Mitogen-activated Protein Kinase (MAPK)-regulated Interactions between Osterix and Runx2 Are Critical for the Transcriptional Osteogenic Program

Artigas, Natalia; Ureña, Cristóbal Pasadas; Rodríguez-Carballo, Eddie; Rosa, José Luís; Ventura, Francesc

doi:10.1074/jbc.m114.576793

Cited by 103 publications

(97 citation statements)

References 53 publications

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“…Taken together, these findings suggest the primary site mediating Sp7's regulation of enhancer activity is the AT-rich motif, although it remains to be investigated whether Sp7 interacts directly at this site. The enrichment of other motifs supports the co-engagement of several other transcriptional regulators in Sp7 bound cis-regulatory modules including Runx (motif 6 in Figure S3A and motif 2 in Figure S3B) and NFAT (motif 4 in Figure S3B) supporting published data on their shared interactions (Artigas et al, 2014; Koga et al, 2005). …”

Section: Resultssupporting

confidence: 80%

Sp7/Osterix Is Restricted to Bone-Forming Vertebrates where It Acts as a Dlx Co-factor in Osteoblast Specification

et al. 2016

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SUMMARY Bone formation in extant species is restricted to vertebrate species. Sp7/Osterix is a key transcriptional determinant of bone-secreting osteoblasts. We performed Sp7 ChIP-seq analysis identifying a large set of predicted osteoblast enhancers and validated a subset of these in cell culture and transgenic mouse assays. Sp-family members bind GC-rich target sequences through their zinc finger domain. Several lines of evidence suggest Sp7 acts differently, engaging osteoblast targets in Dlx-containing regulatory complexes bound to AT-rich motifs. Amino acid differences in the Sp7 zinc finger domain reduce Sp7's affinity for the Sp-family consensus GC-box target; Dlx5 binding maps to this domain of Sp7. The data support a model in which Dlx recruitment of Sp7 to osteoblast enhancers underlies Sp7-directed osteoblast specification. As an Sp7-like zinc finger variant is restricted to vertebrates, the emergence of an Sp7 member within the Sp family was likely closely coupled to evolution of the bone forming vertebrates.

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Section: Resultssupporting

confidence: 80%

Sp7/Osterix Is Restricted to Bone-Forming Vertebrates where It Acts as a Dlx Co-factor in Osteoblast Specification

et al. 2016

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“…Accordingly, MMP13 expression was not detectable in the cartilage of Osterix knockout mice [83]. Consistent with the finding that RUXN2 is involved in MMP13 induction [87], Osterix has been shown to associate with RUNX2 [83,88]. Thus, Osterix seems to play a critical role in upregulation of MMP13 by interacting with RUNX2 (Fig.…”

Section: Coordination Of Endochondral Ossification By Transcriptionalsupporting

confidence: 73%

Regulation of transcriptional network system during bone and cartilage development

Nishimura

Hata

Ikeda

et al. 2015

Journal of Oral Biosciences

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“…OSX and RUNX2 have also been found to interact and exert a transcriptional cooperation that is regulated by p38-and ERKmediated phosphorylations. 43 Modulator of p38 MAPK in osteoblasts. Finally, only one molecular mechanism involved in the regulation of p38 MAPK activity in Figure 2 p38 MAPK signaling in osteoblasts.…”

Section: Upstream Activators Of P38 Mapk In Osteoblastsmentioning

confidence: 99%

Focus on the p38 MAPK signaling pathway in bone development and maintenance

2015

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The p38 mitogen-activated protein kinase (MAPK) signaling pathway can be activated in response to a wide range of extracellular signals. As a consequence, it can generate many different biological effects that depend on the stimulus and on the activated cell type. Therefore, this pathway has been found to regulate many aspects of tissue development and homeostasis. Recent work with the aid of genetically modified mice has highlighted the physiological functions of this pathway in skeletogenesis and postnatal bone maintenance. In this review, emphasis is given to the roles of the p38 MAPK pathway in chondrocyte, osteoblast and osteoclast biology. In particular, we describe the molecular mechanisms of p38 MAPK activation and downstream targets. The requirement of this pathway in physiological bone development and homeostasis is demonstrated by the ability of p38 MAPK to regulate master transcription factors controlling geneses and functions of chondrocytes, osteoblasts and osteoclasts.

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Mitogen-activated Protein Kinase (MAPK)-regulated Interactions between Osterix and Runx2 Are Critical for the Transcriptional Osteogenic Program

Cited by 103 publications

References 53 publications

Sp7/Osterix Is Restricted to Bone-Forming Vertebrates where It Acts as a Dlx Co-factor in Osteoblast Specification

Sp7/Osterix Is Restricted to Bone-Forming Vertebrates where It Acts as a Dlx Co-factor in Osteoblast Specification

Regulation of transcriptional network system during bone and cartilage development

Focus on the p38 MAPK signaling pathway in bone development and maintenance

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