Log in

Relevant bibliographies by topics / Checkpoint in G2 / G2 checkpoint

Contents

Journal articles
Dissertations / Theses
Book chapters
Conference papers
Reports

Academic literature on the topic 'Checkpoint in G2 / G2 checkpoint'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Checkpoint in G2 / G2 checkpoint.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Checkpoint in G2 / G2 checkpoint"

1

Xu, Bo, Seong-Tae Kim, Dae-Sik Lim, and Michael B. Kastan. "Two Molecularly Distinct G2/M Checkpoints Are Induced by Ionizing Irradiation." Molecular and Cellular Biology 22, no. 4 (2002): 1049–59. http://dx.doi.org/10.1128/mcb.22.4.1049-1059.2002.

Full text

Abstract:

ABSTRACT Cell cycle checkpoints are among the multiple mechanisms that eukaryotic cells possess to maintain genomic integrity and minimize tumorigenesis. Ionizing irradiation (IR) induces measurable arrests in the G1, S, and G2 phases of the mammalian cell cycle, and the ATM (ataxia telangiectasia mutated) protein plays a role in initiating checkpoint pathways in all three of these cell cycle phases. However, cells lacking ATM function exhibit both a defective G2 checkpoint and a prolonged G2 arrest after IR, suggesting the existence of different types of G2 arrest. Two molecularly distinct G2

APA, Harvard, Vancouver, ISO, and other styles

2

Qiu, Ling, Andrew Burgess, David P. Fairlie, Helen Leonard, Peter G. Parsons, and Brian G. Gabrielli. "Histone Deacetylase Inhibitors Trigger a G2 Checkpoint in Normal Cells That Is Defective in Tumor Cells." Molecular Biology of the Cell 11, no. 6 (2000): 2069–83. http://dx.doi.org/10.1091/mbc.11.6.2069.

Full text

Abstract:

Important aspects of cell cycle regulation are the checkpoints, which respond to a variety of cellular stresses to inhibit cell cycle progression and act as protective mechanisms to ensure genomic integrity. An increasing number of tumor suppressors are being demonstrated to have roles in checkpoint mechanisms, implying that checkpoint dysfunction is likely to be a common feature of cancers. Here we report that histone deacetylase inhibitors, in particular azelaic bishydroxamic acid, triggers a G2 phase cell cycle checkpoint response in normal human cells, and this checkpoint is defective in a

APA, Harvard, Vancouver, ISO, and other styles

3

Soni, Aashish, Xiaolu Duan, Martin Stuschke, and George Iliakis. "ATR Contributes More Than ATM in Intra-S-Phase Checkpoint Activation after IR, and DNA-PKcs Facilitates Recovery: Evidence for Modular Integration of ATM/ATR/DNA-PKcs Functions." International Journal of Molecular Sciences 23, no. 14 (2022): 7506. http://dx.doi.org/10.3390/ijms23147506.

Full text

Abstract:

The intra-S-phase checkpoint was among the first reported cell cycle checkpoints in mammalian cells. It transiently slows down the rate of DNA replication after DNA damage to facilitate repair and thus prevents genomic instability. The ionizing radiation (IR)-induced intra-S-phase checkpoint in mammalian cells is thought to be mainly dependent upon the kinase activity of ATM. Defects in the intra-S-phase checkpoint result in radio-resistant DNA synthesis (RDS), which promotes genomic instability. ATM belongs to the PI3K kinase family along with ATR and DNA-PKcs. ATR has been shown to be the ke

APA, Harvard, Vancouver, ISO, and other styles

4

Osman, Fekret, Irina R. Tsaneva, Matthew C. Whitby, and Claudette L. Doe. "UV Irradiation Causes the Loss of Viable Mitotic Recombinants in Schizosaccharomyces pombe Cells Lacking the G2/M DNA Damage Checkpoint." Genetics 160, no. 3 (2002): 891–908. http://dx.doi.org/10.1093/genetics/160.3.891.

