TY - JOUR AU - Schmacke, N.A. AU - Hornung, V.* C1 - 74164 C2 - 57360 CY - Campus, 4 Crinan St, London, N1 9xw, England SP - 391–392 TI - Decoding NLRP3: Phase separation enters the scene. JO - Cell Res. VL - 35 PB - Springernature PY - 2025 SN - 1001-0602 ER - TY - JOUR AB - Mutations in the orphan transporter MFSD7c (also known as Flvcr2), are linked to Fowler syndrome. Here, we used Mfsd7c knockout (Mfsd7c-/-) mice and cell-based assays to reveal that MFSD7c is a choline transporter at the blood-brain barrier (BBB). We performed comprehensive metabolomics analysis and detected differential changes of metabolites in the brains and livers of Mfsd7c-/-embryos. Particularly, we found that choline-related metabolites were altered in the brains but not in the livers of Mfsd7c-/- embryos. Thus, we hypothesized that MFSD7c regulates the level of choline in the brain. Indeed, expression of human MFSD7c in cells significantly increased choline uptake. Interestingly, we showed that choline uptake by MFSD7c is greatly increased by choline-metabolizing enzymes, leading us to demonstrate that MFSD7c is a facilitative transporter of choline. Furthermore, single-cell patch clamp analysis showed that the import of choline by MFSD7c is electrogenic. Choline transport function of MFSD7c was shown to be conserved in vertebrates, but not in yeasts. We demonstrated that human MFSD7c is a functional ortholog of HNM1, the yeast choline importer. We also showed that several missense mutations identified in patients exhibiting Fowler syndrome had abolished or reduced choline transport activity. Mice lacking Mfsd7c in endothelial cells of the central nervous system suppressed the import of exogenous choline from blood but unexpectedly had increased choline levels in the brain. Stable-isotope tracing study revealed that MFSD7c was required for exporting choline derived from lysophosphatidylcholine in the brain. Collectively, our work identifies MFSD7c as a choline exporter at the BBB and provides a foundation for future work to reveal the disease mechanisms of Fowler syndrome. AU - Nguyen, X.T.A.* AU - Le, T.N.U.* AU - Nguyen, T.Q.* AU - Thi Thuy Ha, H.* AU - Artati, A. AU - Leong, N.C.P.* AU - Nguyen, D.T.* AU - Lim, P.Y.* AU - Susanto, A.V.* AU - Huang, Q.* AU - Fam, L.* AU - Leong, L.N.* AU - Bonne, I.* AU - Lee, A.* AU - Granadillo, J.L.* AU - Gooch, C.* AU - Yu, D.* AU - Huang, H.* AU - Soong, T.W.* AU - Chang, M.W.* AU - Wenk, M.R.* AU - Adamski, J. AU - Cazenave-Gassiot, A.* AU - Nguyen, L.N.* C1 - 69892 C2 - 55309 CY - Campus, 4 Crinan St, London, N1 9xw, England SP - 245-257 TI - MFSD7c functions as a transporter of choline at the blood-brain barrier. JO - Cell Res. VL - 34 IS - 3 PB - Springernature PY - 2024 SN - 1001-0602 ER - TY - JOUR AU - Niethard, N.* AU - Born, J. C1 - 72867 C2 - 56760 CY - Campus, 4 Crinan St, London, N1 9xw, England SP - 239-240 TI - Tug of war between phosphatase and kinase during sleep. JO - Cell Res. VL - 35 IS - 4 PB - Springernature PY - 2024 SN - 1001-0602 ER - TY - JOUR AU - Träuble, K. AU - Heinig, M. C1 - 72223 C2 - 56524 CY - Campus, 4 Crinan St, London, N1 9xw, England TI - A cross-species foundation model for single cells. JO - Cell Res. PB - Springernature PY - 2024 SN - 1001-0602 ER - TY - JOUR AB - The article Ferroptosis: the Good, the Bad and the Ugly, written by Maceler Aldrovandi & Marcus Conrad, was originally published Online First without Open Access. After publication in volume 30, pages 1061–1062, the author decided to opt for Open Choice and to make the article an Open Access publication. Therefore, the copyright of the article has been changed to © The Author(s) 2020 and the article is forthwith distributed under the terms of the Creative Commons Attribution. