ArticleMolecular biology of the cell2006
Microphthalmia-associated transcription factor interactions with 14-3-3 modulate differentiation of committed myeloid precursors.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 78 citations in OpenAlex.
- Temporal transcriptomic profiling uncovers multilevel suppression of RANKL-driven osteoclast differentiation by 14-3-3ζ.The Journal of biological chemistry · 2026Article
- STING-induced noncanonical autophagy regulates endolysosomal homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- Novel mechanisms of MITF regulation identified in a mouse suppressor screen.EMBO reports · 2024Article
- PDCD4 triggers α-synuclein accumulation and motor deficits via co-suppressing TFE3 and TFEB translation in a model of Parkinson's disease.NPJ Parkinson's disease · 2024Article
- O-GlcNAcylation of MITF regulates its activity and CDK4/6 inhibitor resistance in breast cancer.Nature communications · 2024Article
- 14-3-3ζ suppresses RANKL signaling by destabilizing TRAF6.The Journal of biological chemistry · 2024Article
- LncRNAs as nodes for the cross-talk between autophagy and Wnt signaling in pancreatic cancer drug resistance.International journal of biological sciences · 2024Review
- Article
- Novel mechanisms of MITF regulation and melanoma predisposition identified in a mouse suppressor screen.bioRxiv : the preprint server for biology · 2023Article
- RagD auto-activating mutations impair MiT/TFE activity in kidney tubulopathy and cardiomyopathy syndrome.Nature communications · 2023Article
- A central role for regulated protein stability in the control of TFE3 and MITF by nutrients.Molecular cell · 2023Article
- Autophagy and the Lysosomal System in Cancer.Cells · 2021Review
- The Development of Molecular Biology of Osteoporosis.International journal of molecular sciences · 2021Review
- MiT Family Transcriptional Factors in Immune Cell Functions.Molecules and cells · 2021Review
- Role of Biomolecules in Osteoclasts and Their Therapeutic Potential for Osteoporosis.Biomolecules · 2021Review
- The underestimated role of the microphthalmia-associated transcription factor (MiTF) in normal and pathological haematopoiesis.Cell & bioscience · 2021Review
- TFE3-Mediated Autophagy is Involved in Dopaminergic Neurodegeneration in Parkinson's Disease.Frontiers in cell and developmental biology · 2021Article
- Molecular Mechanisms of Lysosome and Nucleus Communication.Trends in biochemical sciences · 2020Review
- Luminal STIM1 Mutants that Cause Tubular Aggregate Myopathy Promote Autophagic Processes.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The microphthalmia-associated transcription factor (MITF) is required for terminal osteoclast differentiation and is a target for signaling pathways engaged by colony stimulating factor (CSF)-1 and receptor-activator of nuclear factor-kappaB ligand (RANKL). Work presented here demonstrates that MITF can shuttle from cytoplasm to nucleus dependent upon RANKL/CSF-1 action. 14-3-3 was identified as a binding partner of MITF in osteoclast precursors, and overexpression of 14-3-3 in a transgenic model resulted in increased cytosolic localization of MITF and decreased expression of MITF target genes. MITF/14-3-3 interaction was phosphorylation dependent, and Ser173 residue, within the minimal interaction region of amino acid residues 141-191, was required. The Cdc25C-associated kinase (C-TAK)1 interacted with an overlapping region of MITF. C-TAK1 increased MITF/14-3-3 complex formation and thus promoted cytoplasmic localization of MITF. C-TAK1 interaction was disrupted by RANKL/CSF-1 treatment. The results indicate that 14-3-3 regulates MITF activity by promoting the cytosolic localization of MITF in the absence of signals required for osteoclast differentiation. This work identifies a mechanism that regulates MITF activity in monocytic precursors that are capable of undergoing different terminal differentiation programs, and it provides a mechanism that allows committed precursors to rapidly respond to signals in the bone microenvironment to promote specifically osteoclast differentiation.
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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.