a cell must replicate its DNA, segregate the genome and divide into two identical daughter cells with full chromosomes. This… (more)

▼ During the cell cycle, a cell must replicate its DNA, segregate the genome and divide into two identical daughter cells with full chromosomes. This process needs to be specifically coordinated to ensure that cell division does not occur before DNA replication has finished and that the cell septates precisely at midcell to segregate one chromosome to each daughter cell. If cells divide before the chromosome is fully replicated, the chromosome could be guillotined or cell division could occur resulting in cells without chromosomes. If division does not occur properly, the cells elongate but do not divide and form multinucleate filaments. In wild-type cells, DNA replication and cell division appear to be perfectly coordinated. Even at faster doubling times, the cell cycle is synchronized so that DNA replication initiates and terminates once per cell division, the cell division protein FtsZ assembles into a ring precisely at midcell, and cell septation only occurs once the chromosome has replicated and segregated. Despite this apparent coordination, the long-held view in the field is that cell division and DNA replication are independent cycles that are merely coordinated during normal growth. However, it remains widely accepted that cell division is independent from DNA replication in bacteria. In this dissertation, I make 3 contributions to the field of cell cycle regulation. First, I identify a control point that couples cell division with the initiation of DNA replication. Second, I show that long-term inhibitions of cell division lead to terminal cell cycle arrest at a time we have termed the "Point of no return" or PONR. The PONR is equivalent to the eukaryotic G<sub>0<sub> arrest and validates the development of antibiotics that target the cell division machinery. Third, I characterized determinants for assembly of the tubulin-like protein FtsZ using a genetic approach. This work enhances our understanding of what is critical for FtsZ function in vivo and highlights the need to develop better assays for evaluating FtsZ assembly in vitro. Advisors/Committee Members: Petra A Levin.

Subjects/Keywords: cell cycle; cell division; DNA replication; FtsZ

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Arjes, H. A. (2014). Failsafe Mechanisms Coordinate Cell Division and the Initiation of DNA Replication in Bacteria. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/etd/1280

Chicago Manual of Style (16^th Edition):

Arjes, Heidi Ann. “Failsafe Mechanisms Coordinate Cell Division and the Initiation of DNA Replication in Bacteria.” 2014. Doctoral Dissertation, Washington University in St. Louis. Accessed January 22, 2020. https://openscholarship.wustl.edu/etd/1280.

MLA Handbook (7^th Edition):

Arjes, Heidi Ann. “Failsafe Mechanisms Coordinate Cell Division and the Initiation of DNA Replication in Bacteria.” 2014. Web. 22 Jan 2020.

Vancouver:

Arjes HA. Failsafe Mechanisms Coordinate Cell Division and the Initiation of DNA Replication in Bacteria. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2014. [cited 2020 Jan 22]. Available from: https://openscholarship.wustl.edu/etd/1280.

Council of Science Editors:

Arjes HA. Failsafe Mechanisms Coordinate Cell Division and the Initiation of DNA Replication in Bacteria. [Doctoral Dissertation]. Washington University in St. Louis; 2014. Available from: https://openscholarship.wustl.edu/etd/1280

University of Tennessee – Knoxville

23. Stutts, Dustin K. Role of the mitotic cyclin Clb2 in mitotic regulation.

Degree: MS, Biochemistry and Cellular and Molecular Biology, 2010, University of Tennessee – Knoxville

URL: https://trace.tennessee.edu/utk_gradthes/752

► In the budding yeast Saccharomyces cerevisiae, the mitotic cell cycle is regulated by the cyclin-dependent kinase (CDK) Cdc28. Cdc28 is activated by binding to one… (more)

Subjects/Keywords: cyclin; mitosis; Clb2; cell cycle; Cell Biology

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APA (6^th Edition):

Stutts, D. K. (2010). Role of the mitotic cyclin Clb2 in mitotic regulation. (Thesis). University of Tennessee – Knoxville. Retrieved from https://trace.tennessee.edu/utk_gradthes/752

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Stutts, Dustin K. “Role of the mitotic cyclin Clb2 in mitotic regulation.” 2010. Thesis, University of Tennessee – Knoxville. Accessed January 22, 2020. https://trace.tennessee.edu/utk_gradthes/752.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Stutts, Dustin K. “Role of the mitotic cyclin Clb2 in mitotic regulation.” 2010. Web. 22 Jan 2020.

