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Journal articles on the topic 'Checkpoint'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

PAUN, MIHAELA, NICHAMON NAKSINEHABOON, RAJA NASSAR, CHOKCHAI LEANGSUKSUN, STEPHEN L. SCOTT, and NARATE TAERAT. "INCREMENTAL CHECKPOINT SCHEMES FOR WEIBULL FAILURE DISTRIBUTION." International Journal of Foundations of Computer Science 21, no. 03 (2010): 329–44. http://dx.doi.org/10.1142/s0129054110007283.

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Incremental checkpoint mechanism was introduced to reduce high checkpoint overhead of regular (full) checkpointing, especially in high-performance computing systems. To gain an extra advantage from the incremental checkpoint technique, we propose an optimal checkpoint frequency function that globally minimizes the expected wasted time of the incremental checkpoint mechanism. Also, the re-computing time coefficient used to approximate the re-computing time is derived. Moreover, to reduce the complexity in the recovery state, full checkpoints are performed from time to time. In this paper we pre

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Rhind, Nicholas, and Paul Russell. "The Schizosaccharomyces pombe S-Phase Checkpoint Differentiates Between Different Types of DNA Damage." Genetics 149, no. 4 (1998): 1729–37. http://dx.doi.org/10.1093/genetics/149.4.1729.

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Abstract We have identified an S-phase DNA damage checkpoint in Schizosaccharomyces pombe. This checkpoint is dependent on Rad3, the S. pombe homolog of the mammalian ATM/ATR checkpoint proteins, and Cds1. Cds1 had previously been believed to be involved only in the replication checkpoint. The requirement of Cds1 in the DNA damage checkpoint suggests that Cds1 may be a general target of S-phase checkpoints. Unlike other checkpoints, the S. pombe S-phase DNA damage checkpoint discriminates between different types of damage. UV-irradiation, which causes base modification that can be repaired dur

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Naksinehaboon, Nichamon, Mihaela P[un, Raja Nassar, Chokchai Box Leangsuksun, and Stephen Scott. "High Performance Computing Systems with Various Checkpointing Schemes." International Journal of Computers Communications & Control 4, no. 4 (2009): 386. http://dx.doi.org/10.15837/ijccc.2009.4.2455.

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Finding the failure rate of a system is a crucial step in high performance computing systems analysis. To deal with this problem, a fault tolerant mechanism, called checkpoint/ restart technique, was introduced. However, there are additional costs to perform this mechanism. Thus, we propose two models for different schemes (full and incremental checkpoint schemes). The models which are based on the reliability of the system are used to determine the checkpoint placements. Both proposed models consider a balance of between checkpoint overhead and the re-computing time. Due to the extra costs fr

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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.

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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

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Garber, Peter M., and Jasper Rine. "Overlapping Roles of the Spindle Assembly and DNA Damage Checkpoints in the Cell-Cycle Response to Altered Chromosomes in Saccharomyces cerevisiae." Genetics 161, no. 2 (2002): 521–34. http://dx.doi.org/10.1093/genetics/161.2.521.

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Abstract The MAD2-dependent spindle checkpoint blocks anaphase until all chromosomes have achieved successful bipolar attachment to the mitotic spindle. The DNA damage and DNA replication checkpoints block anaphase in response to DNA lesions that may include single-stranded DNA and stalled replication forks. Many of the same conditions that activate the DNA damage and DNA replication checkpoints also activated the spindle checkpoint. The mad2Δ mutation partially relieved the arrest responses of cells to mutations affecting the replication proteins Mcm3p and Pol1p. Thus a previously unrecognize

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Yamada, Ayumi, Brad Duffy, Jennifer A. Perry, and Sally Kornbluth. "DNA replication checkpoint control of Wee1 stability by vertebrate Hsl7." Journal of Cell Biology 167, no. 5 (2004): 841–49. http://dx.doi.org/10.1083/jcb.200406048.

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G2/M checkpoints prevent mitotic entry upon DNA damage or replication inhibition by targeting the Cdc2 regulators Cdc25 and Wee1. Although Wee1 protein stability is regulated by DNA-responsive checkpoints, the vertebrate pathways controlling Wee1 degradation have not been elucidated. In budding yeast, stability of the Wee1 homologue, Swe1, is controlled by a regulatory module consisting of the proteins Hsl1 and Hsl7 (histone synthetic lethal 1 and 7), which are targeted by the morphogenesis checkpoint to prevent Swe1 degradation when budding is inhibited. We report here the identification of X

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Kumar, Parveen, and Rachit Garg. "Soft-Checkpointing Based Hybrid Synchronous Checkpointing Protocol for Mobile Distributed Systems." International Journal of Distributed Systems and Technologies 2, no. 1 (2011): 1–13. http://dx.doi.org/10.4018/jdst.2011010101.

