ArticleJCI insight2022
ARMC5-CUL3 E3 ligase targets full-length SREBF in adrenocortical tumors.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- SREBF2 enhances lipid metabolism and represses anti-tumor immune responses in cervical cancer by increasing ACAT2.Communications biology · 2026Article
- The Proteome of Bilateral Macronodular Adrenocortical Disease (BMAD) Shows Different Profiles Correlating with the Genetic Causes and Reveals Specific Dysregulation of RNA Polymerase II and Cholesterol Biosynthesis Enzymes.Endocrine pathology · 2026Article
- Recent progress in pathophysiology of cortisol-producing adrenal tumor.Endocrine journal · 2026Review
- Bilateral macronodular adrenocortical disease with isolated primary aldosteronism and normocortisolemia: a case report.Frontiers in medicine · 2026Article
- A NovelJCEM case reports · 2025Article
- ARMC5 mutations in primary bilateral macronodular adrenal hyperplasia: a family case report.BMC medical genomics · 2025Article
- The mutational landscape of ARMC5 in Primary Bilateral Macronodular Adrenal Hyperplasia: an update.Orphanet journal of rare diseases · 2025Review
- Cushing syndrome.Nature reviews. Disease primers · 2025Review
- The role of oxidative stress, glucocorticoid receptor and ARMC5 in lipid metabolism.Endocrine journal · 2024Review
- Molecular and Genetics Perspectives on Primary Adrenocortical Hyperfunction Disorders.International journal of molecular sciences · 2024Review
- A NEW-FOUND ARMC5 GERMLINE VARIANT IN PRIMARY BILATERAL MACRONODULAR ADRENAL HYPERPLASIA USING WHOLE-EXOME SEQUENCING AND PROTEIN PREDICTIVE ANALYSIS.Acta endocrinologica (Bucharest, Romania : 2005)Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivating mutations of ARMC5 are responsible for the development of bilateral macronodular adrenal hyperplasia (BMAH). Although ARMC5 inhibits adrenocortical tumor growth and is considered a tumor-suppressor gene, its molecular function is poorly understood. In this study, through biochemical purification using SREBF (SREBP) as bait, we identified the interaction between SREBF and ARMC5 through its Armadillo repeat. We also found that ARMC5 interacted with CUL3 through its BTB domain and underwent self-ubiquitination. ARMC5 colocalized with SREBF1 in the cytosol and induced proteasome-dependent degradation of full-length SREBF through ubiquitination. Introduction of missense mutations in Armadillo repeat of ARMC5 attenuated the interaction between SREBF, and introduction of mutations found in BMAH completely abolished its ability to degrade full-length SREBF. In H295R adrenocortical cells, silencing of ARMC5 increased full-length SREBFs and upregulated SREBF2 target genes. siARMC5-mediated cell growth was abrogated by simultaneous knockdown of SREBF2 in H295R cells. Our results demonstrate that ARMC5 was a substrate adaptor protein between full-length SREBF and CUL3-based E3 ligase, and they suggest the involvement of the SREBF pathway in the development of BMAH.
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