Full text

Abstract:

Abstract Elevated mitotic recombination and cell cycle delays are two of the cellular responses to UV-induced DNA damage. Cell cycle delays in response to DNA damage are mediated via checkpoint proteins. Two distinct DNA damage checkpoints have been characterized in Schizosaccharomyces pombe: an intra-S-phase checkpoint slows replication and a G2/M checkpoint stops cells passing from G2 into mitosis. In this study we have sought to determine whether UV damage-induced mitotic intrachromosomal recombination relies on damage-induced cell cycle delays. The spontaneous and UV-induced recombination

APA, Harvard, Vancouver, ISO, and other styles

5

Li, Fanghua, Emil Mladenov, Rositsa Dueva, Martin Stuschke, Beate Timmermann, and George Iliakis. "Shift in G1-Checkpoint from ATM-Alone to a Cooperative ATM Plus ATR Regulation with Increasing Dose of Radiation." Cells 11, no. 1 (2021): 63. http://dx.doi.org/10.3390/cells11010063.

Full text

Abstract:

The current view of the involvement of PI3-kinases in checkpoint responses after DNA damage is that ATM is the key regulator of G1-, S- or G2-phase checkpoints, that ATR is only partly involved in the regulation of S- and G2-phase checkpoints and that DNA-PKcs is not involved in checkpoint regulation. However, further analysis of the contributions of these kinases to checkpoint responses in cells exposed to ionizing radiation (IR) recently uncovered striking integrations and interplays among ATM, ATR and DNA-PKcs that adapt not only to the phase of the cell cycle in which cells are irradiated,

APA, Harvard, Vancouver, ISO, and other styles

6

Xu, Zhiheng, and David Norris. "The SFP1 Gene Product of Saccharomyces cerevisiae Regulates G2/M Transitions During the Mitotic Cell Cycle and DNA-Damage Response." Genetics 150, no. 4 (1998): 1419–28. http://dx.doi.org/10.1093/genetics/150.4.1419.

Full text

Abstract:

Abstract In eukaryotic cells, checkpoint pathways arrest cell-cycle progression if a particular event has failed to complete appropriately or if an important intracellular structure is defective or damaged. Saccharomyces cerevisiae strains that lack the SFP1 gene fail to arrest at the G2 DNA-damage checkpoint in response to genomic injury, but maintain their ability to arrest at the replication and spindle-assembly checkpoints. sfp1Δ mutants are characterized by a premature entrance into mitosis during a normal (undamaged) cell cycle, while strains that overexpress Sfp1p exhibit delays in G2.

APA, Harvard, Vancouver, ISO, and other styles

7

Xu, Bo, Seong-tae Kim, and Michael B. Kastan. "Involvement of Brca1 in S-Phase and G2-Phase Checkpoints after Ionizing Irradiation." Molecular and Cellular Biology 21, no. 10 (2001): 3445–50. http://dx.doi.org/10.1128/mcb.21.10.3445-3450.2001.

Full text

Abstract:

ABSTRACT Cell cycle arrests in the G1, S, and G2phases occur in mammalian cells after ionizing irradiation and appear to protect cells from permanent genetic damage and transformation. Though Brca1 clearly participates in cellular responses to ionizing radiation (IR), conflicting conclusions have been drawn about whether Brca1 plays a direct role in cell cycle checkpoints. Normal Nbs1 function is required for the IR-induced S-phase checkpoint, but whether Nbs1 has a definitive role in the G2/M checkpoint has not been established. Here we show that Atm and Brca1 are required for both the S-phas

APA, Harvard, Vancouver, ISO, and other styles

8

Dhar, Sonu, Jeremy A. Squire, M. Prakash Hande, Raymund J. Wellinger та Tej K. Pandita. "Inactivation of 14-3-3ς Influences Telomere Behavior and Ionizing Radiation-Induced Chromosomal Instability". Molecular and Cellular Biology 20, № 20 (2000): 7764–72. http://dx.doi.org/10.1128/mcb.20.20.7764-7772.2000.

Full text

Abstract:

ABSTRACT Telomeres are complexes of repetitive DNA sequences and proteins constituting the ends of linear eukaryotic chromosomes. While these structures are thought to be associated with the nuclear matrix, they appear to be released from this matrix at the time when the cells exit from G2 and enter M phase. Checkpoints maintain the order and fidelity of the eukaryotic cell cycle, and defects in checkpoints contribute to genetic instability and cancer. The 14-3-3ς gene has been reported to be a checkpoint control gene, since it promotes G2 arrest following DNA damage. Here we demonstrate that

APA, Harvard, Vancouver, ISO, and other styles

9

Shigetomi, Hiroshi, Tamotsu Sudo, Keiji Shimada та ін. "Inhibition of Cell Death and Induction of G2 Arrest Accumulation in Human Ovarian Clear Cells by HNF-1β Transcription Factor: Chemosensitivity Is Regulated by Checkpoint Kinase CHK1". International Journal of Gynecologic Cancer 24, № 5 (2014): 838–43. http://dx.doi.org/10.1097/igc.0000000000000136.