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. AU - Aldrovandi, M. AU - Conrad, M. C1 - 62841 C2 - 48892 TI - Publisher Correction: Ferroptosis: The Good, the Bad and the Ugly (Cell Research, (2020), 30, 12, (1061-1062), 10.1038/s41422-020-00434-0). JO - Cell Res. PY - 2021 SN - 1001-0602 ER - TY - JOUR AB - Polyunsaturated ether phospholipids, previously thought to oppose propagation of lipid peroxidation, have been reported to promote the cells' susceptibility to ferroptotic cell death. A recent study by Zou and colleagues now sheds a new light on the importance of the peroxisome-ether phospholipid axis in modulating ferroptosis susceptibility and evasion. AU - Aldrovandi, M. AU - Conrad, M. C1 - 60481 C2 - 49970 CY - Campus, 4 Crinan St, London, N1 9xw, England SP - 1061-1062 TI - Ferroptosis: The Good, the Bad and the Ugly. JO - Cell Res. VL - 30 IS - 12 PB - Springernature PY - 2020 SN - 1001-0602 ER - TY - JOUR AB - In a recently published paper in Proc Natl Acad Sci USA, Fang et al. elegantly demonstrated that doxorubicin treatment or transient ischemia/reperfusion in mice triggers ferroptosis, a distinctive form of necrotic cell death marked by irondependent lipid peroxidation, which is the main underlying mechanism in the pathogenesis of cardiomyopathy. AU - Conrad, M. AU - Proneth, B. C1 - 55587 C2 - 46301 CY - Sibs, Cas, 319 Yueyang Road, Shanghai, 200031, Peoples R China SP - 263-264 TI - Broken hearts: Iron overload, ferroptosis and cardiomyopathy. JO - Cell Res. VL - 29 IS - 4 PB - Inst Biochemistry & Cell Biology PY - 2019 SN - 1001-0602 ER - TY - JOUR AB - Chenopodium quinoa is a halophytic pseudocereal crop that is being cultivated in an ever-growing number of countries. Because quinoa is highly resistant to multiple abiotic stresses and its seed has a better nutritional value than any other major cereals, it is regarded as a future crop to ensure global food security. We generated a high-quality genome draft using an inbred line of the quinoa cultivar Real. The quinoa genome experienced one recent genome duplication about 4.3 million years ago, likely reflecting the genome fusion of two Chenopodium parents, in addition to the γ paleohexaploidization reported for most eudicots. The genome is highly repetitive (64.5% repeat content) and contains 54 438 protein-coding genes and 192 microRNA genes, with more than 99.3% having orthologous genes from glycophylic species. Stress tolerance in quinoa is associated with the expansion of genes involved in ion and nutrient transport, ABA homeostasis and signaling, and enhanced basal-level ABA responses. Epidermal salt bladder cells exhibit similar characteristics as trichomes, with a significantly higher expression of genes related to energy import and ABA biosynthesis compared with the leaf lamina. The quinoa genome sequence provides insights into its exceptional nutritional value and the evolution of halophytes, enabling the identification of genes involved in salinity tolerance, and providing the basis for molecular breeding in quinoa. AU - Zou, C.* AU - Chen, A.* AU - Xiao, L.* AU - Müller, H.M.* AU - Ache, P.* AU - Haberer, G. AU - Zhang, M.* AU - Jia, W.* AU - Deng, P.* AU - Huang, R.J.* AU - Lang, D. AU - Li, F.* AU - Zhan, D.* AU - Wu, X.* AU - Zhang, H.* AU - Böhm, J.* AU - Liu, R.* AU - Shabala, S.* AU - Hedrich, R.* AU - Zhu, J.K.* C1 - 52068 C2 - 43708 CY - Shanghai SP - 1327-1340 TI - A high-quality genome assembly of quinoa provides insights into the molecular basis of salt bladder-based salinity tolerance and the exceptional nutritional value. JO - Cell Res. VL - 27 IS - 11 PB - Inst Biochemistry & Cell Biology PY - 2017 SN - 1001-0602 ER -