ArticlePloS one2015
Role of ALADIN in human adrenocortical cells for oxidative stress response and steroidogenesis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
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- Identification of Gβ5 Interactome Associated with Neuronal Development in Neuro-2a Cells through miniTurbo Proximity Labeling.ACS omega · 2026Article
- Pathologies at the gateway: exploring the link between nucleoporins and inherited diseases.Cellular and molecular life sciences : CMLS · 2026Review
- Outcome-specific shifts in homocysteine-androgen correlations in polycystic ovary syndrome.Frontiers in endocrinology · 2026Article
- Article
- Double 'A' phenotypes with mineralocorticoid deficiency: A rare presentation of Allgrove syndrome.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2025Article
- Very early and severe presentation of Triple A syndrome - case report and review of the literature.Frontiers in endocrinology · 2024Review
- Fertility and sexual activity in patients with Triple A syndrome.Frontiers in endocrinology · 2024Article
- SCARB1 downregulation in adrenal insufficiency with Allgrove syndrome.Orphanet journal of rare diseases · 2023Article
- Abiraterone switches castration-resistant prostate cancer dependency from adrenal androgens towards androgen receptor variants and glucocorticoid receptor signalling.The Prostate · 2022Article
- Two novel truncating variants of the AAAS gene causative of the triple A syndrome.Journal of endocrinological investigation · 2020Article
- Active steroid hormone synthesis renders adrenocortical cells highly susceptible to type II ferroptosis induction.Cell death & disease · 2020Article
- A broad range of symptoms in allgrove syndrome: single center experience in Southeast Anatolia.Journal of endocrinological investigation · 2020Article
- 11β-Hydroxysteroid dehydrogenase type 1 inhibition in idiopathic intracranial hypertension: a double-blind randomized controlled trial.Brain communications · 2020Article
- Moonlighting nuclear pore proteins: tissue-specific nucleoporin function in health and disease.Histochemistry and cell biology · 2018Review
- Nicotinamide Nucleotide Transhydrogenase as a Novel Treatment Target in Adrenocortical Carcinoma.Endocrinology · 2018Article
- Compensation for chronic oxidative stress in ALADIN null mice.Biology open · 2018Article
- "Crying without tears" as an early diagnostic sign-post of triple A (Allgrove) syndrome: two case reports.BMC pediatrics · 2018Article
- Triple A patient cells suffering from mitotic defects fail to localize PGRMC1 to mitotic kinetochore fibers.Cell division · 2018Article
- NNT is a key regulator of adrenal redox homeostasis and steroidogenesis in male mice.The Journal of endocrinology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Triple A syndrome is caused by mutations in AAAS encoding the protein ALADIN. We investigated the role of ALADIN in the human adrenocortical cell line NCI-H295R1 by either over-expression or down-regulation of ALADIN. Our findings indicate that AAAS knock-down induces a down-regulation of genes coding for type II microsomal cytochrome P450 hydroxylases CYP17A1 and CYP21A2 and their electron donor enzyme cytochrome P450 oxidoreductase, thereby decreasing biosynthesis of precursor metabolites required for glucocorticoid and androgen production. Furthermore we demonstrate that ALADIN deficiency leads to increased susceptibility to oxidative stress and alteration in redox homeostasis after paraquat treatment. Finally, we show significantly impaired nuclear import of DNA ligase 1, aprataxin and ferritin heavy chain 1 in ALADIN knock-down cells. We conclude that down-regulating ALADIN results in decreased oxidative stress response leading to alteration in steroidogenesis, highlighting our knock-down cell model as an important in-vitro tool for studying the adrenal phenotype in triple A syndrome.
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Registered trials
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.