Stanniocalcin 2 is involved in responding to pancreatic cell injury
The secreted protein Stanniocalcin 2 (STC2) is activated upon Endoplasmic Reticulum stress. The role of STC2 in the (PKR)-like Endoplasmic Reticulum Kinase (PERK) signaling pathway was investigated in vivo in a mouse model of pancreatic injury. Pancreatic acinar cells of transgenic mice over-expressing human STC2 (STC2Tg) displayed altered PERK signaling and increased autophagy. STC2 over-expression also seemed to limit the severity of acinar cell damage following pancreatic injury as indicated by a diminished enzyme activation and increased maintenance of cellular junctions compared to wild type. β-catenin (a marker of adherens junctions, in green) was detected by immunofluorescence in the pancreatic acinar cells of STC2Tg mice. Nuclei were stained with DAPI (blue).
This information is for Figure 5, part G
Taken from: Christopher Pin et al., 2011, BMC Cell Biology [View article]
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