@article{TiegsCostelloIskenetal.2019,
  author    = {Tiegs, Scott D. and Costello, David M. and Isken, Mark W. and Woodward, Guy and McIntyre, Peter B. and Gessner, Mark O. and Chauvet, Eric and Griffiths, Natalie A. and Flecker, Alex S. and Acuna, Vicenc and Albarino, Ricardo and Allen, Daniel C. and Alonso, Cecilia and Andino, Patricio and Arango, Clay and Aroviita, Jukka and Barbosa, Marcus V. M. and Barmuta, Leon A. and Baxter, Colden V. and Bell, Thomas D. C. and Bellinger, Brent and Boyero, Luz and Brown, Lee E. and Bruder, Andreas and Bruesewitz, Denise A. and Burdon, Francis J. and Callisto, Marcos and Canhoto, Cristina and Capps, Krista A. and Castillo, Maria M. and Clapcott, Joanne and Colas, Fanny and Colon-Gaud, Checo and Cornut, Julien and Crespo-Perez, Veronica and Cross, Wyatt F. and Culp, Joseph M. and Danger, Michael and Dangles, Olivier and de Eyto, Elvira and Derry, Alison M. and Diaz Villanueva, Veronica and Douglas, Michael M. and Elosegi, Arturo and Encalada, Andrea C. and Entrekin, Sally and Espinosa, Rodrigo and Ethaiya, Diana and Ferreira, Veronica and Ferriol, Carmen and Flanagan, Kyla M. and Fleituch, Tadeusz and Shah, Jennifer J. Follstad and Frainer, Andre and Friberg, Nikolai and Frost, Paul C. and Garcia, Erica A. and Lago, Liliana Garcia and Garcia Soto, Pavel Ernesto and Ghate, Sudeep and Giling, Darren P. and Gilmer, Alan and Goncalves, Jose Francisco and Gonzales, Rosario Karina and Graca, Manuel A. S. and Grace, Mike and Grossart, Hans-Peter and Guerold, Francois and Gulis, Vlad and Hepp, Luiz U. and Higgins, Scott and Hishi, Takuo and Huddart, Joseph and Hudson, John and Imberger, Samantha and Iniguez-Armijos, Carlos and Iwata, Tomoya and Janetski, David J. and Jennings, Eleanor and Kirkwood, Andrea E. and Koning, Aaron A. and Kosten, Sarian and Kuehn, Kevin A. and Laudon, Hjalmar and Leavitt, Peter R. and Lemes da Silva, Aurea L. and Leroux, Shawn J. and Leroy, Carri J. and Lisi, Peter J. and MacKenzie, Richard and Marcarelli, Amy M. and Masese, Frank O. and Mckie, Brendan G. and Oliveira Medeiros, Adriana and Meissner, Kristian and Milisa, Marko and Mishra, Shailendra and Miyake, Yo and Moerke, Ashley and Mombrikotb, Shorok and Mooney, Rob and Moulton, Tim and Muotka, Timo and Negishi, Junjiro N. and Neres-Lima, Vinicius and Nieminen, Mika L. and Nimptsch, Jorge and Ondruch, Jakub and Paavola, Riku and Pardo, Isabel and Patrick, Christopher J. and Peeters, Edwin T. H. M. and Pozo, Jesus and Pringle, Catherine and Prussian, Aaron and Quenta, Estefania and Quesada, Antonio and Reid, Brian and Richardson, John S. and Rigosi, Anna and Rincon, Jose and Risnoveanu, Geta and Robinson, Christopher T. and Rodriguez-Gallego, Lorena and Royer, Todd V. and Rusak, James A. and Santamans, Anna C. and Selmeczy, Geza B. and Simiyu, Gelas and Skuja, Agnija and Smykla, Jerzy and Sridhar, Kandikere R. and Sponseller, Ryan and Stoler, Aaron and Swan, Christopher M. and Szlag, David and Teixeira-de Mello, Franco and Tonkin, Jonathan D. and Uusheimo, Sari and Veach, Allison M. and Vilbaste, Sirje and Vought, Lena B. M. and Wang, Chiao-Ping and Webster, Jackson R. and Wilson, Paul B. and Woelfl, Stefan and Xenopoulos, Marguerite A. and Yates, Adam G. and Yoshimura, Chihiro and Yule, Catherine M. and Zhang, Yixin X. and Zwart, Jacob A.},
  title     = {Global patterns and drivers of ecosystem functioning in rivers and riparian zones},
