ArticleThe Journal of biological chemistry2019
SIAH1 ubiquitin ligase mediates ubiquitination and degradation of Akt3 in neural development.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- TSG101 Promotes SIAH1 Auto-Ubiquitination to Drive Migration and Invasion in Hepatocellular Carcinoma Cells.Journal of cellular and molecular medicine · 2026Article
- Novel mutations of SRPX facilitate the stemness and malignant progression of glioma.British journal of cancer · 2025Article
- A novel variant inFrontiers in neuroscience · 2025Article
- NovelCase reports in genetics · 2025Article
- Deficiency of SIAH1 promotes the formation of filopodia by increasing the accumulation of FASN in liver cancer.Cell death & disease · 2024Article
- Article
- Molecular glue degrader for tumor treatment.Frontiers in oncology · 2024Review
- Neural crest cells and fetal alcohol spectrum disorders: Mechanisms and potential targets for prevention.Pharmacological research · 2023Review
- Transcriptome-Wide lncRNA and mRNA Profiling of Spleens from Meishan Pigs at Different Development Stages.Animals : an open access journal from MDPI · 2022Article
- Circ-CCNB1 Modulates Trophoblast Proliferation and Invasion in Spontaneous Abortion by Regulating miR-223/SIAH1 axis.Endocrinology · 2022Article
- mMolecular therapy. Nucleic acids · 2022Article
- SIAH1 reverses chemoresistance in epithelial ovarian cancer via ubiquitination of YBX-1.Oncogenesis · 2022Article
- Mechanistic advances in axon pathfinding.Current opinion in cell biology · 2020Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Akt signaling is an important regulator of neural development, but the distinctive function of Akt isoforms in brain development presents a challenge. Here we show Siah1 as an ubiquitin ligase that preferentially interacts with Akt3 and facilitates ubiquitination and degradation of Akt3. Akt3 is enriched in the axonal shaft and branches but not growth cone tips, where Siah1 is prominently present. Depletion of Siah1 enhanced Akt3 levels in the soma and axonal tips, eliciting multiple branching. Brain-specific somatic mutation in Akt3-E17K escapes from Siah1-mediated degradation and causes improper neural development with dysmorphic neurons. Remarkably, coexpression of Siah1 with Akt3-WT restricted disorganization of neural development is caused by Akt3 overexpression, whereas forced expression of Siah1 with the Akt3-E17K mutant fails to cope with malformation of neural development. These findings demonstrate that Siah1 limits Akt3 turnover during brain development and that this event is essential for normal organization of the neural network.
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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.