Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.1 (protein kinase)
 81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low-intensity pulsed ultrasound, a form of mechanical energy transmitted as high-frequency acoustical pressure waves, provides noninvasive therapeutic treatment for accelerating fracture repair and distraction osteogenesis. Relatively young osteoblasts respond to ultrasound by transiently upregulating message levels of immediate-early genes as well as that of osteocalcin and insulin-like growth factor I (IGF-I). Osteocytes derived from newborn rat tibia and calvaria responded to a lesser extent only in c-fos and cyclooxygenase-2 (COX-2) messages. Compared with the stretched osteocytes, which use stretch-activated and parathyroid hormone (PTH)-potentiated Ca2+ influx as an entry route to the protein kinase A (PKA) signal transduction pathways, there was no evidence of Ca2+ internalization by any of the cells tested on exposure to the ultrasound. On the other hand, inhibitors of p38 mitogen-activated protein kinase (MAPK) and upstream phosphoinositide 3-kinase (PI3K) blocked COX-2 and osteocalcin upregulation by the ultrasound-exposed ST2, murine bone marrow-derived cells. This is distinct from the aforementioned osteocytic response to low-frequency stretching and implies the involvement of integrins. Our findings suggested that accelerated fracture repair and distraction osteogenesis by the low-intensity pulsed ultrasound depend, at least in part, on the stimulation of osteoblastic cells at relatively early stages of osteogenic lineage. Bone is under control of multiple regulatory mechanisms so that diverse physical forces can be reflected to the microenvironment of each cell, in turn, to the entire bone.
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PMID:Distinct anabolic response of osteoblast to low-intensity pulsed ultrasound. 1256 14

Osteoclasts are the only cells that destroy and resorb bone. Calcitonin, a calcium regulatory hormone, strongly inhibits bone-resorbing activity of osteoclasts. The calcitonin-induced inhibition of osteoclast function is believed to be due to disruption of cytoskeletal organization (distraction of actin rings) and disappearance of the cellular polarity of osteoclasts. Calcitonin receptors are coupled to both cAMP-PKA- and Ca(2+)-PKC (protein kinase C)-mediated signaling pathways. Using mouse osteoclasts formed in vitro, it is shown that inhibitory effects of calcitonin on bone resorption is mainly mediated by the cAMP-PKA signal. This article describes the mechanism of calcitonin action in the suppression of osteoclast function.
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PMID:[Effects of calcitonin on osteoclast]. 1574 94