| dc.contributor.author | Shrivastava, Richa | |
| dc.date.accessioned | 2024-01-19T07:01:25Z | |
| dc.date.available | 2024-01-19T07:01:25Z | |
| dc.date.issued | 2018-02 | |
| dc.identifier.uri | https://www.sciencedirect.com/science/article/pii/S0024320517306550 | |
| dc.identifier.uri | http://dspace.bits-pilani.ac.in:8080/jspui/xmlui/handle/123456789/13888 | |
| dc.description.abstract | HIF 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.iso | en | en_US |
| dc.publisher | Elsevier | en_US |
| dc.subject | Pharmacy | en_US |
| dc.subject | TAMs | en_US |
| dc.subject | Oncostatin M | en_US |
| dc.subject | HIF-1α | en_US |
| dc.subject | Normoxia | en_US |
| dc.subject | M2 macrophages | en_US |
| dc.title | Oncostatin M upregulates HIF-1α in breast tumor associated macrophages independent of intracellular oxygen concentration | en_US |
| dc.type | Article | en_US |
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