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Minimum-process coordinated checkpointing is a suitable approach to introduce fault tolerance in mobile distributed systems transparently. In order to balance the checkpointing overhead and the loss of computation on recovery, the authors propose a hybrid checkpointing algorithm, wherein an all-process coordinated checkpoint is taken after the execution of minimum-process coordinated checkpointing algorithm for a fixed number of times. In coordinated checkpointing, if a single process fails to take its checkpoint; all the checkpointing effort goes waste, because, each process has to abort its

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8

Islam, Tanzima Zerin, Kathryn Mohror, Saurabh Bagchi, Adam Moody, Bronis R. de Supinski, and Rudolf Eigenmann. "McrEngine: A Scalable Checkpointing System Using Data-Aware Aggregation and Compression." Scientific Programming 21, no. 3-4 (2013): 149–63. http://dx.doi.org/10.1155/2013/341672.

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High performance computing (HPC) systems use checkpoint-restart to tolerate failures. Typically, applications store their states in checkpoints on a parallel file system (PFS). As applications scale up, checkpoint-restart incurs high overheads due to contention for PFS resources. The high overheads force large-scale applications to reduce checkpoint frequency, which means more compute time is lost in the event of failure. We alleviate this problem through a scalable checkpoint-restart system, mcrEngine. McrEngine aggregates checkpoints from multiple application processes with knowledge of the

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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.

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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

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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.

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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

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Moon, Sun Young, Minjoo Han, Gyoungah Ryu, Seong-Ah Shin, Jun Hyuck Lee, and Chang Sup Lee. "Emerging Immune Checkpoint Molecules on Cancer Cells: CD24 and CD200." International Journal of Molecular Sciences 24, no. 20 (2023): 15072. http://dx.doi.org/10.3390/ijms242015072.

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Cancer immunotherapy strategies are based on the utilization of immune checkpoint inhibitors to instigate an antitumor immune response. The efficacy of immune checkpoint blockade, directed at adaptive immune checkpoints, has been demonstrated in select cancer types. However, only a limited subset of patients has exhibited definitive outcomes characterized by a sustained response after discontinuation of therapy. Recent investigations have highlighted the significance of immune checkpoint molecules that are overexpressed in cancer cells and inhibit myeloid lineage immune cells within a tumor mi

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Kumar, Parveen. "A Low-Cost Hybrid Coordinated Checkpointing Protocol for Mobile Distributed Systems." Mobile Information Systems 4, no. 1 (2008): 13–32. http://dx.doi.org/10.1155/2008/982349.

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Mobile distributed systems raise new issues such as mobility, low bandwidth of wireless channels, disconnections, limited battery power and lack of reliable stable storage on mobile nodes. In minimum-process coordinated checkpointing, some processes may not checkpoint for several checkpoint initiations. In the case of a recovery after a fault, such processes may rollback to far earlier checkpointed state and thus may cause greater loss of computation. In all-process coordinated checkpointing, the recovery line is advanced for all processes but the checkpointing overhead may be exceedingly high

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Komolmit, Piyawat. "Immune checkpoint and checkpoint inhibitors in hepatocellular carcinoma." Thai Journal of Hepatology 1, no. 1 (2018): 28–32. http://dx.doi.org/10.30856/th.jhep2018vol1iss1_07.

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การรักษามะเร็งด้วยแนวความคิดของการกระตุ้นให้ภูมิต้านทานของร่างกายไปทำลายเซลล์มะเร็งนั้น ปัจจุบันได้รับการพิสูจน์ชัดว่าวิธีการนี้สามารถหยุดยั้งการแพร่กระจายของเซลล์มะเร็ง โดยไม่ก่อให้เกิดภาวะแทรกซ้อนทางปฏิกิริยาภูมิต้านทานต่ออวัยวะส่วนอื่นที่รุนแรง สามารถนำมาใช้ทางคลินิกได้ ยุคของการรักษามะเร็งกำลังเปลี่ยนจากยุคของยาเคมีบำบัดเข้าสู่การรักษาด้วยภูมิต้านทาน หรือ immunotherapy ยากลุ่ม Immune checkpoint inhibitors โดยเฉพาะ PD-1 กับ CTLA-4 inhibitors จะเข้ามามีบทบาทในการรักษามะเร็งตับในระยะเวลาอันใกล้ จำเป็นแพทย์จะต้องมีความรู้ความเข้าใจในพื้นฐานของ immune checkpoints และยาที่ไปยับยั้งโมเลกุลเหล่านี

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Schollaert, Kaila L., Julie M. Poisson, Jennifer S. Searle, Jennifer A. Schwanekamp, Craig R. Tomlinson, and Yolanda Sanchez. "A Role for Saccharomyces cerevisiae Chk1p in the Response to Replication Blocks." Molecular Biology of the Cell 15, no. 9 (2004): 4051–63. http://dx.doi.org/10.1091/mbc.e03-11-0792.

