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8 results on '"Shivani K. Thaker"'

1. Expression-Based Cell Lineage Analysis in Drosophila Through a Course-Based Research Experience for Early Undergraduates

Author

John M. Olson, Cory J. Evans, Kathy T. Ngo, Hee Jong Kim, Joseph Duy Nguyen, Kayla G. H. Gurley, Truc Ta, Vijay Patel, Lisa Han, Khoa T. Truong-N, Letty Liang, Maggie K. Chu, Hiu Lam, Hannah G. Ahn, Abhik Kumar Banerjee, In Young Choi, Ross G. Kelley, Naseem Moridzadeh, Awais M. Khan, Omair Khan, Szuyao Lee, Elizabeth B. Johnson, Annie Tigranyan, Jay Wang, Anand D. Gandhi, Manish M. Padhiar, Joseph Hargan Calvopina, Kirandeep Sumra, Kristy Ou, Jessie C. Wu, Joseph N. Dickan, Sabrena M. Ahmadi, Donald N. Allen, Van Thanh Mai, Saif Ansari, George Yeh, Earl Yoon, Kimberly Gon, John Y. Yu, Johnny He, Jesse M. Zaretsky, Noemi E. Lee, Edward Kuoy, Alexander N. Patananan, Daniel Sitz, PhuongThao Tran, Minh-Tu Do, Samira J. Akhave, Silverio D. Alvarez, Bobby Asem, Neda Asem, Nicole A. Azarian, Arezou Babaesfahani, Ahmad Bahrami, Manjeet Bhamra, Ragini Bhargava, Rakesh Bhatia, Subir Bhatia, Nicholas Bumacod, Jonathan J. Caine, Thomas A. Caldwell, Nicole A. Calica, Elise M. Calonico, Carman Chan, Helen H.-L. Chan, Albert Chang, Chiaen Chang, Daniel Chang, Jennifer S. Chang, Nauman Charania, Jasmine Y. Chen, Kevin Chen, Lu Chen, Yuyu Chen, Derek J. Cheung, Jesse J. Cheung, Jessica J. Chew, Nicole B. Chew, Cheng-An Tony Chien, Alana M. Chin, Chee Jia Chin, Youngho Cho, Man Ting Chou, Ke-Huan K. Chow, Carolyn Chu, Derrick M. Chu, Virginia Chu, Katherine Chuang, Arunit Singh Chugh, Mark R. Cubberly, Michael Guillermo Daniel, Sangita Datta, Raj Dhaliwal, Jenny Dinh, Dhaval Dixit, Emmylou Dowling, Melinda Feng, Christopher M. From, Daisuke Furukawa, Himaja Gaddipati, Lilit Gevorgyan, Zunera Ghaznavi, Tulika Ghosh, Jaskaran Gill, David J. Groves, Kalkidan K. Gurara, Ali R. Haghighi, Alexandra L. Havard, Nasser Heyrani, Tanya Hioe, Kirim Hong, Justin J. Houman, Molly Howland, Elaine L. Hsia, Justin Hsueh, Stacy Hu, Andrew J. Huang, Jasmine C. Huynh, Jenny Huynh, Chris Iwuchukwu, Michael J. Jang, An An Jiang, Simran Kahlon, Pei-Yun Kao, Manpreet Kaur, Matthew G. Keehn, Elizabeth J. Kim, Hannah Kim, Michelle J. Kim, Shawn J. Kim, Aleksandar Kitich, Ross A. Kornberg, Nicholas G. Kouzelos, Jane Kuon, Bryan Lau, Roger K. Lau, Rona Law, Huy D. Le, Rachael Le, Carrou Lee, Christina Lee, Grace E. Lee, Kenny Lee, Michelle J. Lee, Regina V. Lee, Sean H. K. Lee, Sung Kyu Lee, Sung-Ling D. Lee, Yong Jun Lee, Megan J. Leong, David M. Li, Hao Li, Xingfu Liang, Eric Lin, Michelle M. Lin, Peter Lin, Tiffany Lin, Stacey Lu, Serena S. Luong, Jessica S. Ma, Li Ma, Justin N. Maghen, Sravya Mallam, Shivtaj Mann, Jason H. Melehani, Ryan C. Miller, Nitish Mittal, Carmel M. Moazez, Susie Moon, Rameen Moridzadeh, Kaley Ngo, Hanh H. Nguyen, Kambria Nguyen, Thien H. Nguyen, Angela W. Nieh, Isabella Niu, Seo-Kyung Oh, Jessica R. Ong, Randi K. Oyama, Joseph Park, Yaelim A. Park, Kimberly A. Passmore, Ami Patel, Amy A. Patel, Dhruv Patel, Tirth Patel, Katherine E. Peterson, An Huynh Pham, Steven V. Pham, Melissa E. Phuphanich, Neil D. Poria, Alexandra Pourzia, Victoria Ragland, Riki D. Ranat, Cameron M. Rice, David Roh, Solomon Rojhani, Lili Sadri, Agafe Saguros, Zainab Saifee, Manjot Sandhu, Brooke Scruggs, Lisa M. Scully, Vanessa Shih, Brian A. Shin, Tamir Sholklapper, Harnek Singh, Sumedha Singh, Sondra L. Snyder, Katelyn F. Sobotka, Sae Ho Song, Siddharth Sukumar, Halley C. Sullivan, Mark Sy, Hande Tan, Sara K. Taylor, Shivani K. Thaker, Tulsi Thakore, Gregory E. Tong, Jacinda N. Tran, Jonathan Tran, Tuan D. Tran, Vivi Tran, Cindy L. Trang, Hung G. Trinh, Peter Trinh, Han-Ching H. Tseng, Ted T. Uotani, Akram V. Uraizee, Kent K. T. Vu, Kevin K. T. Vu, Komal Wadhwani, Paluk K. Walia, Rebecca S. Wang, Shuo Wang, Stephanie J. Wang, Danica D. Wiredja, Andrew L. Wong, Daniel Wu, Xi Xue, Griselda Yanez, Yung-Hsuan Yang, Zhong Ye, Victor W. Yee, Cynthia Yeh, Yue Zhao, Xin Zheng, Anke Ziegenbalg, Jon Alkali, Ida Azizkhanian, Akash Bhakta, Luke Berry, Ryen Castillo, Sonja Darwish, Holly Dickinson, Ritika Dutta, Rahul Kumar Ghosh, Riley Guerin, Jonathan Hofman, Garrick Iwamoto, Sarah Kang, Andrew Kim, Brian Kim, Hanwool Kim, Kristine Kim, Suji Kim, Julie Ko, Michael Koenig, Alejandro LaRiviere, Clifton Lee, Jiwon Lee, Brandon Lung, Max Mittelman, Mark Murata, Yujin Park, Daniel Rothberg, Ben Sprung-Keyser, Kunal Thaker, Vivian Yip, Paul Picard, Francie Diep, Nikki Villarasa, Volker Hartenstein, Casey Shapiro, Marc Levis-Fitzgerald, Leslie Jaworski, David Loppato, Ira E. Clark, and Utpal Banerjee

