English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Significance Zinc plays important roles in numerous cellular processes. Deficiency or excess of Zn2+ leads to many diseases. Zn2+ concentration at various cellular compartments is regulated. Imbalance of Zn2+ in mitochondria has been linked to neurodegeneration. However, little is known about how mitochondrial Zn2+ is regulated. We find that SLC-30A9 is required for Zn2+ export from mitochondria in bothCaenorhabditis elegans and human cells. Loss ofslc-30a9 leads to excessive Zn2+ accumulation in mitochondria, severe mitochondrial swelling, compromised mitochondrial metabolic function, reductive stress, and induction of the mitochondrial stress response. SLC-30A9 is also essential for organismal fertility and sperm activation. In neurons,slc-30a9 mutations cause dramatically reduced mitochondria in neurites, providing a potential mechanism for the Birk–Landau–Perez cerebrorenal syndrome.

SLC-30A9 is required for Zn 2+ homeostasis, Zn 2+ mobilization, and mitochondrial health

SLC-30A9 is required for Zn ²⁺ homeostasis, Zn ²⁺ mobilization, and mitochondrial health