Tracking corotating interaction regions from the Sun through to the orbit of Mars using ACE, MEX, VEX, and STEREO

[1] We study the propagation of corotating interaction regions (CIRs) through the inner heliosphere during the solar minimum of 2007–2008 using the Advanced Composition Explorer (ACE), Mars Express (MEX), Venus Express (VEX), and the Solar Terrestrial Relations Observatory (STEREO). We present observations of 24 CIRs observed during the period from 1 July 2007 to 31 August 2008. Using data from ACE, we demonstrate a method for predicting the arrival of CIRs at other locations within the heliosphere. The efficacy of the technique is assessed using observations at Mars and Venus, from MEX and VEX, respectively, and at the STEREO A and STEREO B spacecraft. We also use observations from the STEREO Heliospheric Imagers (HI) to produce another set of CIR arrival time estimates. We show that the estimated arrival times from ACE agree well with the arrival times at other spacecraft, whereas the estimates from STEREO/HI tend to agree less well. This latter difference can be explained through uncertainties in estimates due to difficulties in the unambiguous identification of the corresponding events in the STEREO/HI data

GOT1 inhibition promotes pancreatic cancer cell death by ferroptosis

Cancer metabolism is rewired to support cell survival in response to intrinsic and environmental stressors. Identification of strategies to target these adaptions is an area of active research. We previously described a cytosolic aspartate aminotransaminase (GOT1)-driven pathway in pancreatic cancer used to maintain redox balance. Here, we sought to identify metabolic dependencies following GOT1 inhibition to exploit this feature of pancreatic cancer and to provide additional insight into regulation of redox metabolism. Using pharmacological methods, we identify cysteine, glutathione, and lipid antioxidant function as metabolic vulnerabilities following GOT1 withdrawal. We demonstrate that targeting any of these pathways triggers ferroptosis, an oxidative, iron-dependent form of cell death, in GOT1 knockdown cells. Mechanistically, we reveal that GOT1 inhibition represses mitochondrial metabolism and promotes a catabolic state. Consequently, we find that this enhances labile iron availability through autophagy, which potentiates the activity of ferroptotic stimuli. Overall, our study identifies a biochemical connection between GOT1, iron regulation, and ferroptosis