Pax6 expressed in osteocytes inhibits canonical Wnt signaling
نویسندگان
چکیده
منابع مشابه
The Canonical Wnt Signaling (Wnt/β-Catenin Pathway): A Potential Target for Cancer Prevention and Therapy
Precise regulation of signal transduction pathways is crucial for normal animal development and for maintaining cellular and tissue homeostasis in adults. The Wnt/Frizzled-mediated signaling includes canonical and non-canonical signal transduction pathways. Upregulation or downregulation of the canonical Wnt-signaling (or the Wnt/β-Catenin signal transduction) leads to a variety of human diseas...
متن کاملOsteocytes mediate the anabolic actions of canonical Wnt/β-catenin signaling in bone.
Osteocytes, >90% of the cells in bone, lie embedded within the mineralized matrix and coordinate osteoclast and osteoblast activity on bone surfaces by mechanisms still unclear. Bone anabolic stimuli activate Wnt signaling, and human mutations of components along this pathway underscore its crucial role in bone accrual and maintenance. However, the cell responsible for orchestrating Wnt anaboli...
متن کاملCanonical Wnt signaling inhibits osteoclastogenesis independent of osteoprotegerin
Although Wnt signaling is considered a key regulatory pathway for bone formation, inactivation of β-catenin in osteoblasts does not affect their activity but rather causes increased osteoclastogenesis due to insufficient production of osteoprotegerin (Opg). By monitoring the expression pattern of all known genes encoding Wnt receptors in mouse tissues and bone cells we identified Frizzled 8 (Fz...
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Authors’ Affiliations: Unit of Molecular Oncology, Unit of in vivo Pharmacology, Department of Medicinal Chemistry, Department of Biomolecular Screening, Clinical Development and Department of Pharmacology, Siena Biotech Medicine Research Centre, Siena, Italy. Experimental Therapeutics Centre, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore. The F. M. Kirby Neurobiolo...
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ژورنال
عنوان ژورنال: Molecules and Cells
سال: 2013
ISSN: 1016-8478,0219-1032
DOI: 10.1007/s10059-013-2310-0