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CAP1, a target of miR‐144/451, negatively regulates erythroid differentiation and enucleation

The exact molecular mechanism underlying erythroblast enucleation has been a fundamental biological question for decades. In this study, we found that miR‐144/451 critically regulated erythroid differentiation and enucleation. We further identified CAP1, a G‐actin‐binding protein, as a direct target...

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Detalles Bibliográficos
Autores principales: Huang, Xiaoli, Chao, Ruihua, Zhang, Yanyang, Wang, Pengxiang, Gong, Xueping, Liang, Dongli, Wang, Yuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7933962/
https://www.ncbi.nlm.nih.gov/pubmed/33496386
http://dx.doi.org/10.1111/jcmm.16067
Descripción
Sumario:The exact molecular mechanism underlying erythroblast enucleation has been a fundamental biological question for decades. In this study, we found that miR‐144/451 critically regulated erythroid differentiation and enucleation. We further identified CAP1, a G‐actin‐binding protein, as a direct target of miR‐144/451 in these processes. During terminal erythropoiesis, CAP1 expression declines along with gradually increased miR‐144/451 levels. Enforced CAP1 up‐regulation inhibits the formation of contractile actin rings in erythroblasts and prevents their terminal differentiation and enucleation. Our findings reveal a negative regulatory role of CAP1 in miR‐144/451‐mediated erythropoiesis and thus shed light on how microRNAs fine‐tune terminal erythroid development through regulating actin dynamics.