Vancouver:

Stutts DK. Role of the mitotic cyclin Clb2 in mitotic regulation. [Internet] [Thesis]. University of Tennessee – Knoxville; 2010. [cited 2020 Jan 22]. Available from: https://trace.tennessee.edu/utk_gradthes/752.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Stutts DK. Role of the mitotic cyclin Clb2 in mitotic regulation. [Thesis]. University of Tennessee – Knoxville; 2010. Available from: https://trace.tennessee.edu/utk_gradthes/752

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Illinois – Urbana-Champaign

24. Sridharan, Santhipriyadar. The role of conexin 43 in murine sertoli cell development.

Degree: PhD, 0357, 2010, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/16108

► Sertoli cells are the only somatic cell type present within the seminiferous tubules of the testis. The support of these somatic cells is essential for… (more)

Subjects/Keywords: Sertoli cell; gap junctions; Connexin 43; Sertoli cell development; cell cycle; cell cycle regulators

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APA (6^th Edition):

Sridharan, S. (2010). The role of conexin 43 in murine sertoli cell development. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/16108

Chicago Manual of Style (16^th Edition):

Sridharan, Santhipriyadar. “The role of conexin 43 in murine sertoli cell development.” 2010. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 22, 2020. http://hdl.handle.net/2142/16108.

MLA Handbook (7^th Edition):

Sridharan, Santhipriyadar. “The role of conexin 43 in murine sertoli cell development.” 2010. Web. 22 Jan 2020.

Vancouver:

Sridharan S. The role of conexin 43 in murine sertoli cell development. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2010. [cited 2020 Jan 22]. Available from: http://hdl.handle.net/2142/16108.

Council of Science Editors:

Sridharan S. The role of conexin 43 in murine sertoli cell development. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2010. Available from: http://hdl.handle.net/2142/16108

IUPUI

25. Rohrabaugh, Sara L. Effects of Altering Cell Proliferation on Hematopoietic Stem and Progenitor Cell Function.

Degree: 2011, IUPUI

URL: http://hdl.handle.net/1805/2599

►

Indiana University-Purdue University Indianapolis (IUPUI)

Cell cycle checkpoints guarantee movement through the cell cycle in an appropriate manner. The spindle assembly checkpoint (SAC) ensures the… (more)

▼

Indiana University-Purdue University Indianapolis (IUPUI)

Cell cycle checkpoints guarantee movement through the cell cycle in an appropriate manner. The spindle assembly checkpoint (SAC) ensures the proper segregation of chromosomes into daughter cells during mitosis. Mitotic arrest deficiency 2 (Mad2), a member of the mitotic checkpoint proteins, appears to be crucial for generating the wait anaphase signal to prevent onset of anaphase. We first studied the SAC in hematopoietic stem cells (HSC) to ensure that it was functional. Our previous studies found that prolonged SAC activation was uncoupled from apoptosis initiation in mouse and human embryonic stem cells (ESC). We found that upon treatment with a microtubule-destabilizing agent, HSC arrested in M-phase and subsequently initiated apoptosis. Thus unlike ESC, HSC exhibit coupling of prolonged SAC activation with apoptosis. We studied the effects of Mad2+/- on in vivo recovery of bone marrow HPC from cytotoxic effects and also effects of cytostatic agents on HPC growth in vitro using Mad2-haploinsufficient (Mad2+/-) mice. We found that Mad2+/- HPCs were protected from the cytotoxic effects of cytarabine (Ara-C), a cycle specific agent, consistent with Mad2+/- HPCs being in a slow or non-cycling state. Mad2 haploinsufficiency did not affect recovery of functional HPC after treatment with cyclophosphamide or high sub-lethal dose irradiation, both non-cycle specific agents. There were no differences in immunophenotype defined HSCs in Mad2+/- and Mad2+/+ mice, data confirmed by functional HSC competitive repopulation assays. To better understand the role of Mad2 in HPC, E3330, a cytostatic agent, was used to assess the redox function of Ape1/Ref-1, and colony formation in vitro was examined under normoxic and lowered O2 tension. Mad2+/- HPCs were less responsive to E3330 than Mad2+/+ HPCs, and E3330 was more effective under lowered O2 tension. Mad2+/- HPCs did not exhibit enhanced growth in lowered oxygen tension, in contrast to Mad2+/+ HPCs. Our studies have unexpectedly found that Mad2 haploinsufficiency is protective from the cytotoxic effects of a cycle specific DNA synthesis agent in vivo, and Ape1/Ref-1 inhibitor in vitro.