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Replication blocks and DNA damage incurred during S phase activate the S-phase and intra-S-phase checkpoint responses, respectively, regulated by the Atrp and Chk1p checkpoint kinases in metazoans. In Saccharomyces cerevisiae, these checkpoints are regulated by the Atrp homologue Mec1p and the kinase Rad53p. A conserved role of these checkpoints is to block mitotic progression until DNA replication and repair are completed. In S. cerevisiae, these checkpoints include a transcriptional response regulated by the kinase Dun1p; however, dun1Δ cells are proficient for the S-phase-checkpoint-induced

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15

Heideker, Johanna, Ewa T. Lis, and Floyd E. Romesberg. "Phosphatases, DNA Damage Checkpoints and Checkpoint Deactivation." Cell Cycle 6, no. 24 (2007): 3058–64. http://dx.doi.org/10.4161/cc.6.24.5100.

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Ray, L. B. "Checkpoint, What Checkpoint?" Science's STKE 2007, no. 377 (2007): tw89. http://dx.doi.org/10.1126/stke.3772007tw89.

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Jackson, Robert C. "Modelling malignant progression with a finite state machine supports a two checkpoint theory of cancer." BioDiscovery 1 (July 5, 2012): e8916. https://doi.org/10.7750/BioDiscovery.2012.1.1.

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We postulate the two checkpoints theory of cancer, a model of cancer development suggesting that malignant transformation of cells requires loss of function of both the G1 checkpoint and the mitotic spindle checkpoint. Malignant progression can be described as a process analogous to a genetic algorithm, which we term the malignant progression algorithm. There are two prerequisites for this process: first, there must be competition for reproductive resources, and this is driven by loss of the G1 checkpoint; second, there must be a source of genetic variation, and this is provided by loss of the

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18

Shao, Yizhe, and Chenziqiu Yang. "Immune checkpoint inhibitors for the treatment of Tiple-negative breast cancer." Transactions on Materials, Biotechnology and Life Sciences 6 (September 29, 2024): 78–86. http://dx.doi.org/10.62051/r1g4ph23.

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Recently, the use of immune checkpoint inhibitors (ICIs) on triple negative breast cancer have been a hot research topic. immune checkpoints are vital as they prevent an immune response from being so strong that it kills healthy cells, which is unwanted. When T cell surface proteins bind to partner proteins (immune checkpoint proteins) on other cells, for instance tumor cells, immune checkpoints engage. When the checkpoint and immune checkpoint protein bind together, a signal is released to prevent the cancer from being killed by the immune system. ICIs work by stopping checkpoint proteins fro

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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.

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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

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Zhang, Fangting. "Immune checkpoint inhibitors: the mechanisms, limitations, and improvements." Highlights in Science, Engineering and Technology 8 (August 17, 2022): 14–22. http://dx.doi.org/10.54097/hset.v8i.1105.

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Cancer has been a huge public health concern for decades, with a high incidence and death rate. Traditional therapeutic methods are not effective enough, with many side effects. While immune checkpoint inhibitors, as immunotherapy, are thought to have the most promising future development, aiming at activating immunity against tumor cells for treatment. They worked by blocking immune checkpoints, for example, CTLA-4 and PD-1. These immune checkpoints control T cells expansion, terminate T-cell responses, thus are responsible for the evasion of cancer cells from the immune system, and the immun

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Puntigam, Lisa K., Sandra S. Jeske, Marlies Götz, et al. "Immune Checkpoint Expression on Immune Cells of HNSCC Patients and Modulation by Chemo- and Immunotherapy." International Journal of Molecular Sciences 21, no. 15 (2020): 5181. http://dx.doi.org/10.3390/ijms21155181.

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Endogenous control mechanisms, including immune checkpoints and immunosuppressive cells, are exploited in the process of tumorigenesis to weaken the anti-tumor immune response. Cancer treatment by chemotherapy or immune checkpoint inhibition can lead to changes of checkpoint expression, which influences therapy success. Peripheral blood lymphocytes (PBL) and tumor-infiltrating lymphocytes (TIL) were isolated from head and neck squamous cell carcinoma (HNSCC) patients (n = 23) and compared to healthy donors (n = 23). Immune checkpoint expression (programmed cell death ligand 1 (PD-1), tumor nec

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Sun, Yining, Nan Wang, and Nuo Zhang. "Immune Checkpoint inhibitor Therapy in Various Cancers." Highlights in Science, Engineering and Technology 14 (September 29, 2022): 318–23. http://dx.doi.org/10.54097/hset.v14i.1840.

