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Your search keyword '"Rayannavar, Vinayak"' showing total 13 results
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13 results on '"Rayannavar, Vinayak"'

2. 737 Inhibition of P21-activated kinase 4 (PAK4) reverts immune exclusion and restores anti-tumor immunity in the tumor microenvironment

Author

Zhou, Yu 'Jerry', primary, Chu, Gina, additional, Hendrickson, Eleanore, additional, Gullo-Brown, Johnni, additional, Chavez, Brandy, additional, McAlpine, Indrawan, additional, Rui, Eugene, additional, Doran, Shawn, additional, Timofeevski, Sergei, additional, Heyen, Jonathan, additional, Kinong, Jennifer, additional, Tang, Szu-Yu, additional, Oyer, Jon, additional, Rayannavar, Vinayak, additional, Nager, Andrew, additional, Ching, Keith, additional, Shi, Stephanie, additional, Bhadra, Rajarshi, additional, Dillon, Christopher, additional, and Gururajan, Murali, additional

Published
2021
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4. Human monoclonal antibodies against chikungunya virus target multiple distinct epitopes in the E1 and E2 glycoproteins

Author

Quiroz, Jose A., primary, Malonis, Ryan J., additional, Thackray, Larissa B., additional, Cohen, Courtney A., additional, Pallesen, Jesper, additional, Jangra, Rohit K., additional, Brown, Rebecca S., additional, Hofmann, Daniel, additional, Holtsberg, Frederick W., additional, Shulenin, Sergey, additional, Nyakatura, Elisabeth K., additional, Durnell, Lorellin A., additional, Rayannavar, Vinayak, additional, Daily, Johanna P., additional, Ward, Andrew B., additional, Aman, M. Javad, additional, Dye, John M., additional, Chandran, Kartik, additional, Diamond, Michael S., additional, Kielian, Margaret, additional, and Lai, Jonathan R., additional

Published
2019
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9. Metformin and erlotinib synergize to inhibit basal breast cancer

Author

Lau, Ying-Ka Ingar, primary, Du, Xing, additional, Rayannavar, Vinayak, additional, Hopkins, Benjamin, additional, Shaw, Jacquelyn, additional, Bessler, Eliana, additional, Thomas, Tiffany, additional, Pires, Maira M., additional, Keniry, Megan, additional, Parsons, Ramon E., additional, Cremers, Serge, additional, Szabolcs, Matthias, additional, and Maurer, Matthew A., additional

Published
2014
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12. A Synthetic Dosage Lethal Genetic Interaction Between CKS1Band PLK1Is Conserved in Yeast and Human Cancer Cells

Author

Reid, Robert J D, Du, Xing, Sunjevaric, Ivana, Rayannavar, Vinayak, Dittmar, John, Bryant, Eric, Maurer, Matthew, and Rothstein, Rodney

Abstract

The CKS1Bgene located on chromosome 1q21 is frequently amplified in breast, lung, and liver cancers. CKS1Bcodes for a conserved regulatory subunit of cyclin–CDK complexes that function at multiple stages of cell cycle progression. We used a high throughput screening protocol to mimic cancer-related overexpression in a library of Saccharomyces cerevisiaemutants to identify genes whose functions become essential only when CKS1is overexpressed, a synthetic dosage lethal (SDL) interaction. Mutations in multiple genes affecting mitotic entry and mitotic exit are highly enriched in the set of SDL interactions. The interactions between Cks1 and the mitotic entry checkpoint genes require the inhibitory activity of Swe1 on the yeast cyclin-dependent kinase (CDK), Cdc28. In addition, the SDL interactions of overexpressed CKS1with mutations in the mitotic exit network are suppressed by modulating expression of the CDK inhibitor Sic1. Mutation of the polo-like kinase Cdc5, which functions in both the mitotic entry and mitotic exit pathways, is lethal in combination with overexpressed CKS1. Therefore we investigated the effect of targeting the human Cdc5 ortholog, PLK1, in breast cancers with various expression levels of human CKS1B. Growth inhibition by PLK1knockdown correlates with increased CKS1Bexpression in published tumor cell data sets, and this correlation was confirmed using shRNAs against PLK1in tumor cell lines. In addition, we overexpressed CKS1Bin multiple cell lines and found increased sensitivity to PLK1knockdown and PLK1 drug inhibition. Finally, combined inhibition of WEE1 and PLK1 results in less apoptosis than predicted based on an additive model of the individual inhibitors, showing an epistatic interaction and confirming a prediction of the yeast data. Thus, identification of a yeast SDL interaction uncovers conserved genetic interactions that can affect human cancer cell viability.

Published
2016
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13. Prenatal Stress Induces Schizophrenia-Like Alterations of Serotonin 2A and Metabotropic Glutamate 2 Receptors in the Adult Offspring: Role of Maternal Immune System.

Author

Holloway, Terrell, Moreno, José L., Umali, Adrienne, Rayannavar, Vinayak, Hodes, Georgia E., Russo, Scott J., and González-Maeso, Javier

Subjects
SCHIZOPHRENIA risk factors, GLUTAMATE receptors, PSYCHOLOGICAL stress, IMMUNE system, SEROTONIN receptors, PREGNANCY complications, ANTIPSYCHOTIC agents, DRUG development
Abstract

It has been suggested that severe adverse life events during pregnancy increase the risk of schizophrenia in the offspring. The serotonin 5-HT2A and the metabotropic glutamate 2 (mGlu2) receptors both have been the target of considerable attention regarding schizophrenia and antipsychotic drug development. We tested the effects of maternal variable stress during pregnancy on expression and behavioral function of these two receptors in mice. Prenatal stress increased 5-HT2A and decreased mGlu2 expression in frontal cortex, a brain region involved in perception, cognition, and mood. This pattern of expression of 5-HT2A and mGlu2 receptors was consistent with behavioral alterations, including increased head-twitch response to the hallucinogenic 5-HT2A agonist DOI [l-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane] and decreased mGlu2-dependent antipsychotic-like effect of the mGlu2/3 agonist LY379268 (lfl,4i?,5S,6.R-2-oxa-4-aminobicyclo[3.1.0]hexane-4,6-dicarboxylate) in adult, but not prepubertal, mice born to stressed mothers during pregnancy. Cross-fostering studies determined that these alterations were not attributable to effects of prenatal stress on maternal care. Additionally, a similar pattern of biochemical and behavioral changes were observed in mice born to mothers injected with polyinosiniepolycytidylic acid [poly(I:C)] during pregnancy as a model of prenatal immune activation. These data strengthen pathophysiological hypotheses that propose an early neurodevelopmental origin for schizophrenia and other psychiatric disorders. [ABSTRACT FROM AUTHOR]

Published
2013
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