Advisors/Committee Members: Broxmeyer, Hal E., Pelus, Louis, Roman, Ann, Yoder, Mervin C..

Subjects/Keywords: hematopoietic stem cell, hematopoietic progenitor cell, cell cycle; Hematopoietic stem cells; Cell cycle – Regulation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rohrabaugh, S. L. (2011). Effects of Altering Cell Proliferation on Hematopoietic Stem and Progenitor Cell Function. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/2599

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rohrabaugh, Sara L. “Effects of Altering Cell Proliferation on Hematopoietic Stem and Progenitor Cell Function.” 2011. Thesis, IUPUI. Accessed January 22, 2020. http://hdl.handle.net/1805/2599.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rohrabaugh, Sara L. “Effects of Altering Cell Proliferation on Hematopoietic Stem and Progenitor Cell Function.” 2011. Web. 22 Jan 2020.

Vancouver:

Rohrabaugh SL. Effects of Altering Cell Proliferation on Hematopoietic Stem and Progenitor Cell Function. [Internet] [Thesis]. IUPUI; 2011. [cited 2020 Jan 22]. Available from: http://hdl.handle.net/1805/2599.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rohrabaugh SL. Effects of Altering Cell Proliferation on Hematopoietic Stem and Progenitor Cell Function. [Thesis]. IUPUI; 2011. Available from: http://hdl.handle.net/1805/2599

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Université de Grenoble

26. Vu Hong, Lien. Les Benzo[e]pyridoindoles, une nouvelle famille d'inhibiteurs de kinase à activité anti-proliférative : Benzo[e]pyridoindole, the novel kinase inhibitor family with antiproliferative activity.

Degree: Docteur es, Biologie cellulaire, 2011, Université de Grenoble

URL: http://www.theses.fr/2011GRENV049

►

Les Benzo[e]pyridoindoles sont identifiés comme inhibiteurs des kinases Aurora. La molécule la plus active, C1, inhibe efficacement à la fois Aurora B et CHK2. Nous… (more)

▼

Les Benzo[e]pyridoindoles sont identifiés comme inhibiteurs des kinases Aurora. La molécule la plus active, C1, inhibe efficacement à la fois Aurora B et CHK2. Nous avons donc exploité cette potentialité dans des applications de traitements combinés en se basant sur la spécificité restreinte mais multiple de cet inhibiteur. Nous avons mis en place le traitement combiné (Etoposide et C1) sur des lignées cellulaires et des effets additifs pour H358 et synergiques pour U2OS et HL60 sont notés. Ce traitement empêche efficacement la croissance des sphéroides et l'expansion des xénogreffes cellulaires. Un des avantages majeur de cette combinaison est la diminution des doses d'agents de dommages à l'ADN. C1 ouvre une piste pharmacologique basée sur l'altération simultanée de la mitose et de la réparation. La famille des benzo[e]pyridoindoles possède une forme penta-hétérocyclique avec 3 chaines latérales dont les variations peuvent influencer l'activité inhibitrice. Nous avons donc mesuré l'activité antimitotique de différents benzo[e]pyridoindoles. Cette étude structure/fonction permet de définir la contribution des chaînes latérales dans l'activité inhibitrice et d'orienter les futures synthèses. Nous nous sommes également intéressés au composé C4 qui avait un profil atypique d'inhibition de phosphorylation de l'histone H3. Il inhibe cette phosphorylation uniquement en entrée de mitose. Nous avons ainsi pu montrer que la phosphorylation de l'histone H3 n'est pas nécessaire à l'assemblage des chromosomes. Enfin, nous avons caractérisé l'efficacité de la molécule C21, un composé à forte activité anti-proliférative, sur différents modèles cellulaires et animaux. Ce travail révèle les potentialités multiples des benzo[e]pyridoindoles comme nouvelles molécules anti-prolifératives

