ArticlePloS one2012
Slc39a7/zip7 plays a critical role in development and zinc homeostasis in zebrafish.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 48 citations in OpenAlex.
- Molecular insights into CRIP1 as an immunometabolic regulator revealed by CRIP1 knockout and single-cell transcriptomics.Frontiers in immunology · 2026Article
- Single-Cell Analysis of Alternative Splicing and Gene Regulatory Network Reveals Remarkable Expression and Regulation Dynamics During Human Early Embryonic Development.FASEB bioAdvances · 2025Article
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- Review
- Noninvasive and Spatiotemporal Control of DNAzyme-Based Imaging of Metal IonsJournal of the American Chemical Society · 2022Article
- Zinc transporter ZIP7 is a novel determinant of ferroptosis.Cell death & disease · 2021Article
- Interactions of Environmental Chemicals and Natural Products With ABC and SLC Transporters in the Digestive System of Aquatic Organisms.Frontiers in physiology · 2021Article
- Article
- Systematic genetic mapping of necroptosis identifies SLC39A7 as modulator of death receptor trafficking.Cell death and differentiation · 2019Article
- An essential role for the ZnNature immunology · 2019Article
- Optical Control of Metal Ion Probes in Cells and Zebrafish Using Highly Selective DNAzymes Conjugated to Upconversion Nanoparticles.Journal of the American Chemical Society · 2018Article
- Article
- Knockdown of SLC39A7 suppresses cell proliferation, migration and invasion in cervical cancer.EXCLI journal · 2017Article
- Zinc transporter ZIP10 forms a heteromer with ZIP6 which regulates embryonic development and cell migration.The Biochemical journal · 2016Article
- Long-term expression of zinc transporters in hippocampus following penicillin-induced developmental seizures and its regulation by E-64d.Experimental and therapeutic medicine · 2016Article
- 3D imaging of transition metals in the zebrafish embryo by X-ray fluorescence microtomography.Metallomics : integrated biometal science · 2014Article
- X-ray fluorescence imaging reveals subcellular biometal disturbances in a childhood neurodegenerative disorder.Chemical science · 2014Article
- Deregulation of subcellular biometal homeostasis through loss of the metal transporter, Zip7, in a childhood neurodegenerative disorder.Acta neuropathologica communications · 2014Article
- Genome wide identification, phylogeny and expression of zinc transporter genes in common carp.PloS one · 2014Article
- Zebrafish in the sea of mineral (iron, zinc, and copper) metabolism.Frontiers in pharmacology · 2014Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSlc39a7/Zip7, also known as Ke4, is a member of solute carrier family 39 (Slc39a) and plays a critical role in regulating cell growth and death. Because the function of Zip7 in vivo was unclear, the present study investigated the function of zip7 in vertebrate development and zinc metabolism using zebrafish as a model organism. PRINCIPAL FINDING: Using real-time PCR to determine the gene expression pattern of zip7 during zebrafish development, we found that zip7 mRNA is expressed throughout embryonic development and into maturity. Interestingly, whole mount in situ hybridization revealed that while zip7 mRNA is ubiquitously expressed until 12 hours post-fertilization (hpf); at 24 hpf and beyond, zip7 mRNA was specifically detected only in eyes. Morpholino-antisense (MO) gene knockdown assay revealed that downregulation of zip7 expression resulted in several morphological defects in zebrafish including decreased head size, smaller eyes, shorter palates, and shorter and curved spinal cords. Analysis by synchrotron radiation X-ray fluorescence (SR-XRF) showed reduced concentrations of zinc in brain, eyes, and gills of zip7-MO-injected embryos. Furthermore, incubation of the zip7 knockdown embryos in a zinc-supplemented solution was able to rescue the MO-induced morphological defects. SIGNIFICANCE: Our data suggest that zip7 is required for eye, brain, and skeleton formation during early embryonic development in zebrafish. Moreover, zinc supplementation can partially rescue defects resulting from zip7 gene knockdown. Taken together, our data provide critical insight into a novel function of zip7 in development and zinc homeostasis in vivo in zebrafish.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.