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95 results on '"Shah, Jagesh V."'

51. APC16 is a conserved subunit of the anaphase-promoting complex/cyclosome

Author

Kops, Geert J. P. L., primary, van der Voet, Monique, additional, Manak, Michael S., additional, van Osch, Maria H. J., additional, Naini, Said Movahedi, additional, Brear, Andrea, additional, McLeod, Ian X., additional, Hentschel, Dirk M., additional, Yates, John R., additional, van den Heuvel, Sander, additional, and Shah, Jagesh V., additional

Published
2015
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53. LRF maintains genome integrity by regulating the non-homologous end joining pathway of DNA repair

Author

Liu, Xue-Song, primary, Chandramouly, Gurushankar, additional, Rass, Emilie, additional, Guan, Yinghua, additional, Wang, Guocan, additional, Hobbs, Robin M., additional, Rajendran, Anbazhagan, additional, Xie, Anyong, additional, Shah, Jagesh V., additional, Davis, Anthony J., additional, Scully, Ralph, additional, Lunardi, Andrea, additional, and Pandolfi, Pier Paolo, additional

Published
2015
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55. Live-cell multiphoton fluorescence correlation spectroscopy with an improved large Stokes shift fluorescent protein

Author

Guan, Yinghua, primary, Meurer, Matthias, additional, Raghavan, Sarada, additional, Rebane, Aleksander, additional, Lindquist, Jake R., additional, Santos, Sofia, additional, Kats, Ilia, additional, Davidson, Michael W., additional, Mazitschek, Ralph, additional, Hughes, Thomas E., additional, Drobizhev, Mikhail, additional, Knop, Michael, additional, and Shah, Jagesh V., additional

Published
2015
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57. ANKS6 is the critical activator of NEK8 kinase in embryonic situs determination and organ patterning

Author

Czarnecki, Peter G., primary, Gabriel, George C., additional, Manning, Danielle K., additional, Sergeev, Mikhail, additional, Lemke, Kristi, additional, Klena, Nikolai T., additional, Liu, Xiaoqin, additional, Chen, Yu, additional, Li, You, additional, San Agustin, Jovenal T., additional, Garnaas, Maija K., additional, Francis, Richard J., additional, Tobita, Kimimasa, additional, Goessling, Wolfram, additional, Pazour, Gregory J., additional, Lo, Cecilia W., additional, Beier, David R., additional, and Shah, Jagesh V., additional

Published
2015
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60. Interfilament interactions in the cytoskeleton : single filament measurements and mechanical consequences

Author

Paul A. Janmey., Harvard University--MIT Division of Health Sciences and Technology., Shah, Jagesh V. (Jagesh Vijaykumar), Paul A. Janmey., Harvard University--MIT Division of Health Sciences and Technology., and Shah, Jagesh V. (Jagesh Vijaykumar)

Abstract

Thesis (Ph.D.)--Harvard--Massachusetts Institute of Technology Division of Health Sciences and Technology, 1999., Includes bibliographical references (leaves 115-128)., by Jagesh V. Shah., Ph.D.

Published
2014

62. Monoalkoxy BODIPYs—A Fluorophore Class for Bioimaging

Author

Courtis, Alexandra M., primary, Santos, Sofia A., additional, Guan, Yinghua, additional, Hendricks, J. Adam, additional, Ghosh, Balaram, additional, Szantai-Kis, D. Miklos, additional, Reis, Surya A., additional, Shah, Jagesh V., additional, and Mazitschek, Ralph, additional

Published
2014
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65. Cytosolic phospholipase A2α regulates G1 progression through modulating FOXO1 activity.

Author

Naini, Said Movahedi, Choukroun, Gabriel J., Ryan, James R., Hentsche, Dirk M., Shah, Jagesh V., and Bonventre, Joseph V.