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Immune checkpoint inhibitors (ICIs) are a new way of immunotherapy, not simply refers to the improvement of immunity to the body, but by improving the immune microenvironment around the tumor, thereby activating immune cell activity in vivo to achieve anti-tumor purposes. Now, CTLA‐4 and PD‐1 or PD‐L1 monoclonal antibody are mainly developed relatively successfully for immune checkpoints, in addition to other new immune checkpoints that have been discovered and clinically tested. However, while immune checkpoint inhibitors have been developed successively, some vague problems still need to be

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Jiang, Zhijun, Yuhang Liu, and Haohui Wang. "Immune Checkpoint Inhibitors Current Advances and Future Perspective." Highlights in Science, Engineering and Technology 74 (December 29, 2023): 1426–30. http://dx.doi.org/10.54097/ykhjgh37.

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Immune therapy has become the fourth method to treat tumors after the traditional methods including radiotherapy, chemotherapy and surgery. Immune therapies use humans’ innate immune system to fight against tumors. Nowadays there are many immune therapies used in clinic, including immune checkpoint inhibitors, cancer vaccines, cytokine therapies, and so on. One of the most mature and widely used immune therapies is immune checkpoint inhibitors (ICIs). Because tumor surface have some proteins that can bind to the receptors on the immune cells, once they are bound the function of the immune syst

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Chauhan, Sachin Kumar Singh, Ulrike Koehl, and Stephan Kloess. "Harnessing NK Cell Checkpoint-Modulating Immunotherapies." Cancers 12, no. 7 (2020): 1807. http://dx.doi.org/10.3390/cancers12071807.

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During the host immune response, the precise balance of the immune system, regulated by immune checkpoint, is required to avoid infection and cancer. These immune checkpoints are the mainstream regulator of the immune response and are crucial for self-tolerance. During the last decade, various new immune checkpoint molecules have been studied, providing an attractive path to evaluate their potential role as targets for effective therapeutic interventions. Checkpoint inhibitors have mainly been explored in T cells until now, but natural killer (NK) cells are a newly emerging target for the dete

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Clémenson, Céline, and Marie-Claude Marsolier-Kergoat. "The Spindle Assembly Checkpoint Regulates the Phosphorylation State of a Subset of DNA Checkpoint Proteins in Saccharomyces cerevisiae." Molecular and Cellular Biology 26, no. 24 (2006): 9149–61. http://dx.doi.org/10.1128/mcb.00310-06.

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ABSTRACT The DNA and the spindle assembly checkpoints play key roles in maintaining genomic integrity by coordinating cell responses to DNA lesions and spindle dysfunctions, respectively. These two surveillance pathways seem to operate mostly independently of one another, and little is known about their potential physiological connections. Here, we show that in Saccharomyces cerevisiae, the activation of the spindle assembly checkpoint triggers phosphorylation changes in two components of the DNA checkpoint, Rad53 and Rad9. These modifications are independent of the other DNA checkpoint protei

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Bashkirov, Vladimir I., Jeff S. King, Elena V. Bashkirova, Jacqueline Schmuckli-Maurer, and Wolf-Dietrich Heyer. "DNA Repair Protein Rad55 Is a Terminal Substrate of the DNA Damage Checkpoints." Molecular and Cellular Biology 20, no. 12 (2000): 4393–404. http://dx.doi.org/10.1128/mcb.20.12.4393-4404.2000.

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ABSTRACT Checkpoints, which are integral to the cellular response to DNA damage, coordinate transient cell cycle arrest and the induced expression of DNA repair genes after genotoxic stress. DNA repair ensures cellular survival and genomic stability, utilizing a multipathway network. Here we report evidence that the two systems, DNA damage checkpoint control and DNA repair, are directly connected by demonstrating that the Rad55 double-strand break repair protein of the recombinational repair pathway is a terminal substrate of DNA damage and replication block checkpoints. Rad55p was specificall

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YANG, ZHONGHUA, CHENGZHENG SUN, YUAN MIAO, ABDUL SATTAR, and YANYAN YANG. "GUARANTEED MUTUALLY CONSISTENT CHECKPOINTING IN DISTRIBUTED COMPUTATIONS." International Journal of Foundations of Computer Science 11, no. 01 (2000): 153–66. http://dx.doi.org/10.1142/s0129054100000089.

