ArticleJournal of cellular and molecular medicine2017
A novel P53/POMC/Gαs/SASH1 autoregulatory feedback loop activates mutated SASH1 to cause pathologic hyperpigmentation.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- SASH1 as a Context-Dependent Multi-Docking Scaffold Linking Receptor Signaling to Cytoskeletal Dynamics.International journal of molecular sciences · 2026Review
- Genetic Pigmentary Disorders: From Molecular Mechanisms to Clinical Manifestations.The Journal of dermatology · 2026Review
- Solution NMR backbone assignment of the SASH1 SLy proteins associated disordered region (SPIDER).Biomolecular NMR assignments · 2023Article
- The Structural Dynamics, Complexity of Interactions, and Functions in Cancer of Multi-SAM Containing Proteins.Cancers · 2023Review
- SAM1 domain of SASH1 harbors distinctive structural heterogeneity.Journal of structural biology · 2022Article
- Two novel SASH1 mutations in Chinese families with dyschromatosis universalis hereditaria.Journal of clinical laboratory analysis · 2021Article
- SASH1 is a prognostic indicator and potential therapeutic target in non-small cell lung cancer.Scientific reports · 2020Article
- Mutated SASH1 promotes Mitf expression in a heterozygous mutated SASH1 knock‑in mouse model.International journal of molecular medicine · 2020Article
- Transcriptional regulation of P63 on the apoptosis of male germ cells and three stages of spermatogenesis in mice.Cell death & disease · 2018Article
- p53 regulates ERK1/2/CREB cascade via a novel SASH1/MAP2K2 crosstalk to induce hyperpigmentation.Journal of cellular and molecular medicine · 2017Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53-Transcriptional-regulated proteins interact with a large number of other signal transduction pathways in the cell, and a number of positive and negative autoregulatory feedback loops act upon the p53 response. P53 directly controls the POMC/α-MSH productions induced by ultraviolet (UV) and is associated with UV-independent pathological pigmentation. When identifying the causative gene of dyschromatosis universalis hereditaria (DUH), we found three mutations encoding amino acid substitutions in the gene SAM and SH3 domain containing 1 (SASH1), and SASH1 was associated with guanine nucleotide-binding protein subunit-alpha isoforms short (Gαs). However, the pathological gene and pathological mechanism of DUH remain unknown for about 90 years. We demonstrate that SASH1 is physiologically induced by p53 upon UV stimulation and SASH and p53 is reciprocally induced at physiological and pathophysiological conditions. SASH1 is regulated by a novel p53/POMC/α-MSH/Gαs/SASH1 cascade to mediate melanogenesis. A novel p53/POMC/Gαs/SASH1 autoregulatory positive feedback loop is regulated by SASH1 mutations to induce pathological hyperpigmentation phenotype. Our study demonstrates that a novel p53/POMC/Gαs/SASH1 autoregulatory positive feedback loop is regulated by SASH1 mutations to induce pathological hyperpigmentation phenotype.
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