Subjects
g-trace, gene expression, education, stem, cure, Genetics, QH426-470
Abstract

A variety of genetic techniques have been devised to determine cell lineage relationships during tissue development. Some of these systems monitor cell lineages spatially and/or temporally without regard to gene expression by the cells, whereas others correlate gene expression with the lineage under study. The GAL4 Technique for Real-time and Clonal Expression (G-TRACE) system allows for rapid, fluorescent protein-based visualization of both current and past GAL4 expression patterns and is therefore amenable to genome-wide expression-based lineage screens. Here we describe the results from such a screen, performed by undergraduate students of the University of California, Los Angeles (UCLA) Undergraduate Research Consortium for Functional Genomics (URCFG) and high school summer scholars as part of a discovery-based education program. The results of the screen, which reveal novel expression-based lineage patterns within the brain, the imaginal disc epithelia, and the hematopoietic lymph gland, have been compiled into the G-TRACE Expression Database (GED), an online resource for use by the Drosophila research community. The impact of this discovery-based research experience on student learning gains was assessed independently and shown to be greater than that of similar programs conducted elsewhere. Furthermore, students participating in the URCFG showed considerably higher STEM retention rates than UCLA STEM students that did not participate in the URCFG, as well as STEM students nationwide.

Published
2019
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2. Viral hijacking of cellular metabolism

Author

Shivani K. Thaker, James Ch’ng, and Heather R. Christofk

Subjects
Biology (General), QH301-705.5
Abstract

Abstract This review discusses the current state of the viral metabolism field and gaps in knowledge that will be important for future studies to investigate. We discuss metabolic rewiring caused by viruses, the influence of oncogenic viruses on host cell metabolism, and the use of viruses as guides to identify critical metabolic nodes for cancer anabolism. We also discuss the need for more mechanistic studies identifying viral proteins responsible for metabolic hijacking and for in vivo studies of viral-induced metabolic rewiring. Improved technologies for detailed metabolic measurements and genetic manipulation will lead to important discoveries over the next decade.