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In this paper, we explore the isomorphism between vector time and causality to characterize consistency of a set of checkpoints in a distributed computing. A necessary and sufficient condition, to determine if a set of local checkpoints can form a consistent global checkpoint, is presented and proved using the isomorphic power of vector time and causality. To the best of our knowledge, this is the first attempt to use the isomorphism for this purpose. This condition leads to a simple and straightforward algorithm for a guaranteed mutually consistent global checkpointing. In our approach, a pro

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Toh, G. W. L., and N. F. Lowndes. "Role of the Saccharomyces cerevisiae Rad9 protein in sensing and responding to DNA damage." Biochemical Society Transactions 31, no. 1 (2003): 242–46. http://dx.doi.org/10.1042/bst0310242.

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Eukaryotic cells have evolved surveillance mechanisms, known as DNA-damage checkpoints, that sense and respond to genome damage. DNA-damage checkpoint pathways ensure co-ordinated cellular responses to DNA damage, including cell cycle delays and activation of repair mechanisms. RAD9, from Saccharomyces cerevisiae, was the first damage checkpoint gene to be identified, although its biochemical function remained unknown until recently. This review examines briefly work that provides significant insight into how Rad9 activates the checkpoint signalling kinase Rad53.

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Klein, Hannah L. "Spontaneous Chromosome Loss in Saccharomyces cerevisiae Is Suppressed by DNA Damage Checkpoint Functions." Genetics 159, no. 4 (2001): 1501–9. http://dx.doi.org/10.1093/genetics/159.4.1501.

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Abstract Genomic instability is one of the hallmarks of cancer cells and is often the causative factor in revealing recessive gene mutations that progress cells along the pathway to unregulated growth. Genomic instability can take many forms, including aneuploidy and changes in chromosome structure. Chromosome loss, loss and reduplication, and deletions are the majority events that result in loss of heterozygosity (LOH). Defective DNA replication, repair, and recombination can significantly increase the frequency of spontaneous genomic instability. Recently, DNA damage checkpoint functions tha

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Yaothanee, Jumpol, and Kasidit Chanchio. "A checkpointing mechanism for virtual clusters using memory-bound time-multiplexed data transfers." International Journal of Electrical and Computer Engineering (IJECE) 14, no. 1 (2024): 1147. http://dx.doi.org/10.11591/ijece.v14i1.pp1147-1165.

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Transparent hypervisor-level checkpoint-restart mechanisms for virtual clusters (VCs) or clusters of virtual machines (VMs) offer an attractive fault tolerance capability for cloud data centers. However, existing mechanisms have suffered from high checkpoint downtimes and overheads. This paper introduces Mekha, a novel hypervisor-level, in-memory coordinated checkpoint-restart mechanism for VCs that leverages precopy live migration. During a VC checkpoint event, Mekha creates a shadow VM for each VM and employs a novel memory-bound timed-multiplex data (MTD) transfer mechanism to replicate the

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Moertel, Christopher, G. Elizabeth Pluhar, and Michael Olin. "TRLS-09. USE OF A PAN-PEPTIDE CHECKPOINT INHIBITOR IN THE TREATMENT OF CENTRAL NERVOUS SYSTEM TUMORS." Neuro-Oncology 25, Supplement_1 (2023): i81. http://dx.doi.org/10.1093/neuonc/noad073.312.

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Abstract Immunotherapy has revolutionized clinical management of a select group of malignancies by offering a long-term, durable treatment response. Unfortunately, only a small percentage of brain cancers respond. The combination of multiple checkpoint inhibitors may result in serious immune-related adverse events. We have developed a Pan-Immune Checkpoint Ligand that simultaneously controls multiple immune checkpoints. The CD200 immune checkpoint modulates the immune system through a single inhibitory receptor (CD200R1) and multiple activation receptors (CD200ARs). We developed a peptide liga

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Clarke, Duncan J., Guillaume Mondesert, Marisa Segal, et al. "Dosage Suppressors of pds1 Implicate Ubiquitin-Associated Domains in Checkpoint Control." Molecular and Cellular Biology 21, no. 6 (2001): 1997–2007. http://dx.doi.org/10.1128/mcb.21.6.1997-2007.2001.

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ABSTRACT In budding yeast, anaphase initiation is controlled by ubiquitin-dependent degradation of Pds1p. Analysis of pds1mutants implicated Pds1p in the DNA damage, spindle assembly, and S-phase checkpoints. Though some components of these pathways are known, others remain to be identified. Moreover, the essential function of Pds1p, independent of its role in checkpoint control, has not been elucidated. To identify loci that genetically interact withPDS1, we screened for dosage suppressors of a temperature-sensitive pds1 allele, pds1-128, defective for checkpoint control at the permissive tem

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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.

