Fig. 5: The ERK1/2 pathway-independent activation of the JAK1/STAT1 pathway in Shoc2-depleted HDLEC.
From: Signaling scaffold Shoc2 regulates lymphangiogenesis by suppressing mTORC1-mediated IFN responses
A Schematic representation of the major signaling pathway activated by IFNs - the Janus kinase/signal transducer and activator of transcription (JAK1/STAT1) pathway. Activation of the JAK1/STAT1 pathway at the plasma membrane and rapid phosphorylation and nuclear translocation of STAT1 lead to the expression of IFN-stimulated genes (ISGs) containing ISREs (Interferon-Stimulated Response Elements) and GAS (Gamma Interferon-Activated Sites) DNA cis-elements. B Western blot of whole cell lysates extracted from human dermal lymphatic endothelial cells (HDLEC) expressing lentivirally supplied non-targeting shRNA (NT), Shoc2 shRNA (KD), or Shoc2 shRNA together with Shoc2-tagRFP (SE) for 3 and 6 days. Cell lysates were probed using antibodies to the indicated proteins. C Western blot of whole cell lysates extracted from HDLEC expressing lentivirally supplied non-targeting shRNA (NT), Shoc2 shRNA (KD), or Shoc2 shRNA together with Shoc2-tagRFP (SE) for 6 days. Cells were treated with 10 µM MEK inhibitor PD50042 for 24 h before Western blot. Cell lysates were probed using antibodies to the indicated proteins. D Western blot of whole cell lysates extracted from HDLEC expressing lentivirally supplied non-targeting shRNA (NT), Shoc2 shRNA (KD), or Shoc2 shRNA together with Shoc2-tagRFP (SE) for 6 days. Cells were treated with 5 µM JAK1 inhibitor ruxolitinib for 24 h before Western blot. Cell lysates were probed using antibodies to the indicated proteins. The results in each panel are representative of at least three independent experiments.
