Article ; Online: Essentiality of Nfatc1 short isoform in osteoclast differentiation and its self-regulation.
2023 Volume 13, Issue 1, Page(s) 18797
Abstract: During osteoclast differentiation, the expression of the transcription factor nuclear factor of activated T cell 1 (Nfatc1) increases in an autoproliferative manner. Nfatc1 isoforms are of three sizes, and only the short isoform increases during ... ...
Abstract | During osteoclast differentiation, the expression of the transcription factor nuclear factor of activated T cell 1 (Nfatc1) increases in an autoproliferative manner. Nfatc1 isoforms are of three sizes, and only the short isoform increases during osteoclast differentiation. Genetic ablation of the whole Nfatc1 gene demonstrated that it is essential for osteoclastogenesis; however, the specific role of the Nfatc1 short form (Nfatc1/αA) remains unknown. In this study, we engineered Nfatc1 short form-specific knockout mice and found that these mice died in utero by day 13.5. We developed a novel osteoclast culture system in which hematopoietic stem cells were cultured, proliferated, and then differentiated into osteoclasts in vitro. Using this system, we show that the Nfatc1/αA isoform is essential for osteoclastogenesis and is responsible for the expression of various osteoclast markers, the Nfatc1 short form itself, and Nfatc1 regulators. |
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MeSH term(s) | Mice ; Animals ; Osteoclasts/metabolism ; NFATC Transcription Factors/genetics ; NFATC Transcription Factors/metabolism ; T-Lymphocytes/metabolism ; Cell Differentiation/genetics ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Self-Control ; RANK Ligand/metabolism |
Chemical Substances | NFATC Transcription Factors ; Protein Isoforms ; RANK Ligand ; Nfatc1 protein, mouse |
Language | English |
Publishing date | 2023-11-01 |
Publishing country | England |
Document type | Journal Article ; Research Support, Non-U.S. Gov't |
ZDB-ID | 2615211-3 |
ISSN | 2045-2322 ; 2045-2322 |
ISSN (online) | 2045-2322 |
ISSN | 2045-2322 |
DOI | 10.1038/s41598-023-45909-3 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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