Please use this identifier to cite or link to this item: http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/1539
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dc.contributor.authorTripathi, Subhash K.en_US
dc.contributor.authorSHETTY, ANKITHAen_US
dc.contributor.authorGALANDE, SANJEEV et al.en_US
dc.date.accessioned2019-01-24T09:13:26Z
dc.date.available2019-01-24T09:13:26Z
dc.date.issued2019-01en_US
dc.identifier.citationiScience, 11, 334-355.en_US
dc.identifier.issn-en_US
dc.identifier.urihttp://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/1539-
dc.identifier.urihttps://doi.org/10.1016/j.isci.2018.12.020en_US
dc.description.abstractTh17 cells contribute to pathogenesis of inflammatory and autoimmune diseases and cancer. To reveal the Th17 cell-specific proteomic signature regulating Th17 cell differentiation and function in human we used a label-free mass spectrometry-based approach. Further, a comprehensive analysis of the proteome and transcriptome of cells during human Th17 differentiation revealed a high degree of overlap between the datasets. However, when compared to a corresponding published mouse data, we found very limited overlap between the proteins differentially regulated in response to Th17 differentiation. Validations were made for a panel of selected proteins with known and unknown functions. Finally, using RNA interference (RNAi), we showed that SATB1 negatively regulates human Th17 cell differentiation. Overall, the current study illustrates a comprehensive picture of the global protein landscape during early human Th17 cell differentiation. Poor overlap with mouse data underlines the importance of human studies for translational research.en_US
dc.language.isoenen_US
dc.publisherElsevier B.V.en_US
dc.subjectHumanen_US
dc.subjectTh17 cell differentiationen_US
dc.subjectProteomicsen_US
dc.subjectMass spectrometryen_US
dc.subjectSATB1en_US
dc.subjectTOC-JAN-2019en_US
dc.subject2019en_US
dc.titleQuantitative mass spectrometry-based proteomics reveals the dynamic protein landscape during initiation of human Th17 cell polarizationen_US
dc.typeArticleen_US
dc.contributor.departmentDept. of Biologyen_US
dc.identifier.sourcetitleiScienceen_US
dc.publication.originofpublisherForeignen_US
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