Subjects
CYTOSOL, PHOSPHOLIPASE A2, GENE expression, ENZYME activation, CHEMICAL inhibitors, NEOPLASTIC cell transformation
Abstract

Group IVA phospholipase A² [cytosolic phospholipase A²α (cPLA²α)] is a key mediator of inflammation and tumorigenesis. In this study, by using a combination of chemical inhibition and genetic approaches in zebrafish and murine cells, we identify a mechanism by which cPLA²α promotes cell proliferation. We identified 2 cplA²α genes in zebrafish, cplA²αa and cplA²αb, with conserved phospholipase activity. In zebrafish, loss of cplA²α expression or inhibition of cplA²α activity diminished G1 progression through the cell cycle. This phenotype was also seen in both mouse embryonic fibroblasts and mesangial cells. G1 progression was rescued by the addition of arachidonic acid or prostaglandin E2 (PGE2), indicating a phospholipase-dependent mechanism. We further show that PGE2, through PI3K/AKT activation, promoted Forkhead box protein O1 (FOXO1) phosphorylation and FOXO1 nuclear export. This led to up-regulation of cyclin D1 and down-regulation of p27Kip1, thus promoting G1 progression. Finally, using pharmacologic inhibitors, we show that cPLA²α, rapidly accelerated fibrosarcoma (RAF)/MEK/ERK, and PI3K/AKT signaling pathways cooperatively regulate G1 progression in response to platelet-derived growth factor stimulation. In summary, these data indicate that cPLA²α, through its phospholipase activity, is a critical effector of G1 phase progression through the cell cycle and suggest that pharmacological targeting of this enzyme may have important therapeutic benefits in disease mechanisms that involve excessive cell proliferation, in particular, cancer and proliferative glomerulopathies. [ABSTRACT FROM AUTHOR]

Published
2016
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72. PC16 is a conserved subunit of the anaphase-promoting complex/cyclosome

Author

Kops, Geert J. P. L., primary, van der Voet, Monique, additional, Manak, Michael S., additional, van Osch, Maria H. J., additional, Naini, Said M., additional, Brear, Andrea, additional, McLeod, Ian X., additional, Hentschel, Dirk M., additional, Yates, John R., additional, van den Heuvel, Sander, additional, and Shah, Jagesh V., additional

Published
2010
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73. APC16 is a conserved subunit of the anaphase-promoting complex/cyclosome

Author

Kops, Geert J. P. L., primary, van der Voet, Monique, additional, Manak, Michael S., additional, van Osch, Maria H. J., additional, Naini, Said M., additional, Brear, Andrea, additional, McLeod, Ian X., additional, Hentschel, Dirk M., additional, Yates, John R., additional, van den Heuvel, Sander, additional, and Shah, Jagesh V., additional

Published
2010
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74. Small-molecule kinase inhibitors provide insight into Mps1 cell cycle function

Author

Kwiatkowski, Nicholas, primary, Jelluma, Nannette, additional, Filippakopoulos, Panagis, additional, Soundararajan, Meera, additional, Manak, Michael S, additional, Kwon, Mijung, additional, Choi, Hwan Geun, additional, Sim, Taebo, additional, Deveraux, Quinn L, additional, Rottmann, Sabine, additional, Pellman, David, additional, Shah, Jagesh V, additional, Kops, Geert J P L, additional, Knapp, Stefan, additional, and Gray, Nathanael S, additional

Published
2010
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76. THM1 negatively modulates mouse sonic hedgehog signal transduction and affects retrograde intraflagellar transport in cilia

Author

Tran, Pamela V, primary, Haycraft, Courtney J, additional, Besschetnova, Tatiana Y, additional, Turbe-Doan, Annick, additional, Stottmann, Rolf W, additional, Herron, Bruce J, additional, Chesebro, Allyson L, additional, Qiu, Haiyan, additional, Scherz, Paul J, additional, Shah, Jagesh V, additional, Yoder, Bradley K, additional, and Beier, David R, additional

Published
2008
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79. Group IVA Cytosolic Phospholipase A2 Regulates the G2-to-M Transition by Modulating the Activity of Tumor Suppressor SIRT2.

Author

Naini, Said Movahedi, Sheridan, Alice M., Force, Thomas, Shah, Jagesh V., and Bonventre, Joseph V.