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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,

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Cowley, Dale O., Ginger W. Muse, and Terry Van Dyke. "A Dominant Interfering Bub1 Mutant Is Insufficient To Induce or Alter Thymic Tumorigenesis In Vivo, Even in a Sensitized Genetic Background." Molecular and Cellular Biology 25, no. 17 (2005): 7796–802. http://dx.doi.org/10.1128/mcb.25.17.7796-7802.2005.

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ABSTRACT Aneuploidy is a common feature of human tumors, often correlating with poor prognosis. The mitotic spindle checkpoint is thought to play a major role in aneuploidy suppression. To investigate the role of the spindle checkpoint in tumor suppression in vivo, we developed transgenic mice in which thymocytes express a dominant interfering fragment of Bub1, a kinase regulator of the spindle checkpoint. We report that, despite high-level expression of dominant-negative Bub1 (Bub1DN), a protein known to inhibit spindle checkpoint activity in cultured cells, thymocytes show no evidence of spi

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Corellou, F., S. R. Bisgrove, D. L. Kropf, L. Meijer, B. Kloareg, and F. Y. Bouget. "A S/M DNA replication checkpoint prevents nuclear and cytoplasmic events of cell division including centrosomal axis alignment and inhibits activation of cyclin-dependent kinase-like proteins in fucoid zygotes." Development 127, no. 8 (2000): 1651–60. http://dx.doi.org/10.1242/dev.127.8.1651.

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S/M checkpoints prevent various aspects of cell division when DNA has not been replicated. Such checkpoints are stringent in yeast and animal somatic cells but are usually partial or not present in animal embryos. Because little is known about S/M checkpoints in plant cells and embryos, we have investigated the effect of aphidicolin, a specific inhibitor of DNA polymerases (alpha) and (delta), on cell division and morphogenesis in Fucus and Pelvetia zygotes. Both DNA replication and cell division were inhibited by aphidicolin, indicating the presence, in fucoid zygotes, of a S/M checkpoint. Th

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Buckle, Irina, and Camille Guillerey. "Inhibitory Receptors and Immune Checkpoints Regulating Natural Killer Cell Responses to Cancer." Cancers 13, no. 17 (2021): 4263. http://dx.doi.org/10.3390/cancers13174263.

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The discovery of immune checkpoints provided a breakthrough for cancer therapy. Immune checkpoints are inhibitory receptors that are up-regulated on chronically stimulated lymphocytes and have been shown to hinder immune responses to cancer. Monoclonal antibodies against the checkpoint molecules PD-1 and CTLA-4 have shown early clinical success against melanoma and are now approved to treat various cancers. Since then, the list of potential candidates for immune checkpoint blockade has dramatically increased. The current paradigm stipulates that immune checkpoint blockade therapy unleashes pre

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MURAKAMI, Hiroshi, and Paul NURSE. "DNA replication and damage checkpoints and meiotic cell cycle controls in the fission and budding yeasts." Biochemical Journal 349, no. 1 (2000): 1–12. http://dx.doi.org/10.1042/bj3490001.

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The cell cycle checkpoint mechanisms ensure the order of cell cycle events to preserve genomic integrity. Among these, the DNA-replication and DNA-damage checkpoints prevent chromosome segregation when DNA replication is inhibited or DNA is damaged. Recent studies have identified an outline of the regulatory networks for both of these controls, which apparently operate in all eukaryotes. In addition, it appears that these checkpoints have two arrest points, one is just before entry into mitosis and the other is prior to chromosome separation. The former point requires the central cell-cycle re

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Cai, Huiming, Ge Liu, Jianfeng Zhong, et al. "Immune Checkpoints in Viral Infections." Viruses 12, no. 9 (2020): 1051. http://dx.doi.org/10.3390/v12091051.

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As evidence has mounted that virus-infected cells, such as cancer cells, negatively regulate the function of T-cells via immune checkpoints, it has become increasingly clear that viral infections similarly exploit immune checkpoints as an immune system escape mechanism. Although immune checkpoint therapy has been successfully used in cancer treatment, numerous studies have suggested that such therapy may also be highly relevant for treating viral infection, especially chronic viral infections. However, it has not yet been applied in this manner. Here, we reviewed recent findings regarding immu

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Forbes, Kristi Chrispell, Timothy Humphrey, and Tamar Enoch. "Suppressors of Cdc25p Overexpression Identify Two Pathways That Influence the G2/M Checkpoint in Fission Yeast." Genetics 150, no. 4 (1998): 1361–75. http://dx.doi.org/10.1093/genetics/150.4.1361.