Full text

Abstract:

ObjectiveAppropriate cell cycle checkpoints are essential for the maintenance of normal cells and chemosensitivity of cancer cells. Clear cell adenocarcinoma (CCA) of the ovary is highly resistant to chemotherapy. Hepatocyte nuclear factor-1β (HNF-1β) is known to be overexpressed in CCA, but its role and clinical significance is unclear. We investigated the role of HNF-1β in regulation of the cell cycle in CCA.MethodsTo clarify the effects of HNF-1β on cell cycle checkpoints, we compared the cell cycle distribution and the expression of key proteins involved in CCA cells in which HNF-1β had be

APA, Harvard, Vancouver, ISO, and other styles

10

Rhind, Nicholas, and Paul Russell. "Roles of the Mitotic Inhibitors Wee1 and Mik1 in the G2 DNA Damage and Replication Checkpoints." Molecular and Cellular Biology 21, no. 5 (2001): 1499–508. http://dx.doi.org/10.1128/mcb.21.5.1499-1508.2001.

Full text

Abstract:

ABSTRACT The G2 DNA damage and DNA replication checkpoints in many organisms act through the inhibitory phosphorylation of Cdc2 on tyrosine-15. This phosphorylation is catalyzed by the Wee1/Mik1 family of kinases. However, the in vivo role of these kinases in checkpoint regulation has been unclear. We show that, in the fission yeastSchizosaccharomyces pombe, Mik1 is a target of both checkpoints and that the regulation of Mik1 is, on its own, sufficient to delay mitosis in response to the checkpoints. Mik1 appears to have two roles in the DNA damage checkpoint; one in the establishment of the c

APA, Harvard, Vancouver, ISO, and other styles

More sources

Dissertations / Theses on the topic "Checkpoint in G2 / G2 checkpoint"

1

Carrassa, Laura. "Molecular mechanisms regulating the G2 checkpoint induced after DNA damage." Thesis, Open University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434262.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Ahmad, Syed Saif. "Deciphering the role of BRCA2 at the damage-induced G2 checkpoint." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/278013.

Full text

Abstract:

Loss of DNA damage-induced G2 checkpoint control is associated with genome instability, tumour formation and the therapeutic response of tumours to genotoxic agents. The large 3418 residue protein encoded by BRCA2 – heterozygous germline mutations in which predispose to cancer - has recently been implicated in G2 checkpoint maintenance. However, the mechanistic basis of BRCA2’s role in the G2 checkpoint remains unknown. The overall aim of my research is to understand the mechanism by which BRCA2 regulates the G2 checkpoint. Domain mapping studies, using overlapping fragments encoding the full-

APA, Harvard, Vancouver, ISO, and other styles

3

Tao, Yungan. "Interruption of G2-M and mitotic checkpoint : Influence on tumor radiosensitivity." Paris 11, 2008. http://www.theses.fr/2008PA11T062.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Zhou, Yan. "Regulation of Aurora A activity during checkpoint recovery." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-181746.

Full text

Abstract:

Cell division requires accurate DNA replication and cells develop checkpoint mechanisms toensure the correct passage of the genetic material. Cells arrest by a checkpoint when DNAdamage is found. After the checkpoint is silenced, the cell cycle can be resumed. Polo-likekinase 1 (Plk1) and Aurora A kinase (AurA) are both important regulators for checkpointrecovery. The question how AurA is activated was studied by many researchers, but the exactmechanism stays unclear.We developed a new setup to study AurA activation during checkpoint recovery. Quantitativeimmunofluorescence of fixed cells as w

APA, Harvard, Vancouver, ISO, and other styles

5

Daviknes, Ingrid Marie Eriksen. "G2 checkpoint siRNA screen in irradiated cancer cells: validation of candidate positive hits." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for bioteknologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-14145.

Full text

Abstract:

Prior to this project, a high throughput assay was developed in order to perform automated RNAi screens with siRNA- libraries targeting potential regulators of the G2 checkpoint. The libraries were covering the human kinases, phosphatases and DNA repair. The aim of this project was to validate the candidate hits from the phosphatome screen as possible G2 checkpoint regulators. To validate the candidate hits, esiRNAs were applied in order to down regulate the target proteins, and G2 checkpoint abrogation was assayed by flow cytometry analysis. To confirm that the assay did work, the effects of

APA, Harvard, Vancouver, ISO, and other styles

6

Putnam, Charles Wellington. "Integration of G2/M checkpoint, spindle assembly checkpoint,and Ran cycle regulators in the Saccharomyces cerevisiae DNA damage mitotic arrest response." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280738.

