ArticleThe EMBO journal2014
MiR-135b is a direct PAX6 target and specifies human neuroectoderm by inhibiting TGF-β/BMP signaling.
Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
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- microRNA Expression in the Late Embryonic Pax6-Null Mouse Cerebellum.Molecular neurobiology · 2025Article
- Post-replicative initial expression of PAX6 during neuroectoderm differentiation.The EMBO journal · 2025Article
- Inactivation of major hepcidin pathways leads to systemic and hepatic iron overload during development of chemically-induced liver cirrhosis in rats.Journal of toxicologic pathology · 2025Article
- MiRNAs as major players in brain health and disease: current knowledge and future perspectives.Cell death discovery · 2025Review
- miR-135b: An emerging player in cardio-cerebrovascular diseases.Journal of pharmaceutical analysis · 2024Review
- MeCP2 dysfunction prevents proper BMP signaling and neural progenitor expansion in brain organoid.Annals of clinical and translational neurology · 2023Article
- Role of Some microRNA/ADAM Proteins Axes in Gastrointestinal Cancers as a Novel Biomarkers and Potential Therapeutic Targets-A Review.Current issues in molecular biology · 2023Review
- Identification and coregulation pattern analysis of long noncoding RNAs following subacute spinal cord injury.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022Article
- G-quadruplex DNA structures in human stem cells and differentiation.Nature communications · 2022Article
- Role of circular RNA expression in the pathological progression after spinal cord injury.Neural regeneration research · 2021Article
- The Clinical Assessment of MicroRNA Diagnostic, Prognostic, and Theranostic Value in Colorectal Cancer.Cancers · 2021Review
- Article
- Kinetic modeling of stem cell transcriptome dynamics to identify regulatory modules of normal and disturbed neuroectodermal differentiation.Nucleic acids research · 2020Article
- Possible involvement of TGF‑β‑SMAD‑mediated epithelial‑mesenchymal transition in pro‑metastatic property of PAX6.Oncology reports · 2020Article
- The Spectrum ofGenes · 2019Review
- MicroRNA Signature in Human Normal and Tumoral Neural Stem Cells.International journal of molecular sciences · 2019Review
- mRNA and miRNA expression profiles in an ectoderm-biased substate of human pluripotent stem cells.Scientific reports · 2019Article
- Pax 6 Controls Neural Crest Potential of Limbal Niche Cells to Support Self-Renewal of Limbal Epithelial Stem Cells.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several transcription factors (TFs) have been implicated in neuroectoderm (NE) development, and recently, the TF PAX6 was shown to be critical for human NE specification. However, microRNA networks regulating human NE development have been poorly documented. We hypothesized that microRNAs activated by PAX6 should promote NE development. Using a genomics approach, we identified PAX6 binding sites and active enhancers genome-wide in an in vitro model of human NE development that was based on neural differentiation of human embryonic stem cells (hESC). PAX6 binding to active enhancers was found in the proximity of several microRNAs, including hsa-miR-135b. MiR-135b was activated during NE development, and ectopic expression of miR-135b in hESC promoted differentiation toward NE. MiR-135b promotes neural conversion by targeting components of the TGF-β and BMP signaling pathways, thereby inhibiting differentiation into alternate developmental lineages. Our results demonstrate a novel TF-miRNA module that is activated during human neuroectoderm development and promotes the irreversible fate specification of human pluripotent cells toward the neural lineage.
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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.