Relevant bibliographies by topics / Synthetic Dosage Lethality

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

Academic literature on the topic 'Synthetic Dosage Lethality'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Synthetic Dosage Lethality"

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Kroll, Eugene S., Katherine M. Hyland, Philip Hieter, and Joachim J. Li. "Establishing Genetic Interactions by a Synthetic Dosage Lethality Phenotype." Genetics 143, no. 1 (1996): 95–102. http://dx.doi.org/10.1093/genetics/143.1.95.

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Abstract We have devised a genetic screen, termed synthetic dosage lethality, in which a cloned “reference” gene is inducibly overexpressed in a set of mutant strains carrying potential “target” mutations. To test the specificity of the method, two reference genes, CTF13, encoding a centromere binding protein, and ORC6, encoding a subunit of the origin of replication binding complex, were overexpressed in a large collection of mutants defective in either chromosome segregation or replication. CTF13 overexpression caused synthetic dosage lethality in combination with ctf14-42 (cbf2, ndc10), ctf
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Zimmermann, Christine, Ignacio Garcia, Manja Omerzu, Pierre Chymkowitch, Beibei Zhang, and Jorrit M. Enserink. "Mapping the Synthetic Dosage Lethality Network ofCDK1/CDC28." G3: Genes|Genomes|Genetics 7, no. 6 (2017): 1753–66. http://dx.doi.org/10.1534/g3.117.042317.

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Gupta, Anuradha, Anas Ahmad, Aqib Iqbal Dar, and Rehan Khan. "Synthetic Lethality: From Research to Precision Cancer Nanomedicine." Current Cancer Drug Targets 18, no. 4 (2018): 337–46. http://dx.doi.org/10.2174/1568009617666170630141931.

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Cancer is an evolutionary disease with multiple genetic alterations, accumulated due to chromosomal instability and/or aneuploidy and it sometimes acquires drug-resistant phenotype also. Whole genome sequencing and mutational analysis helped in understanding the differences among persons for predisposition of a disease and its treatment non-responsiveness. Thus, molecular targeted therapies came into existence. Among them, the concept of synthetic lethality have enthralled great attention as it is a pragmatic approach towards exploiting cancer cell specific mutations to specifically kill cance
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Lee, Amanda R., Anna Tangiyan, Isha Singh, and Peter S. Choi. "Incomplete paralog compensation generates selective dependency on TRA2A in cancer." PLOS Genetics 21, no. 5 (2025): e1011685. https://doi.org/10.1371/journal.pgen.1011685.

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Paralogs often exhibit functional redundancy, allowing them to effectively compensate for each other’s loss. However, this buffering mechanism is frequently disrupted in cancer, exposing unique paralog-specific vulnerabilities. Here, we identify a selective dependency on the splicing factor TRA2A. We find that TRA2A and its paralog TRA2B are synthetic lethal partners that function as widespread and largely redundant activators of both alternative and constitutive splicing. While loss of TRA2A alone is typically neutral due to compensation by TRA2B, we discover that a subset of cancer cell line
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Dandage, Rohan, and Elena Kuzmin. "Abstract B012: Predicting targetable paralog synthetic lethalities and functional redundancies in cancer genomes." Molecular Cancer Therapeutics 23, no. 6_Supplement (2024): B012. http://dx.doi.org/10.1158/1538-8514.synthleth24-b012.

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Abstract Paralogs are prevalent in the human genome and are considered a rich source of synthetic lethality due to functional redundancy. For a cancer cell carrying a gene with Loss-Of-Function (LOF) mutation, inactivation of its paralog using gene editing can induce a selective decrease in viability, leaving normal cells that do not harbor the mutation unharmed. Previous studies have exploited this vulnerability of cancer genomes. However, the cancer-specificity of such synthetic lethality limits its application across different cancer types. Furthermore, the role of functional redundancy whi
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Megchelenbrink, Wout, Rotem Katzir, Xiaowen Lu, Eytan Ruppin, and Richard A. Notebaart. "Synthetic dosage lethality in the human metabolic network is highly predictive of tumor growth and cancer patient survival." Proceedings of the National Academy of Sciences 112, no. 39 (2015): 12217–22. http://dx.doi.org/10.1073/pnas.1508573112.

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Synthetic dosage lethality (SDL) denotes a genetic interaction between two genes whereby the underexpression of gene A combined with the overexpression of gene B is lethal. SDLs offer a promising way to kill cancer cells by inhibiting the activity of SDL partners of activated oncogenes in tumors, which are often difficult to target directly. As experimental genome-wide SDL screens are still scarce, here we introduce a network-level computational modeling framework that quantitatively predicts human SDLs in metabolism. For each enzyme pair (A, B) we systematically knock out the flux through A c
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Gilad, Oren, Barzin Y. Nabet, Ryan L. Ragland, et al. "Combining ATR Suppression with Oncogenic Ras Synergistically Increases Genomic Instability, Causing Synthetic Lethality or Tumorigenesis in a Dosage-Dependent Manner." Cancer Research 70, no. 23 (2010): 9693–702. http://dx.doi.org/10.1158/0008-5472.can-10-2286.