Subjects
TUMOR suppressor proteins, TUMOR suppressor genes, PHOSPHOLIPASES, CYCLIN genetics, CENTROSOMES, OXIDATIVE phosphorylation
Abstract

The G2-to-M transition (or prophase) checkpoint of the cell cycle is a critical regulator of mitotic entry. SIRT2, a tumor suppressor gene, contributes to the control of this checkpoint by blocking mitotic entry under cellular stress. However, the mechanism underlying both SIRT2 activation and regulation of the G2-to-M transition remains largely unknown. Here, we report the formation of a multiprotein complex at the G2-to-M transition in vitro and in vivo. Group IVA cytosolic phospholipase A2 (cPLA2α) acts as a bridge in this complex to promote binding of SIRT2 to cyclin A-Cdk2. Cyclin A-Cdk2 then phosphorylates SIRT2 at Ser331. This phosphorylation reduces SIRT2 catalytic activity and its binding affinity to centrosomes and mitotic spindles, promoting G2-to-M transition. We show that the inhibitory effect of cPLA2α on SIRT2 activity impacts various cellular processes, including cellular levels of histone H4 acetylated at K16 (Ac-H4K16) and Ac-α-tubulin. This regulatory effect of cPLA2α on SIRT2 defines a novel function of cPLA2α independent of its phospholipase activity and may have implications for the impact of SIRT2-related effects on tumorigenesis and age-related diseases. [ABSTRACT FROM AUTHOR]

Published
2015
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80. Systematic proteomics of the VCP-UBXD adaptor network identifies a role for UBXN10 in regulating ciliogenesis.

Author

Sergeev, Mikhail, Garnaas, Maija, Goessling, Wolfram, Shah, Jagesh V., Raman, Malavika, Lydeard, John R., Huttlin, Edward L., and Harper, J. Wade

Subjects
PROTEOMICS, ADENOSINE triphosphate, UBIQUITIN, CILIARY body, ZEBRA danio
Abstract

The AAA-ATPase VCP (also known as p97 or CDC48) uses ATP hydrolysis to 'segregate' ubiquitylated proteins from their binding partners. VCP acts through UBX-domain-containing adaptors that provide target specificity, but the targets and functions of UBXD proteins remain poorly understood. Through systematic proteomic analysis of UBXD proteins in human cells, we reveal a network of over 195 interacting proteins, implicating VCP in diverse cellular pathways. We have explored one such complex between an unstudied adaptor UBXN10 and the intraflagellar transport B (IFT-B) complex, which regulates anterograde transport into cilia. UBXN10 localizes to cilia in a VCP-dependent manner and both VCP and UBXN10 are required for ciliogenesis. Pharmacological inhibition of VCP destabilized the IFT-B complex and increased trafficking rates. Depletion of UBXN10 in zebrafish embryos causes defects in left-right asymmetry, which depends on functional cilia. This study provides a resource for exploring the landscape of UBXD proteins in biology and identifies an unexpected requirement for VCP-UBXN10 in ciliogenesis. [ABSTRACT FROM AUTHOR]

Published
2015
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87. Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury.

Author

Li Yang, Besschetnova, Tatiana Y., Brooks, Craig R., Shah, Jagesh V., and Bonventre, Joseph V.

Subjects
EPITHELIAL cells, CELL cycle, ACUTE kidney failure, KIDNEY diseases, FIBROSIS, FOCAL adhesion kinase, COLLAGEN diseases, GENETICS, DIAGNOSIS, PHYSIOLOGY
Abstract