Benzo[e]pyridoindole is identified as the novel Aurora inhibiteurs. The most potent compound, C1, inhibits efficiently both Aurora B and CHK2. Thus, we exploited the potency of this molecule in combined treatment applications based on its sharp and multiple specificities. We set up the combined treatments (Etoposide plus C1) on different cell lines and obtained an additive effect on H358 and a synergic one for HL60 and U2OS cells. This combination prevents the spheroid development as well as the cellular xenograft expansion. One of the main advantages of this combination is to decrease the dose of DNA damage agents in therapy leading to the reduction of their toxicity. C1 inhibiting both CHK2 and Aurora B open the way to targeted pharmacology based on simultaneous alteration of mitotic onset and DNA damage defences. Benzo[e]pyridoindole family has a penta-heterocyclic form with 3 lateral chains. The variations of these lateral chains can affect the inhibitory activity of the compounds. We researched the antimitotic efficiency of several benzo[e]pyridoindoles. This structure/function study drives to define the contribution of lateral chains in inhibitory activity and will direct future synthesis. We focused on compound C4 that induced an unusual…

Advisors/Committee Members: Molla, Annie (thesis director).

Subjects/Keywords: Mitose; Kinase; Cycle cellulaire; Cycle cellulaire; Kinase; Cell cycle; 570

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APA (6^th Edition):

Vu Hong, L. (2011). Les Benzo[e]pyridoindoles, une nouvelle famille d'inhibiteurs de kinase à activité anti-proliférative : Benzo[e]pyridoindole, the novel kinase inhibitor family with antiproliferative activity. (Doctoral Dissertation). Université de Grenoble. Retrieved from http://www.theses.fr/2011GRENV049

Chicago Manual of Style (16^th Edition):

Vu Hong, Lien. “Les Benzo[e]pyridoindoles, une nouvelle famille d'inhibiteurs de kinase à activité anti-proliférative : Benzo[e]pyridoindole, the novel kinase inhibitor family with antiproliferative activity.” 2011. Doctoral Dissertation, Université de Grenoble. Accessed January 22, 2020. http://www.theses.fr/2011GRENV049.

MLA Handbook (7^th Edition):

Vu Hong, Lien. “Les Benzo[e]pyridoindoles, une nouvelle famille d'inhibiteurs de kinase à activité anti-proliférative : Benzo[e]pyridoindole, the novel kinase inhibitor family with antiproliferative activity.” 2011. Web. 22 Jan 2020.

Vancouver:

Vu Hong L. Les Benzo[e]pyridoindoles, une nouvelle famille d'inhibiteurs de kinase à activité anti-proliférative : Benzo[e]pyridoindole, the novel kinase inhibitor family with antiproliferative activity. [Internet] [Doctoral dissertation]. Université de Grenoble; 2011. [cited 2020 Jan 22]. Available from: http://www.theses.fr/2011GRENV049.

