Timothy J Walker, Eduardo Reyes-Alvarez ... Lois M Mulligan
TMEM127 depletion alters membrane dynamics, promoting cell surface accumulation and constitutive activity of growth factor receptors, and ultimately providing a novel paradigm for oncogenesis through aberrant receptor localization and signaling.
Simona Bolamperti, Hiroaki Saito ... Hanna Taipaleenmäki
A novel mechanism underlying the regulation of osteoblast morphology, adherence, and migration that has implications in bone remodeling, regeneration, and response to the pharmacological effects of PTH treatment.
Analysis of mice lacking the precursor for irisin, FNDC5, provides evidence for a sex-specific role of irisin in calcium release from bone due to osteocytic osteolysis.
A comprehensive review focusing on the role of osteoclasts as active regulators of bone homeostasis by influencing osteoblast function explores the currently known mechanisms and coupling factors involved in osteoclast–osteoblast communication and their potential as treatments for bone diseases.
Live imaging, transcriptional profiling and mouse models demonstrated that the mesenchyme controls the growth pace but not the mode of branching of the mammary epithelium and unveiled a unique function for Igf1/Igfr1 in embryonic development mammary gland.
Osteoblast glucose metabolism is impaired in a mouse model for type II diabetes and can be boosted pharmacologically or genetically to alleviate diabetic osteopenia.
Loss or PTH1R-mediated repression of Zfp467 results in a pathway that increases Pth1r transcription via NFκB1 and thus cellular responsiveness to PTH/PTHrP, ultimately leading to enhanced bone formation.
Impaired bone microstructure and bone strength are prominent characteristics of rats with hemizygous E10-16del mutation in PLS3, and treatment with alendronate or teriparatide can improve bone mineral density and bone microstructure of this novel rat model with PLS3-related early-onset osteoporosis.