Fibrosis is responsible for chronic progressive kidney failure, which is present in a large number of adults in the developed world. It is increasingly appreciated that acute kidney injury (AKI), resulting in aberrant incomplete repair, is a major contributor to chronic fibrotic kidney disease. The mechanism that triggers the fibrogenic response after injury is not well understood. In ischemic, toxic and obstructive models of AKI, we demonstrate a causal association between epithelial cell cycle G2/M arrest and a fibrotic outcome. G2/M-arrested proximal tubular cells activate c-jun NH2-terminal kinase (JNK) signaling, which acts to upregulate profibrotic cytokine production. Treatment with a JNK inhibitor, or bypassing the G2/M arrest by administration of a p53 inhibitor or the removal of the contralateral kidney, rescues fibrosis in the unilateral ischemic injured kidney. Hence, epithelial cell cycle arrest at G2/M and its subsequent downstream signaling are hitherto unrecognized therapeutic targets for the prevention of fibrosis and interruption of the accelerated progression of kidney disease. [ABSTRACT FROM AUTHOR]

Published
2010
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88. Systematic VCP-UBXD Adaptor Network Proteomics Identifies a Role for UBXN10 in Regulating Ciliogenesis

Author

Raman, Malavika, Sergeev, Mikhail, Garnaas, Maija, Lydeard, John R., Huttlin, Edward L., Goessling, Wolfram, Shah, Jagesh V., and Harper, J. Wade

Abstract

The AAA-ATPase VCP (also known as p97 or CDC48) uses ATP hydrolysis to “segregate” ubiquitinated proteins from their binding partners. VCP acts via UBX-domain containing adaptors that provide target specificity, but targets and functions of UBXD proteins remain poorly understood. Through systematic proteomic analysis of UBXD proteins in human cells, we reveal a network of over 195 interacting proteins, implicating VCP in diverse cellular pathways. We have explored one such complex between an unstudied adaptor UBXN10 and the intraflagellar transport B (IFT-B) complex, which regulates anterograde transport into cilia. UBXN10 localizes to cilia in a VCP-dependent manner and both VCP and UBXN10 are required for ciliogenesis. Pharmacological inhibition of VCP destabilized the IFT-B complex and increased trafficking rates. Depletion of UBXN10 in zebrafish embryos causes defects in left-right asymmetry, which depends on functional cilia. This study provides a resource for exploring the landscape of UBXD proteins in biology and identifies an unexpected requirement for VCP-UBXN10 in ciliogenesis.

Published
2015
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89. p31cometacts to ensure timely spindle checkpoint silencing subsequent to kinetochore attachment

Author

Hagan, Robert S., Manak, Michael S., Buch, Håkon Kirkeby, Meier, Michelle G., Meraldi, Patrick, Shah, Jagesh V., Sorger, Peter K., and Doxsey, Stephen J

Abstract

The spindle assembly checkpoint links the onset of anaphase to completion of chromosome-microtubule attachment and is mediated by the binding of Mad and Bub proteins to kinetochores of unattached or maloriented chromosomes. Mad2 and BubR1 traffic between kinetochores and the cytosol, thereby transmitting a "wait anaphase" signal to the anaphase-promoting complex. It is generally assumed that this signal dissipates automatically upon kinetochore-microtubule binding, but it has been shown that under conditions of nocodazole-induced arrest p31comet, a Mad2-binding protein, is required for mitotic progression. In this article we investigate the localization and function of p31cometduring normal, unperturbed mitosis in human and marsupial cells. We find that, like Mad2, p31comettraffics on and off kinetochores and is also present in the cytosol. Cells depleted of p31cometarrest in metaphase with mature bipolar kinetochore-microtubule attachments, a satisfied checkpoint, and high cyclin B levels. Thus p31cometis required for timely mitotic exit. We propose that p31cometis an essential component of the machinery that silences the checkpoint during each cell cycle.

Published
2011

90. Chromosome Tips Damaged in Anaphase Inhibit Cytokinesis

Author

Baker, Norman M., Zeitlin, Samantha G., Shi, Linda Z., Berns, Michael W., and Shah, Jagesh V.