Full text

Abstract:

It is axiomatic that genomic stability is dependent upon regulatory pathways, termed checkpoints, which sense perturbations of cell cycle execution including damage to chromosomal DNA. In Saccharomyces cerevisiae, the principal DNA damage checkpoint is at G2/M. Heretofore, this and other checkpoints, such as the spindle assembly checkpoint, which is also operative at the metaphase/anaphase transition, have been viewed as essentially linear pathways, responding to a specific type of damage, signaling via sui generis proteins, and targeting a limited number of effectors for arrest. In a 1999 rep

APA, Harvard, Vancouver, ISO, and other styles

7

Cervigni, Romina Ines. "Analysis of the molecular mechanisms of the Golgi-based G2/M cell cycle checkpoint." Thesis, Open University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.580685.

Full text

Abstract:

This thesis is focused on the role of Golgi fragmentation in the regulation of the G2/M transition of the cell cycle, and it is based on previous findings that Golgi fragmentation is required to enter into mitosis. The Golgi complex is composed of many cisternal stacks that are interconnected by tubules, to form a continuous 'ribbon-like' structure. During mitosis, the Golgi ribbon undergoes extensive fragmentation through a multi stage process that promotes its correct partitioning and inheritance by the daughter cells. The first part of my work is focused on the understanding of the mechanis

APA, Harvard, Vancouver, ISO, and other styles

8

Thanasoula, Maria. "ATM/ATR-dependent responses to dysfunctional telomeres at the G2/M transition." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:b9f806e3-88e5-4dc4-b2e9-8ecf854249d1.

Full text

Abstract:

Mammalian telomeres are nucleoprotein complexes at the end of chromosomes containing a specific protein complex, called shelterin. Shelterin protects chromosome ends from the DNA damage response (DDR), by facilitating the formation of a telomeric capping structure, called the T-loop. During their elongation in S phase, telomeres become transiently uncapped and can be sensed as DNA damage in G2 phase. This leads to the recruitment of DDR factors, such as phosphorylated histone H2AX (γH2AX), to the telomeres forming the so-called, telomere dysfunction-induced foci (TIFs). My PhD work described h

APA, Harvard, Vancouver, ISO, and other styles

9

Xu, Lin. "Novel G2 cell cycle checkpoint inhibitors and antimitotic agents isolated through two new HTS bioassays." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61207.pdf.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Feeney, Katherine M. "Investigations of G2/M decatenation checkpoint control, using the DNA topoisomerase II inhibitor ICRF-193." Thesis, University of Ulster, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.529562.

Full text

APA, Harvard, Vancouver, ISO, and other styles

More sources

Book chapters on the topic "Checkpoint in G2 / G2 checkpoint"

1

Kaufmann, William K. "Decatenation G2 Checkpoint." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1541-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Kaufmann, William K. "Decatenation G2 Checkpoint." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_1541.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Kaufmann, William K. "Decatenation G2 Checkpoint." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1541.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Maller, J. L., B. G. Gabrielli, L. M. Roy, D. H. Walker, and T. Izumi. "Regulating the G2 Checkpoint in the Cell Cycle." In Tyrosine Phosphorylation/Dephosphorylation and Downstream Signalling. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78247-3_42.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Tapia-Alveal, Claudia, and Matthew J. O’Connell. "Methods for Studying the G2 DNA Damage Checkpoint in Mammalian Cells." In Cell Cycle Checkpoints. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Kuang, Jian, and Ruoning Wang. "Mechanisms of G2 Phase Arrest in DNA Damage-Induced Checkpoint Response." In Checkpoint Controls and Targets in Cancer Therapy. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-178-3_3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Kaufmann, William K. "Analysis of the Topoisomerase II-Dependent Decatenation G2 Checkpoint and Checkpoint Kinases in Human Cells." In Methods in Molecular Biology. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-340-4_13.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Ye, Xiang S., and Stephen A. Osmani. "Regulation of p34cdc2/cylinB H1 and NIMA kinases during the G2/M transition and checkpoint responses in Aspergillus nidulans." In Progress in Cell Cycle Research. Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5371-7_17.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Willis, Nicholas, and Nicholas Rhind. "Studying G2 DNA Damage Checkpoints Using the Fission Yeast Schizosaccharomyces pombe." In Cell Cycle Checkpoints. Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

"G2 Checkpoint Abrogation." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2293.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Checkpoint in G2 / G2 checkpoint"

1

Li, G., S. S. Nair, S. J. Lees, and F. W. Booth. "Regulation of G2/M Transition in Mammalian Cells by Oxidative Stress." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-82349.

