Draft:Marcus Conrad

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  • Comment: Did you personally take the photo of him as claimed? 331dot (talk) 09:16, 30 October 2023 (UTC)

Marcus Conrad is a German biologist. He is currently the director of the Institute of Metabolism and Cell Death[1] at the Helmholtz Zentrum München in Munich. He is known for having contributed to the discovery of ferroptosis.

Early Life and Education[edit]

Marcus Conrad was born in Pfullendorf (Germany). He studied biology at the University of Konstanz graduating with his diploma thesis entitled "Thymidylat-Synthase als Modellenzym für molekulare Adaptation an hochosmolare Umwelt". He then pursued his doctoral studies at the LMU Munich working on the role of phospholipid hydroperoxide glutathione peroxidase (PHGPx) in fertility, now known as GPX4. He graduated in 2001 receiving the highest possible mark (summa cum laude).[2]

Career[edit]

Subseqeunt to receiving his PhD he was appointed as a Postdoctoral researcher from 2001 to 2004 at the Institute of Clinical Molecular Biology and Tumor Genetics at the Helmholtz Zentrum München in Munich. Since 2005 is was appointed as a group leader with a short stint at the Yamagata University in Tsuruoka (Japan) during 2007 and a sabbatical working as a senior scientist in Laboratory of Arne Östman at the Karolinska Institute in Stockholm in Sweden[2]. In 2008 he was the first to show that loss of GPX4 triggered cell death in mice iconically describing this phenomenon as a "yet-unrecognized cell death pathway",[3] today known as ferroptosis.

In 2009 briefly left academia to become head of the global drug discovery platform at Bayer-Shering Pharma in Berlin before reurtuning to Munich and becoming the head of the transgenic core unit at the German Centre for neurodegenerative diseases (DZNE).

In 2018 he reported on the role of selenium in ferroptosis[4] and in 2019 on a second axis of ferroptosis protection mediated by AIFM2, recoined as Ferroptosis suppressor protein 1 (FSP1).[5]

References[edit]

  1. ^ "Helmholtz Munich". Helmholtz Munich. Retrieved 2024-01-08.
  2. ^ a b "PI Biography". Conrad Laboratory. Retrieved 2024-01-08.
  3. ^ Seiler, Alexander; Schneider, Manuela; Förster, Heidi; Roth, Stephan; Wirth, Eva K.; Culmsee, Carsten; Plesnila, Nikolaus; Kremmer, Elisabeth; Rådmark, Olof; Wurst, Wolfgang; Bornkamm, Georg W.; Schweizer, Ulrich; Conrad, Marcus (September 2008). "Glutathione peroxidase 4 senses and translates oxidative stress into 12/15-lipoxygenase dependent- and AIF-mediated cell death". Cell Metabolism. 8 (3): 237–248. doi:10.1016/j.cmet.2008.07.005. ISSN 1932-7420. PMID 18762024.
  4. ^ Ingold, Irina; Berndt, Carsten; Schmitt, Sabine; Doll, Sebastian; Poschmann, Gereon; Buday, Katalin; Roveri, Antonella; Peng, Xiaoxiao; Porto Freitas, Florencio; Seibt, Tobias; Mehr, Lisa; Aichler, Michaela; Walch, Axel; Lamp, Daniel; Jastroch, Martin (2018-01-25). "Selenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis". Cell. 172 (3): 409–422.e21. doi:10.1016/j.cell.2017.11.048. ISSN 1097-4172. PMID 29290465.
  5. ^ Doll, Sebastian; Freitas, Florencio Porto; Shah, Ron; Aldrovandi, Maceler; da Silva, Milene Costa; Ingold, Irina; Goya Grocin, Andrea; Xavier da Silva, Thamara Nishida; Panzilius, Elena; Scheel, Christina H.; Mourão, André; Buday, Katalin; Sato, Mami; Wanninger, Jonas; Vignane, Thibaut (November 2019). "FSP1 is a glutathione-independent ferroptosis suppressor". Nature. 575 (7784): 693–698. Bibcode:2019Natur.575..693D. doi:10.1038/s41586-019-1707-0. ISSN 1476-4687. PMID 31634899. S2CID 204833583.

External links[edit]