Published
2019
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3. Viral hijacking of cellular metabolism

Author

James Ch’ng, Shivani K. Thaker, and Heather R. Christofk

Subjects
Future studies, Anabolism, Physiology, viruses, Plant Science, Computational biology, Review, Biology, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, 0302 clinical medicine, Structural Biology, Neoplasms, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, Aetiology, lcsh:QH301-705.5, Ecology, Evolution, Behavior and Systematics, 030304 developmental biology, Cancer, 0303 health sciences, Cellular metabolism, Extramural, Cell Biology, Biological Sciences, 3. Good health, Infectious Diseases, lcsh:Biology (General), Viruses, Host-Pathogen Interactions, General Agricultural and Biological Sciences, Infection, 030217 neurology & neurosurgery, Oncovirus, Metabolic Networks and Pathways, Biotechnology, Developmental Biology
Abstract

This review discusses the current state of the viral metabolism field and gaps in knowledge that will be important for future studies to investigate. We discuss metabolic rewiring caused by viruses, the influence of oncogenic viruses on host cell metabolism, and the use of viruses as guides to identify critical metabolic nodes for cancer anabolism. We also discuss the need for more mechanistic studies identifying viral proteins responsible for metabolic hijacking and for in vivo studies of viral-induced metabolic rewiring. Improved technologies for detailed metabolic measurements and genetic manipulation will lead to important discoveries over the next decade.

Published
2019

4. Differential Metabolic Reprogramming by Zika Virus Promotes Cell Death in Human versus Mosquito Cells

Author

Travis J. Chapa, Ernst W. Schmid, Shivani K. Thaker, Heather R. Christofk, Danyang Gong, Ren Sun, Vaithilingaraja Arumugaswami, and Gustavo Garcia

Subjects
0301 basic medicine, Male, Programmed cell death, Physiology, Citric Acid Cycle, Foreskin, Receptor, Interferon alpha-beta, Retinal Pigment Epithelium, Carbohydrate metabolism, Biology, AMP-Activated Protein Kinases, Article, Zika virus, Pentose Phosphate Pathway, 03 medical and health sciences, Mice, 0302 clinical medicine, Aedes, Chlorocebus aethiops, Animals, Humans, Phosphorylation, Protein kinase A, Molecular Biology, Vero Cells, Mice, Knockout, Cell Death, Zika Virus Infection, AMPK, Epithelial Cells, Cell Biology, Metabolism, Zika Virus, Fibroblasts, biology.organism_classification, Cell biology, Citric acid cycle, 030104 developmental biology, Glucose, Apoptosis, 030217 neurology & neurosurgery
Abstract

Zika virus is a pathogen that poses serious consequences, including congenital microcephaly. Although many viruses reprogram host cell metabolism, whether Zika virus alters cellular metabolism and the functional consequences of Zika-induced metabolic changes remain unknown. Here, we show that Zika virus infection differentially reprograms glucose metabolism in human versus C6/36 mosquito cells by increasing glucose use in the tricarboxylic acid cycle in human cells versus increasing glucose use in the pentose phosphate pathway in mosquito cells. Infection of human cells selectively depletes nucleotide triphosphate levels, leading to elevated AMP/ATP ratios, AMP-activated protein kinase (AMPK) phosphorylation, and caspase-mediated cell death. AMPK is also phosphorylated in Zika virus-infected mouse brain. Inhibiting AMPK in human cells decreases Zika virus-mediated cell death, whereas activating AMPK in mosquito cells promotes Zika virus-mediated cell death. These findings suggest that the differential metabolic reprogramming during Zika virus infection of human versus mosquito cells determines whether cell death occurs.

Published
2018

5. In vivo genetic dissection of tumor growth and the Warburg effect

Author

Shivani K. Thaker, Cheng-Wei Wang, Utpal Banerjee, Arunima Purkayastha, and Kevin T. Jones

Subjects
0301 basic medicine, MAPK/ERK pathway, Pvr, Oxidative Phosphorylation, Neoplasms, cell biology, Drosophila Proteins, 2.1 Biological and endogenous factors, Glycolysis, Gene Regulatory Networks, Biology (General), Aetiology, D. melanogaster, General Neuroscience, General Medicine, Warburg effect, Cell biology, Gene Expression Regulation, Neoplastic, DNA-Binding Proteins, Biochemistry, Medicine, Drosophila, Research Article, LDH, warburg effect, QH301-705.5, Science, Pyruvate Dehydrogenase Complex, Biology, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, developmental biology, stem cells, Genetics, Animals, cancer, Protein kinase B, hypoxia-inducible factor, PI3K/AKT/mTOR pathway, Neoplastic, General Immunology and Microbiology, Oncogene, Animal, Cell Biology, Metabolic pathway, Disease Models, Animal, 030104 developmental biology, Developmental Biology and Stem Cells, Gene Expression Regulation, Anaerobic glycolysis, Disease Models, Biochemistry and Cell Biology, metabolism
Abstract

