ArticleJournal of molecular biology2012
LIV-1 ZIP ectodomain shedding in prion-infected mice resembles cellular response to transition metal starvation.
Article in Journal of molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Research progress on the molecular structure, function, and application in tumor therapy of zinc transporter ZIP4.International journal of biological sciences · 2024Review
- Redox mechanisms and their pathological role in prion diseases: The road to ruin.PLoS pathogens · 2023Review
- The LIV-1 Subfamily of Zinc Transporters: From Origins to Present Day Discoveries.International journal of molecular sciences · 2023Review
- Why and how to investigate the role of protein phosphorylation in ZIP and ZnT zinc transporter activity and regulation.Cellular and molecular life sciences : CMLS · 2020Review
- SheddomeDB: the ectodomain shedding database for membrane-bound shed markers.BMC bioinformatics · 2017Review
- Physiological roles of zinc transporters: molecular and genetic importance in zinc homeostasis.The journal of physiological sciences : JPS · 2017Review
- A ZIP6-ZIP10 heteromer controls NCAM1 phosphorylation and integration into focal adhesion complexes during epithelial-to-mesenchymal transition.Scientific reports · 2017Article
- Prion Protein Deficiency Causes Diverse Proteome Shifts in Cell Models That Escape Detection in Brain Tissue.PloS one · 2016Article
- Prion protein functions as a ferrireductase partner for ZIP14 and DMT1.Free radical biology & medicine · 2015Article
- Review
- The Cellular Prion Protein: A Player in Immunological Quiescence.Frontiers in immunology · 2015Review
- Zinc transporter SLC39A10/ZIP10 facilitates antiapoptotic signaling during early B-cell development.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Zinc transporter SLC39A10/ZIP10 controls humoral immunity by modulating B-cell receptor signal strength.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Comparative genomic analysis of slc39a12/ZIP12: insight into a zinc transporter required for vertebrate nervous system development.PloS one · 2014Article
- Lipid rafts: linking prion protein to zinc transport and amyloid-β toxicity in Alzheimer's disease.Frontiers in cell and developmental biology · 2014Article
- A mechanism for epithelial-mesenchymal transition and anoikis resistance in breast cancer triggered by zinc channel ZIP6 and STAT3 (signal transducer and activator of transcription 3).The Biochemical journal · 2013Article
- The ZIP5 ectodomain co-localizes with PrP and may acquire a PrP-like fold that assembles into a dimer.PloS one · 2013Article
- Zinc transporters and their functional integration in mammalian cells.The Journal of biological chemistryReview
- Review
- Article
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
We recently documented the co-purification of members of the LIV-1 subfamily of ZIP (Zrt-, Irt-like Protein) zinc transporters (LZTs) with the cellular prion protein (PrP(C)) and, subsequently, established that the prion gene family descended from an ancestral LZT gene. Here, we begin to address whether the study of LZTs can shed light on the biology of prion proteins in health and disease. Starting from an observation of an abnormal LZT immunoreactive band in prion-infected mice, subsequent cell biological analyses uncovered a surprisingly coordinated biology of ZIP10 (an LZT member) and prion proteins that involves alterations to N-glycosylation and endoproteolysis in response to manipulations to the extracellular divalent cation milieu. Starving cells of manganese or zinc, but not copper, causes shedding of the N1 fragment of PrP(C) and of the ectodomain of ZIP10. For ZIP10, this posttranslational biology is influenced by an interaction between its PrP-like ectodomain and a conserved metal coordination site within its C-terminal multi-spanning transmembrane domain. The transition metal starvation-induced cleavage of ZIP10 can be differentiated by an immature N-glycosylation signature from a constitutive cleavage targeting the same site. Data from this work provide a first glimpse into a hitherto neglected molecular biology that ties PrP to its LZT cousins and suggest that manganese or zinc starvation may contribute to the etiology of prion disease in mice.
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