Council of Science Editors:

Vu Hong L. Les Benzo[e]pyridoindoles, une nouvelle famille d'inhibiteurs de kinase à activité anti-proliférative : Benzo[e]pyridoindole, the novel kinase inhibitor family with antiproliferative activity. [Doctoral Dissertation]. Université de Grenoble; 2011. Available from: http://www.theses.fr/2011GRENV049

27. Keifenheim, Daniel L. Cell Size Control in the Fission Yeast Schizosaccharomyces pombe: A Dissertation.

Degree: Interdisciplinary Graduate Program, Biochemistry and Molecular Pharmacology, 2015, U of Massachusetts : Med

URL: http://escholarship.umassmed.edu/gsbs_diss/784

► The coordination between cell growth and division is a highly regulated process that is intimately linked to the cell cycle. Efforts to identify an… (more)

▼ The coordination between cell growth and division is a highly regulated process that is intimately linked to the cell cycle. Efforts to identify an independent mechanism that measures cell size have been unsuccessful. Instead, we propose that size control is an intrinsic function of the basic cell cycle machinery. My work shows that in the fission yeast Schizosaccharomyces pombe Cdc25 accumulates in a size dependent manner. This accumulation of Cdc25 occurs over a large range of cell sizes. Additionally, experiments with short pulses of cycloheximide have shown that Cdc25 is an inherently unstable protein that quickly returns to a size dependent equilibrium in the cell suggesting that Cdc25 concentration is dependent on size and not time. Thus, Cdc25 can act as a sizer for the cell. However, cells are still viable when Cdc25 is constitutively expressed suggesting that there is another sizer in the case that Cdc25 expression is compromised. Cdc13 is a likely candidate due to the similar characteristics to Cdc25 and the ability to activate Cdc2. Cdc13 accumulates during the cell cycle in a manner similar to Cdc25. I show that in the absence of Cdc2 tyrosine phosphorylation, the cell size is sensitive to Cdc13 activity showing that Cdc13 accumulation can determine when cells enter mitosis. These results suggest a two sizer model where Cdc25 is the main sizer with Cdc13 acting as a backup sizer in the event of Cdc25 expression is compromised. Additionally, in the absence of Cdc2 phosphorylation by the kinases Wee1 and Mik1, mitotic entry is regulated by the activity of Cdc2. In the absence of Cdc2 phosphorylation, this activity is regulated by binding of cyclins to Cdc2. Under these circumstances, the activity of Cdc13 can regulate mitotic entry provide further evidence that Cdc13 could be a sizer of the cell in the case where Cdc25 expression is compromised. The results I present in this dissertation provide the groundwork for understanding how cells regulate size and how this size regulation affects cell cycle control in S. pombe . The results show how the intrinsic cell cycle machinery can act as a sizer for the G2/M transition in S. pombe . Interestingly, this mitotic commitment pathway is well conserved suggesting a general solution for size control in eukaryotes at the G2/M transition. Understanding the mechanism of how protein concentration is regulated in a size dependent manner will give much needed insight into how cells control size. Elucidating the mechanism for size control will capitalize on decades of research and deepen our understanding of basic cell biology. Advisors/Committee Members: Nick Rhind, PhD.

Subjects/Keywords: Cell Size; Cell Cycle; Cell Cycle Checkpoints; Cell Division; Schizosaccharomyces; Cell Biology; Cellular and Molecular Physiology

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APA (6^th Edition):

Keifenheim, D. L. (2015). Cell Size Control in the Fission Yeast Schizosaccharomyces pombe: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/784

Chicago Manual of Style (16^th Edition):

Keifenheim, Daniel L. “Cell Size Control in the Fission Yeast Schizosaccharomyces pombe: A Dissertation.” 2015. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 22, 2020. http://escholarship.umassmed.edu/gsbs_diss/784.

MLA Handbook (7^th Edition):

Keifenheim, Daniel L. “Cell Size Control in the Fission Yeast Schizosaccharomyces pombe: A Dissertation.” 2015. Web. 22 Jan 2020.

Vancouver:

Keifenheim DL. Cell Size Control in the Fission Yeast Schizosaccharomyces pombe: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2015. [cited 2020 Jan 22]. Available from: http://escholarship.umassmed.edu/gsbs_diss/784.