Full text

Abstract:

The regulation of the G2/M transition for the mammalian cell cycle has been modeled using 19 states to investigate the G2 checkpoint dynamics in response to oxidative stress. A detailed network model of G2/M regulation is presented and then a “core” subsystem is extracted from the full network. An existing model of Mitosis control is extended by adding two important pathways regulating G2/M transition in response to DNA damage induced by oxidative stress. Model predictions indicate that the p53 dependent pathway is not required for initial G2 arrest as the Chk1/Cdc25C pathway can arrest the ce

APA, Harvard, Vancouver, ISO, and other styles

2

Slangen, Paul, Mariska van Geldorp, Mark de Gooijer, Olaf van Tellingen, and Gerben Borst. "Abstract 92: Increasing TTFields treatment efficacy by targeting G2 cell cycle checkpoint." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-92.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Rorà, Andrea Ghelli Luserna di, Ilaria Iacobucci, Enrica Imbrogno, et al. "Abstract 294: Override the doxorubicin-induced G2/M checkpoint using cell-cycle checkpoint inhibitors on acute lymphoblastic leukemia." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-294.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Simhadri, Srilatha R., Hong Cai, and Bing Xia. "Abstract 636: Role of PALB2 and the BRCA complex in G2/M checkpoint control." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-636.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Yang, Linlin, Cory Pettit, Andrew Hu, Tianyun Li, and Terence M. Williams. "Abstract 981: Wee-1 kinase inhibitor AZD-1775 radiosensitizes esophageal cancer through targeting G2 checkpoint activation." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-981.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Gery, Sigal, Takayuki Tabasyhi, Verena Nowak, Rocio Alvarez, Julia Sohn, and Phillip H. Koeffler. "Abstract 3871: Per1 is phosphorylated by ATM/ATR and is involved in the G2/M checkpoint response." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3871.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Parsels, Leslie A., Daria M. Tanska, Joshua D. Parsels, et al. "Abstract 2964: AZD7762-mediated gemcitabine sensitization does not require G2-M checkpoint abrogation in pancreatic cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2964.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Chiyoda, Tatsuyuki, Shinji Kuninaka, Kenta Masuda, et al. "Abstract 562: The Hippo pathway component LATS1 phosphorylates MYPT1 to counteract PLK1 and regulate G2 DNA damage checkpoint." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-562.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Ghosh-Choudhury, Triparna, Holli A. Loomans, Ying-Wooi Wan, Zhangdon Liu, Shannon M. Hawkins, and Matthew L. Anderson. "Abstract 3113: Hyperactivation of FOXM1 drives ovarian cancer growth and metastasis independent of the G2-M cell cycle checkpoint." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3113.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Chatterjee, Suman, and Timothy F. Burns. "Abstract 762: Ganetespib resistance inKRASmutant NSCLC is mediated through bypassing the G2/M checkpoint and reactivating the PI3K/MTOR pathway." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-762.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Checkpoint in G2 / G2 checkpoint"

1

Britt, Anne. G2 Checkpoint Responses in Arabidopsis. Office of Scientific and Technical Information (OSTI), 2013. http://dx.doi.org/10.2172/1116357.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Besley, Blair D., and Scott K. Davey. Analysis of hRad1, a Human G2 Checkpoint Control Gene. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada407538.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Hall, Eric J., Lubomir B. Smilenov, and Erik F. Young. Genetic Control of the Trigger for the G2/M Checkpoint. Office of Scientific and Technical Information (OSTI), 2013. http://dx.doi.org/10.2172/1095188.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Oesterreich, Steffi. The Scaffold Attachment Factor SAFB1P: A New Player in G2/M Checkpoint Control. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada435280.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

McGowan, Clare H. The Role of G2/M Checkpoint Controls in Cytotoxic Treatment of Breast Cancer. Defense Technical Information Center, 1997. http://dx.doi.org/10.21236/ada340581.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!