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Autophagy is a highly regulated process of degrading and recycling damaged proteins and organelles in response to cellular stress.1, 2 It is mediated by a unique vesicle called the autophagosome, which is assembled by the formation of a double membrane around the cellular component marked for destruction.1 The autophagosome vesicle then fuses with the lysosome to deliver its contents for degradation by lysosomal hydrolases.
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The MEK inhibitors cobimetinib and trametinib are used in combination with BRAF inhibitors to treat metastatic melanoma but increase rates of hemorrhage relative to BRAF inhibitors alone. Platelets express several members of the MAPK signalling cascade including MEK1 and MEK2 and ERK1 and ERK2 but their role in platelet function and haemostasis is ambiguous as previous reports have been contradictory. It is therefore unclear if MEK inhibitors might be causing platelet dysfunction and contributing to increased hemorrhage. In the present study we performed pharmacological characterisation of cobimetinib and trametinib in vitro to investigate potential for MEK inhibitors to cause platelet dysfunction.
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The Park NX12 is an inverted optical microscope based SPM platform for SICM, SECM, and SECCM, in addition to atomic force microscopy for research on a broad range of materials from organic to inorganic, transparent to opaque, and soft to hard. Park NX12 is suited for advanced research on materials such as membranes, organic devices and electronics, and biological and pathological samples in both air and liquid, plus a solution and platform for pipette-based SPM techniques.