A well-characterized metabolic landmark for aggressive cancers is the reprogramming from oxidative phosphorylation to aerobic glycolysis, referred to as the Warburg effect. Models mimicking this process are often incomplete due to genetic complexities of tumors and cell lines containing unmapped collaborating mutations. In order to establish a system where individual components of oncogenic signals and metabolic pathways can be readily elucidated, we induced a glycolytic tumor in the Drosophila wing imaginal disc by activating the oncogene PDGF/VEGF-receptor (Pvr). This causes activation of multiple oncogenic pathways including Ras, PI3K/Akt, Raf/ERK, Src and JNK. Together this network of genes stabilizes Hifα (Sima) that in turn, transcriptionally up-regulates many genes encoding glycolytic enzymes. Collectively, this network of genes also causes inhibition of pyruvate dehydrogenase (PDH) activity resulting in diminished ox-phos levels. The high ROS produced during this process functions as a feedback signal to consolidate this metabolic reprogramming. DOI: http://dx.doi.org/10.7554/eLife.18126.001

Published
2016

7. MYC-induced reprogramming of glutamine catabolism supports optimal virus replication

Author

Shivani K. Thaker, Jun Feng, Minh Thai, Daniel Braas, Yushen Du, Thomas G. Graeber, Hailiang Hu, Ting-Ting Wu, and Heather R. Christofk

Subjects
viruses, Glutamine, General Physics and Astronomy, Biology, medicine.disease_cause, Virus Replication, Article, General Biochemistry, Genetics and Molecular Biology, Cell Line, Adenoviridae, Proto-Oncogene Proteins c-myc, Downregulation and upregulation, medicine, Humans, 2.1 Biological and endogenous factors, Adenovirus infection, Aetiology, chemistry.chemical_classification, Multidisciplinary, Glutaminase, General Chemistry, medicine.disease, 3. Good health, Enzyme, Infectious Diseases, Biochemistry, chemistry, Viral replication, Cell culture, Mutation, Infection
Abstract

Viruses rewire host cell glucose and glutamine metabolism to meet the bioenergetic and biosynthetic demands of viral propagation. However, the mechanism by which viruses reprogram glutamine metabolism and the metabolic fate of glutamine during adenovirus infection have remained elusive. Here, we show MYC activation is necessary for adenovirus-induced upregulation of host cell glutamine utilization and increased expression of glutamine transporters and glutamine catabolism enzymes. Adenovirus-induced MYC activation promotes increased glutamine uptake, increased use of glutamine in reductive carboxylation and increased use of glutamine in generating hexosamine pathway intermediates and specific amino acids. We identify glutaminase (GLS) as a critical enzyme for optimal adenovirus replication and demonstrate that GLS inhibition decreases replication of adenovirus, herpes simplex virus 1 and influenza A in cultured primary cells. Our findings show that adenovirus-induced reprogramming of glutamine metabolism through MYC activation promotes optimal progeny virion generation, and suggest that GLS inhibitors may be useful therapeutically to reduce replication of diverse viruses., Viruses can reprogram glutamine metabolism of host cells to support bioenergetics demands of viral replication. Here the authors show that adenoviral infection leads to enhanced glutamine metabolism through virus-mediated activation of MYC, which is required for optimal progeny virion generation.

Published
2015
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8. In vivo genetic dissection of tumor growth and the Warburg effect

Author

Cheng-Wei Wang, Arunima Purkayastha, Kevin T Jones, Shivani K Thaker, and Utpal Banerjee

Subjects
cancer, metabolism, warburg effect, Pvr, hypoxia-inducible factor, LDH, Medicine, Science, Biology (General), QH301-705.5
Abstract

A well-characterized metabolic landmark for aggressive cancers is the reprogramming from oxidative phosphorylation to aerobic glycolysis, referred to as the Warburg effect. Models mimicking this process are often incomplete due to genetic complexities of tumors and cell lines containing unmapped collaborating mutations. In order to establish a system where individual components of oncogenic signals and metabolic pathways can be readily elucidated, we induced a glycolytic tumor in the Drosophila wing imaginal disc by activating the oncogene PDGF/VEGF-receptor (Pvr). This causes activation of multiple oncogenic pathways including Ras, PI3K/Akt, Raf/ERK, Src and JNK. Together this network of genes stabilizes Hifα (Sima) that in turn, transcriptionally up-regulates many genes encoding glycolytic enzymes. Collectively, this network of genes also causes inhibition of pyruvate dehydrogenase (PDH) activity resulting in diminished ox-phos levels. The high ROS produced during this process functions as a feedback signal to consolidate this metabolic reprogramming.

Published
2016
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