ReviewHuman mutation2026
Zinc Transporter Gene Variants (SLC30A and SLC39A) in Human Disease: From Metal Homeostasis Disruption to Convergent Signaling Pathways.
Review in Human mutation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
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0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Zinc, an indispensable trace element, performs critical functions in human physiology. As a versatile cofactor, zinc participates in over 1000 enzymatic reactions and regulates more than 2000 transcription factors, orchestrating diverse cellular signaling pathways. The transmembrane transport of zinc is mediated by specialized transporter proteins, which are categorized into two families: zinc transporters (ZnTs) and Zrt- and Irt-like proteins (ZIPs). These transporters are pivotal for maintaining cellular and systemic zinc homeostasis. Pathogenic variants in ZnT/ZIP genes are associated with a spectrum of severe human diseases. This review systematically examines the pathophysiological connections between ZnT/ZIP gene variants and human diseases, providing a conceptual framework for future mechanistic investigations.
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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 Socratic graph.