ArticleExperimental and therapeutic medicine2020
ZMIZ1 promotes the proliferation and migration of melanocytes in vitiligo.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Blockade of ZMIZ1-GATA4 Axis Regulation Restores Youthfulness to Aged Cartilage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Association ofGenes · 2024Article
- Genomic insights into local adaptation and phenotypic diversity of Wenchang chickens.Poultry science · 2024Article
- Zmiz1 is a novel regulator of lymphatic endothelial cell gene expression and function.PloS one · 2024Article
- Zmiz1 is a novel regulator of lymphatic endothelial cell gene expression and function.bioRxiv : the preprint server for biology · 2023Article
- Stimulatory effects ofFrontiers in pharmacology · 2023Article
- ZMIZ proteins: partners in transcriptional regulation and risk factors for human disease.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Prostate Cancer Susceptibility Loci Identified inInternational journal of genomics · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome wide association studies have revealed that the zinc finger MIZ-type containing 1 (ZMIZ1) is involved in the pathogenesis of vitiligo; however, the underlying mechanism remains unclear. The present study aimed to investigate the effects of ZMIZ1 on the proliferation, apoptosis and migration of the human melanocyte cell lines PIG1 and PIG3V. ZMIZ1 overexpression and knockdown PIG1 and PIG3V cell models were established by lentivirus infection, and the effects of ZMIZ1 on cell proliferation and apoptosis were determined using an MTT assay and flow cytometry, respectively. Furthermore, the expression levels of proliferation- and apoptosis-associated proteins were analyzed using western blotting. Additionally, Transwell assays were performed to determine the effect of ZMIZ1 on the migration of PIG1 and PIG3V cells. Finally, the effect of ZMIZ1 on cytoskeletal remodeling in PIG1 and PIG3V cells was analyzed using immunocytochemistry. The overexpression of ZMIZ1 promoted the proliferation and inhibited the apoptosis of PIG1 and PIG3V cells, whereas the genetic knockdown of ZMIZ1 resulted in the opposite effects. Furthermore, ZMIZ1 overexpression increased the migration, whereas the knockdown of ZMIZ1 inhibited the migration and altered remodeling of the actin cytoskeleton in PIG1 and PIG3V cells. In conclusion, the results of the present study suggest that ZMIZ1 regulates the proliferation, apoptosis and migration of PIG1 and PIG3V cells, and indicate that ZMIZ1 may serve as a potential therapeutic target for vitiligo.
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