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Thu, Yee Mon. "How Not To Be in the Wrong Place at the Wrong Time: An Education Primer for Use with “Deposition of Centromeric Histone H3 Variant CENP-A/Cse4 into Chromatin Is Facilitated by Its C-Terminal Sumoylation”." Genetics 216, no. 2 (2020): 333–42. http://dx.doi.org/10.1534/genetics.120.303493.

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Recent work by Kentaro Ohkuni and colleagues exemplifies how a series of molecular mechanisms contribute to a cellular outcome—equal distribution of chromosomes. Failure to maintain structural and numerical integrity of chromosomes is one contributing factor in genetic diseases such as cancer. Specifically, the authors investigated molecular events surrounding centromeric histone H3 variant Cse4 deposition—a process important for chromosome segregation, using Saccharomyces cerevisiae as a model organism. This study illustrates an example of a post-translational modification—sumoylation—regulat
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Liu, Chang, Dewald van Dyk, Yue Li, Brenda Andrews, and Hai Rao. "A genome-wide synthetic dosage lethality screen reveals multiple pathways that require the functioning of ubiquitin-binding proteins Rad23 and Dsk2." BMC Biology 7, no. 1 (2009): 75. http://dx.doi.org/10.1186/1741-7007-7-75.

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Young, Barry P., Kathryn L. Post, Jesse T. Chao, Fabian Meili, Kurt Haas, and Christopher Loewen. "Sentinel interaction mapping – a generic approach for the functional analysis of human disease gene variants using yeast." Disease Models & Mechanisms 13, no. 7 (2020): dmm044560. http://dx.doi.org/10.1242/dmm.044560.

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ABSTRACTAdvances in sequencing technology have led to an explosion in the number of known genetic variants of human genes. A major challenge is to now determine which of these variants contribute to diseases as a result of their effect on gene function. Here, we describe a generic approach using the yeast Saccharomyces cerevisiae to quickly develop gene-specific in vivo assays that can be used to quantify the level of function of a genetic variant. Using synthetic dosage lethality screening, ‘sentinel’ yeast strains are identified that are sensitive to overexpression of a human disease gene. V
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Dissertations / Theses on the topic "Synthetic Dosage Lethality"

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Sharifpoor, Sara. "Global Analysis of Kinase Interactions in Budding Yeast using Synthetic Dosage Lethality." Thesis, 2011. http://hdl.handle.net/1807/31937.

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To date, most genome-scale approaches designed to explore kinase pathways have been targeted towards substrate identification for individual kinases but provide little functional information and only a limited view of the interplay of kinases and their targets in key biological processes. I attempted to tackle the complexity of kinase networks using an unbiased integrated global analysis in budding yeast. I used functional genomics screens to study the yeast kinome using combinatorial genetic perturbations. I first assessed the effects of gene overexpression on the fitness of non-essential ki
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Dittmar, John. "A Novel Platform to Perform Cancer-Relevant Synthetic Dosage Lethality Screens in Saccharomyces cerevisiae." Thesis, 2013. https://doi.org/10.7916/D89029VH.

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The most significant challenge in developing cancer therapies is to selectively kill cancer cells while leaving normal cells unharmed. One approach to specifically target tumors is to exploit gene expression changes specific to cancer cells. For example, synthetic dosage lethal (SDL) interactions occur when increased gene dosage is lethal only in combination with a specific gene disruption. Since cancer cells often specifically over-express a host of gene products, discovering SDL interactions could reveal new therapeutic targets for cancer treatment. In this situation, cancer cells over-expre
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Books on the topic "Synthetic Dosage Lethality"

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Dittmar, John. A Novel Platform to Perform Cancer-Relevant Synthetic Dosage Lethality Screens in Saccharomyces cerevisiae. [publisher not identified], 2013.

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Book chapters on the topic "Synthetic Dosage Lethality"

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Measday, Vivien, and Philip Hieter. "Synthetic dosage lethality." In Guide to Yeast Genetics and Molecular and Cell Biology - Part B. Elsevier, 2002. http://dx.doi.org/10.1016/s0076-6879(02)50971-x.

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Conference papers on the topic "Synthetic Dosage Lethality"

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Hansen, Ryan J., Bryan Strouse, Kenna Anderes, Gregg Smith, and Christian Hassig. "Abstract B181: The Chk1 inhibitor, SRA737, demonstrates chemical synthetic lethality with replication stress-inducing agents, including low-dose gemcitabine, in preclinical models of cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b181.

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Journal articles
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