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dc.contributor.authorShrivastava, Richa-
dc.date.accessioned2024-01-19T07:01:25Z-
dc.date.available2024-01-19T07:01:25Z-
dc.date.issued2018-02-
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S0024320517306550-
dc.identifier.urihttp://dspace.bits-pilani.ac.in:8080/jspui/xmlui/handle/123456789/13888-
dc.description.abstractHIF is an important transcription-regulator for adaptation to cellular stress in cells of myeloid origin. Classically, expression and activity of HIF1-α is regulated by oxygen-concentration within cell. However, there exists an alternative regulatory mechanism affecting HIF1-α levels independent of oxygen concentration particularly in inflammatory cells like macrophages. Here we report the mechanism of HIF1-α upregulation in TAMs by Oncostatin-M (OSM) independent of cellular oxygen concentration.en_US
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.subjectPharmacyen_US
dc.subjectTAMsen_US
dc.subjectOncostatin Men_US
dc.subjectHIF-1αen_US
dc.subjectNormoxiaen_US
dc.subjectM2 macrophagesen_US
dc.titleOncostatin M upregulates HIF-1α in breast tumor associated macrophages independent of intracellular oxygen concentrationen_US
dc.typeArticleen_US
Appears in Collections:Department of Pharmacy

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