Subjects
biophysics, replication and repair, cell biology, cell growth and division
Abstract

Genome maintenance is ensured by a variety of biochemical sensors and pathways that repair accumulated damage. During mitosis, the mechanisms that sense and resolve DNA damage remain elusive. Studies have demonstrated that damage accumulated on lagging chromosomes can activate the spindle assembly checkpoint. However, there is little known regarding damage to DNA after anaphase onset. In this study, we demonstrate that laser-induced damage to chromosome tips (presumptive telomeres) in anaphase of Potorous tridactylis cells (PtK2) inhibits cytokinesis. In contrast, equivalent irradiation of non-telomeric chromosome regions or control irradiations in either the adjacent cytoplasm or adjacent to chromosome tips near the spindle midzone during anaphase caused no change in the eventual completion of cytokinesis. Damage to only one chromosome tip caused either complete absence of furrow formation, a prolonged delay in furrow formation, or furrow regression. When multiple chromosome tips were irradiated in the same cell, the cytokinesis defects increased, suggesting a potential dose-dependent mechanism. These results suggest a mechanism in which dysfunctional telomeres inhibit mitotic exit.

Published
2010
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91. In VivoDelivery of a CD20 CAR Using a CD8-Targeted Fusosome in Southern Pig-Tail Macaques (M. nemestrina) Results in B Cell Depletion

Author

Cunningham, Justine, Chandra, Sundeep, Emmanuel, Akinola, Mazzarelli, Allyse, Passaro, Carmela, Baldwin, Paige, Nguyen-McCarty, Michelle, Rocca, Carrie, Joyce, Shannon, Kim, Joohwan, Vagin, Vasily, Kaczmarek, James, Chavan, Hemant, Jewell, Heather, Lipsitz, Yonatan, Shamashkin, Misha, Hlavaty, Kelan, Rodriguez, Jason, Co, Carl, Cruite, Pattie, Ennajdaoui, Hanane, Duback, Victoria, Elman, Jess, Amatya, Shirisha, Harding, Caspian, Lyubinetsky, Sergey, Patel, Vidur, Pepper, Lauren, Ruzo, Albert, Iovino, Salvatore, Varghese, Bindu, Foster, Aaron E., Gorovits, Boris, Elpek, Kutlu, Laska, Michael, McGill, Trevor, Shah, Jagesh V, Fry, Terry J., and Dambach, Donna

Abstract

Introduction: Ex vivomanufactured chimeric antigen receptor (CAR) T cell therapies are highly effective for treating B cell malignancies. However, the complexity, cost and time required to manufacture CAR T cells limits access. To overcome conventional ex vivoCAR T limitations, a novel gene therapy platform has been developed that can deliver CAR transgenes directly to T cells through systemic administration of a fusosome, an engineered, target-directed novel paramyxovirus-based integrating vector that binds specific cell surface receptors for gene delivery through membrane fusion. Here, we demonstrate that systemic administration of a CD8a-targeted, integrating vector envelope (i.e., fusogen) encoding an anti-CD20 CAR into Southern pig-tail macaques (M. nemestrina), which is a species permissive to the integrating vector-mediated transduction, results in T cell transduction and B cell depletion with no treatment-related toxicities.

Published
2021
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95. Chemical and Physical Determinants of Cell Migration

Author

Prentice Mott, Harrison Valentine, Shah, Jagesh V., and Mahadevan, Lakshminarayanan

Subjects
Biology, Physics, Biophysics, Chemotaxis, Hydrualic Resistance, Memory, Microfluidics, Neutrophil, Polarization
Abstract

The phenomenon of directed cell motion in response to external directional cues has drawn significant interest for more than a century, with the first recorded observations of bacterial chemotaxis at the end of the 19th century. Furthermore, movies generated by David Rogers while at Vanderbilt University of a peripheral blood neutrophil tracking a bacterium are a staple of any college biology class to demonstrate the phenomenon of eukaryotic chemotaxis. In just the last decade, our understanding of the biochemical mechanisms underlying the process of directed eukaryotic cell migration. As a result, several generalized processes have been identified, connecting multiple phenomena from cancer metastasis to axon guidance. Making further sense of the complex biochemical pathways requires both quantitative mathematical models and fine control over the external cellular environment. To this end, microfluidics has proven extremely useful, allowing for precise quantification of both the external environment and the cellular response.

Published
2014

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