Regular ArticleAP-1 Transcription Factor Complex Is a Target of Signals from Both WNT-7a and N-Cadherin-Dependent Cell–Cell Adhesion Complex during the Regulation of Limb Mesenchymal Chondrogenesis
References (30)
- et al.
Cellular interactions and signaling in cartilage development
Osteoarthr. Cart.
(2000) - et al.
Activation of the Wnt signaling pathway: A molecular mechanism for lithium action
Dev. Biol.
(1997) - et al.
Activation of protein kinase C decreases phosphorylation of c-Jun at sites that negatively regulate its DNA-binding activity
Cell
(1991) - et al.
Glycogen synthase kinase-3: Functions in oncogenesis and development
Biochim. Biophys. Acta
(1992) - et al.
Opposing role of mitogen-activated protein kinase subtypes, Erk-1/2 and p38, in regulation of chondrogenesis of mesenchymes
J. Biol. Chem.
(2000) - et al.
Interaction between the signaling molecules WNT7a and SHH during vertebrate limb development: Dorsal signals regulate anteroposterior patterning
Cell
(1995) - et al.
Chondrogenesis of limb bud mesenchyme in vitro: Stimulation by cations
Dev. Biol.
(1986) - et al.
Regulation of human involucrin promoter activity by a protein kinase C, Ras, MEKK1, MEK3, p38/RK, AP-1 signal transduction pathway
J. Biol. Chem.
(1998) - et al.
Isolation and characterization of the promoter region of the chicken N-cadherin gene
Gene
(1997) - et al.
AP-1 function and regulation
Curr. Opin. Cell. Biol.
(1997)
Cadherins as predictive markers of nodal metastasis in breast cancer
Mod. Pathol.
The chondrocyte pericellular matrix: A model for hyaluronan-mediated cell-matrix interactions
Biochem. Soc. Trans.
Wnt regulation of Limb mesenchymal chondrogenesis is accompanied by altered N-cadherin-related functions
FASEB J.
Molecular to pharmacologic control of osteoblast proliferation and differentiation
J. Cell. Biochem.
Cited by (51)
CDH2 and CDH11 act as regulators of stem cell fate decisions
2015, Stem Cell ResearchCitation Excerpt :CDH2 was required for the initial condensation phase but decreased significantly during terminal chondrogenic differentiation (Oberlender and Tuan, 1994; Woods et al., 2007). In agreement, it has been reported that the cleavage of CDH2 was required during chondrogenic differentiation (Nakazora et al., 2010), while inhibition of commitment to chondrogenic lineage by the Wnt7a inhibitor led to enhanced CDH2 expression and stabilization of AJs (Tufan and Tuan, 2001; Tufan et al., 2002a, b). Interestingly, loss of CDH2 led to increased levels of CDH11, suggesting that compensatory mechanisms might be at work (Luo et al., 2005).
Activator protein-1 (AP-1) and response to pathogen infection in the Hong Kong oyster (Crassostrea hongkongensis)
2014, Fish and Shellfish ImmunologyMultipotent mesenchymal stromal cells in articular diseases
2008, Best Practice and Research: Clinical RheumatologyCitation Excerpt :By contrast, Wnt5a and Wnt5b promote early chondrogenesis in vitro while inhibiting terminal differentiation in vivo.65 Whereas it has been clearly demonstrated that Wnt7a blocks chondrogenesis,66,67 the exact role of Wnt3a is more controversial. Indeed, Wnt3a has the capacity to enhance BMP-2-mediated chondrogenesis of mesenchymal micromass cultures via the regulation of N-cadherin-mediated adhesion, the inhibition of GSK-3β kinase activity and the nuclear signalling of β-catenin and LEF-1.68
Roles of Wnt7a in embryo development, tissue homeostasis, and human diseases
2019, Journal of Cellular Biochemistry
- 1
To whom correspondence and reprint requests should be addressed at Cartilage Biology and Orthopaedics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Building 13, 3W17, MSC 5755, Bethesda, MD 20892-5755. Fax: (301) 480-4315. E-mail: [email protected].