Council of Science Editors:

Keifenheim DL. Cell Size Control in the Fission Yeast Schizosaccharomyces pombe: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2015. Available from: http://escholarship.umassmed.edu/gsbs_diss/784

University of Illinois – Chicago

28. Rady, Brian. Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes.

Degree: 2013, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/10071

► This work pertains to the search for genetic targets to induce beta-cell proliferation. This proliferation was intended to support the advancement of islet cell transplant… (more)

Subjects/Keywords: Diabetes; cell therapy; beta-cell proliferation; cell-cycle

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rady, B. (2013). Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/10071

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rady, Brian. “Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes.” 2013. Thesis, University of Illinois – Chicago. Accessed January 22, 2020. http://hdl.handle.net/10027/10071.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rady, Brian. “Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes.” 2013. Web. 22 Jan 2020.

Vancouver:

Rady B. Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes. [Internet] [Thesis]. University of Illinois – Chicago; 2013. [cited 2020 Jan 22]. Available from: http://hdl.handle.net/10027/10071.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rady B. Transcription Factors E2F Have a Role in Proliferation of Beta-Cells and Development of Type-2 Diabetes. [Thesis]. University of Illinois – Chicago; 2013. Available from: http://hdl.handle.net/10027/10071

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

The Ohio State University

29. Collins, Mark Leo. DHFR RNA metabolism during the cell cycle : a critical review.

Degree: PhD, Graduate School, 1983, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487238791269318

Subjects/Keywords: Chemistry; Cell cycle

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Collins, M. L. (1983). DHFR RNA metabolism during the cell cycle : a critical review. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1487238791269318

Chicago Manual of Style (16^th Edition):

Collins, Mark Leo. “DHFR RNA metabolism during the cell cycle : a critical review.” 1983. Doctoral Dissertation, The Ohio State University. Accessed January 22, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487238791269318.

MLA Handbook (7^th Edition):

Collins, Mark Leo. “DHFR RNA metabolism during the cell cycle : a critical review.” 1983. Web. 22 Jan 2020.

Vancouver:

Collins ML. DHFR RNA metabolism during the cell cycle : a critical review. [Internet] [Doctoral dissertation]. The Ohio State University; 1983. [cited 2020 Jan 22]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487238791269318.

Council of Science Editors:

Collins ML. DHFR RNA metabolism during the cell cycle : a critical review. [Doctoral Dissertation]. The Ohio State University; 1983. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487238791269318

The Ohio State University

30. Evans, David Alan. Modification of the frequency of mitotic crossing in Nicotiana tabacum, Glycine max, and Lycopersicon esculentum using X-rays.

Degree: PhD, Graduate School, 1977, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487064256736819

Subjects/Keywords: Biology; Cell cycle

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Evans, D. A. (1977). Modification of the frequency of mitotic crossing in Nicotiana tabacum, Glycine max, and Lycopersicon esculentum using X-rays. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1487064256736819

Chicago Manual of Style (16^th Edition):

Evans, David Alan. “Modification of the frequency of mitotic crossing in Nicotiana tabacum, Glycine max, and Lycopersicon esculentum using X-rays.” 1977. Doctoral Dissertation, The Ohio State University. Accessed January 22, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487064256736819.

MLA Handbook (7^th Edition):

Evans, David Alan. “Modification of the frequency of mitotic crossing in Nicotiana tabacum, Glycine max, and Lycopersicon esculentum using X-rays.” 1977. Web. 22 Jan 2020.

Vancouver:

Evans DA. Modification of the frequency of mitotic crossing in Nicotiana tabacum, Glycine max, and Lycopersicon esculentum using X-rays. [Internet] [Doctoral dissertation]. The Ohio State University; 1977. [cited 2020 Jan 22]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487064256736819.

Council of Science Editors:

Evans DA. Modification of the frequency of mitotic crossing in Nicotiana tabacum, Glycine max, and Lycopersicon esculentum using X-rays. [Doctoral Dissertation]. The Ohio State University; 1977. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487064256736819

Open Access Theses and Dissertations