  series = {Science Advances},
  volume    = {5},
  journal   = {Science Advances},
  number    = {1},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  issn      = {2375-2548},
  doi       = {10.1126/sciadv.aav0486},
  pages     = {8},
  year      = {2019},
  abstract  = {River ecosystems receive and process vast quantities of terrestrial organic carbon, the fate of which depends strongly on microbial activity. Variation in and controls of processing rates, however, are poorly characterized at the global scale. In response, we used a peer-sourced research network and a highly standardized carbon processing assay to conduct a global-scale field experiment in greater than 1000 river and riparian sites. We found that Earth's biomes have distinct carbon processing signatures. Slow processing is evident across latitudes, whereas rapid rates are restricted to lower latitudes. Both the mean rate and variability decline with latitude, suggesting temperature constraints toward the poles and greater roles for other environmental drivers (e.g., nutrient loading) toward the equator. These results and data set the stage for unprecedented "next-generation biomonitoring" by establishing baselines to help quantify environmental impacts to the functioning of ecosystems at a global scale.},
  language  = {en}
}
@article{FujiharaZhangJacksonetal.2022,
  author    = {Fujihara, Kenji M. and Zhang, Bonnie Z. and Jackson, Thomas D. and Ogunkola, Moses and Nijagal, Brunda and Milne, Julia V. and Sallman, David A. and Ang, Ching-Seng and Nikolic, Iva and Kearney, Conor J. and Hogg, Simon J. and Cabalag, Carlos S. and Sutton, Vivien R. and Watt, Sally and Fujihara, Asuka T. and Trapani, Joseph A. and Simpson, Kaylene J. and Stojanovski, Diana and Leimk{\"u}hler, Silke and Haupt, Sue and Phillips, Wayne A. and Clemons, Nicholas J.},
  title     = {Eprenetapopt triggers ferroptosis, inhibits NFS1 cysteine desulfurase, and synergizes with serine and glycine dietary restriction},
  series = {Science Advances},
  volume    = {8},
  journal   = {Science Advances},
  number    = {37},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  issn      = {2375-2548},
  doi       = {10.1126/sciadv.abm9427},
  pages     = {13},
  year      = {2022},
  abstract  = {The mechanism of action of eprenetapopt (APR-246, PRIMA-1MET) as an anticancer agent remains unresolved, al-though the clinical development of eprenetapopt focuses on its reported mechanism of action as a mutant-p53 reactivator. Using unbiased approaches, this study demonstrates that eprenetapopt depletes cellular antioxidant glutathione levels by increasing its turnover, triggering a nonapoptotic, iron-dependent form of cell death known as ferroptosis. Deficiency in genes responsible for supplying cancer cells with the substrates for de novo glutathione synthesis (SLC7A11, SHMT2, and MTHFD1L), as well as the enzymes required to synthesize glutathione (GCLC and GCLM), augments the activity of eprenetapopt. Eprenetapopt also inhibits iron-sulfur cluster biogenesis by limit-ing the cysteine desulfurase activity of NFS1, which potentiates ferroptosis and may restrict cellular proliferation. The combination of eprenetapopt with dietary serine and glycine restriction synergizes to inhibit esophageal xenograft tumor growth. These findings reframe the canonical view of eprenetapopt from a mutant-p53 reactivator to a ferroptosis inducer.},
  language  = {en}
}