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Abstract Checkpoints maintain the order of cell-cycle events. At G2/M, a checkpoint blocks mitosis in response to damaged or unreplicated DNA. There are significant differences in the checkpoint responses to damaged DNA and unreplicated DNA, although many of the same genes are involved in both responses. To identify new genes that function specifically in the DNA replication checkpoint pathway, we searched for high-copy suppressors of overproducer of Cdc25p (OPcdc25+), which lacks a DNA replication checkpoint. Two classes of suppressors were isolated. One class includes a new gene encoding a p

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Pankratz, Daniel G., and Susan L. Forsburg. "Meiotic S-Phase Damage Activates Recombination without Checkpoint Arrest." Molecular Biology of the Cell 16, no. 4 (2005): 1651–60. http://dx.doi.org/10.1091/mbc.e04-10-0934.

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Checkpoints operate during meiosis to ensure the completion of DNA synthesis and programmed recombination before the initiation of meiotic divisions. Studies in the fission yeast Schizosaccharomyces pombe suggest that the meiotic response to DNA damage due to a failed replication checkpoint response differs substantially from the vegetative response, and may be influenced by the presence of homologous chromosomes. The checkpoint responses to DNA damage during fission yeast meiosis are not well characterized. Here we report that DNA damage induced during meiotic S-phase does not activate checkp

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Yates, Luke A., Xiaodong Zhang, and Peter M. Burgers. "DNA Damage and Replication Stress Checkpoints." Annual Review of Biochemistry 94, no. 1 (2025): 195–221. https://doi.org/10.1146/annurev-biochem-072324-031915.

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DNA damage checkpoints are key regulatory signaling cascades that arrest cell cycle progression upon DNA damage or upon DNA replication stalling and allow time for repair or correction. Failure to elicit these checkpoints can lead to genomic instability that can result in cell death or mutations, ultimately leading to diseases such as cancer. Components of the DNA damage checkpoint are attractive targets for precision medicine to treat cancers. Over the last several years, cutting-edge structural techniques have provided molecular insights into the highly coordinated checkpoint signaling that

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Wang, Tian Xi, Ming Hua Jiang, Jing Liang, Chang Long Zhou, Feng Yu, and Xi Wu. "Application of Process Migration in Intelligent Router Based on BLCR." Applied Mechanics and Materials 721 (December 2014): 724–27. http://dx.doi.org/10.4028/www.scientific.net/amm.721.724.

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Implement a checkpoint mechanism in the system of loaded BLCR project, to set up checkpoints on the progress which need a quick recovery. The router can receive and save the checkpoint files sent by the other system. When the process need to quickly migrate to the other machines, to use the checkpoint files to recover, ensure the process runs on the other computer from a previous running state. In this way can save a lot of time and resources, and can meet the need of many applications.

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GUPTA, SUNIL KUMAR, R. K. CHAUHAN, and PARVEEN KUMAR. "A MINIMUM-PROCESS COORDINATED CHECKPOINTING PROTOCOL FOR MOBILE COMPUTING SYSTEMS." International Journal of Foundations of Computer Science 19, no. 04 (2008): 1015–38. http://dx.doi.org/10.1142/s0129054108006108.

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Checkpoint is a designated place in a program at which normal process is interrupted specifically to preserve the status information necessary to allow resumption of processing at a later time. A checkpoint algorithm for mobile distributed systems needs to handle many new issues like: mobility, low bandwidth of wireless channels, lack of stable storage on mobile nodes, disconnections, limited battery power and high failure rate of mobile nodes. These issues make traditional checkpointing techniques unsuitable for such environments. Minimum-process coordinated checkpointing is an attractive app

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Chin, Cheen Fei, and Foong May Yeong. "Safeguarding Entry into Mitosis: the Antephase Checkpoint." Molecular and Cellular Biology 30, no. 1 (2009): 22–32. http://dx.doi.org/10.1128/mcb.00687-09.

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ABSTRACT Maintenance of genomic stability is needed for cells to survive many rounds of division throughout their lifetime. Key to the proper inheritance of intact genome is the tight temporal and spatial coordination of cell cycle events. Moreover, checkpoints are present that function to monitor the proper execution of cell cycle processes. For instance, the DNA damage and spindle assembly checkpoints ensure genomic integrity by delaying cell cycle progression in the presence of DNA or spindle damage, respectively. A checkpoint that has recently been gaining attention is the antephase checkp

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Zhou, Qing, Kieu T. M. Pham, Huiqing Hu, Yasuhiro Kurasawa, and Ziyin Li. "A kinetochore-based ATM/ATR-independent DNA damage checkpoint maintains genomic integrity in trypanosomes." Nucleic Acids Research 47, no. 15 (2019): 7973–88. http://dx.doi.org/10.1093/nar/gkz476.

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Abstract DNA damage-induced cell cycle checkpoints serve as surveillance mechanisms to maintain genomic stability, and are regulated by ATM/ATR-mediated signaling pathways that are conserved from yeast to humans. Trypanosoma brucei, an early divergent microbial eukaryote, lacks key components of the conventional DNA damage-induced G2/M cell cycle checkpoint and the spindle assembly checkpoint, and nothing is known about how T. brucei controls its cell cycle checkpoints. Here we discover a kinetochore-based, DNA damage-induced metaphase checkpoint in T. brucei. MMS-induced DNA damage triggers a

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Goff, Peter H., Rashmi Bhakuni, Thomas Pulliam, Jung Hyun Lee, Evan T. Hall, and Paul Nghiem. "Intersection of Two Checkpoints: Could Inhibiting the DNA Damage Response Checkpoint Rescue Immune Checkpoint-Refractory Cancer?" Cancers 13, no. 14 (2021): 3415. http://dx.doi.org/10.3390/cancers13143415.

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Metastatic cancers resistant to immunotherapy require novel management strategies. DNA damage response (DDR) proteins, including ATR (ataxia telangiectasia and Rad3-related), ATM (ataxia telangiectasia mutated) and DNA-PK (DNA-dependent protein kinase), have been promising therapeutic targets for decades. Specific, potent DDR inhibitors (DDRi) recently entered clinical trials. Surprisingly, preclinical studies have now indicated that DDRi may stimulate anti-tumor immunity to augment immunotherapy. The mechanisms governing how DDRi could promote anti-tumor immunity are not well understood; howe

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Benoit, Anne, Saurabh K. Raina, and Yves Robert. "Efficient checkpoint/verification patterns." International Journal of High Performance Computing Applications 31, no. 1 (2016): 52–65. http://dx.doi.org/10.1177/1094342015594531.

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Errors have become a critical problem for high-performance computing. Checkpointing protocols are often used for error recovery after fail-stop failures. However, silent errors cannot be ignored, and their peculiarity is that such errors are identified only when the corrupted data is activated. To cope with silent errors, we need a verification mechanism to check whether the application state is correct. Checkpoints should be supplemented with verifications to detect silent errors. When a verification is successful, only the last checkpoint needs to be kept in memory because it is known to be

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Iyer, Divya Ramalingam, and Nicholas Rhind. "Checkpoint regulation of replication forks: global or local?" Biochemical Society Transactions 41, no. 6 (2013): 1701–5. http://dx.doi.org/10.1042/bst20130197.

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Cell-cycle checkpoints are generally global in nature: one unattached kinetochore prevents the segregation of all chromosomes; stalled replication forks inhibit late origin firing throughout the genome. A potential exception to this rule is the regulation of replication fork progression by the S-phase DNA damage checkpoint. In this case, it is possible that the checkpoint is global, and it slows all replication forks in the genome. However, it is also possible that the checkpoint acts locally at sites of DNA damage, and only slows those forks that encounter DNA damage. Whether the checkpoint r

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Rhind, N., and P. Russell. "Chk1 and Cds1: linchpins of the DNA damage and replication checkpoint pathways." Journal of Cell Science 113, no. 22 (2000): 3889–96. http://dx.doi.org/10.1242/jcs.113.22.3889.

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Recent work on the mechanisms of DNA damage and replication cell cycle checkpoints has revealed great similarity between the checkpoint pathways of organisms as diverse as yeasts, flies and humans. However, there are differences in the ways these organisms regulate their cell cycles. To connect the conserved checkpoint pathways with various cell cycle targets requires an adaptable link that can target different cell cycle components in different organisms. The Chk1 and Cds1 protein kinases, downstream effectors in the checkpoint pathways, seem to play just such roles. Perhaps more surprisingly

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Nabieva, Malika. "DEVELOPMENT OF CUSTOMS SERVICE MECHANISMS IN THE CONTEXT OF INTELLIGENT CHECKPOINTS." Russian Journal of Management 12, no. 4 (2025): 703–15. https://doi.org/10.29039/2500-1469-2024-12-4-703-715.

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The paper presents the results of an analysis of the development of intelligent checkpoint technologies in the context of their potential impact on the development of customs services at an intelligent checkpoint. The analysis of the current state of research aimed at improving the efficiency of checkpoints shows the presence of only individual functional solutions that pointwise implement fragmented tasks of instrumental control at checkpoints outside of complex solutions that integrate well-known technical solutions and select and implement advanced technologies of instrumental control in th

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