The University of Osaka · Environmental Science
Professor Daisuke Inoue's research lab focuses on cellular and molecular mechanisms underlying bone metabolism, neuronal signaling, and ion channel regulation. The lab investigates how mechanical forces and biochemical signals regulate bone formation through transcription factors like FosB/DeltaFosB and explores the role of membrane proteins such as meltrin family members in bone cell function. Additionally, the lab examines signaling pathways in sympathetic neurons, particularly the GPR41-ERK1/2-synapsin 2 axis activated by short-chain fatty acids, and the impact of metabolites like palmitylcarnitine on cardiac ion channels. These studies integrate molecular biology, cell signaling, and physiology to uncover mechanisms relevant to bone diseases, neurological disorders, and cardiac dysfunction.
Figures are computed from collected data and may differ slightly.
Here we report the cloning and initial biochemical characterization of the mouse metalloprotease/disintegrin/cysteine-rich (MDC) protein meltrin beta and the analysis of the mRNA expression of four MDC genes (meltrin alpha, meltrin beta, mdc9, and mdc15) in bone cells, including osteoclasts and osteoblasts. Like most other MDC proteins, the predicted meltrin beta protein consists of a signal sequence, prodomain, metalloprotease domain with a predicted catalytic site, disintegrin domain, cysteine
Mechanical stress to bone plays a critical role in maintaining bone mass and strength. However, the molecular mechanism of mechanical stress-induced bone formation is not fully understood. In the present study, we demonstrate that FosB and its spliced variant DeltaFosB, which is known to increase bone mass by stimulating bone formation in vivo, is rapidly induced by mechanical loading in mouse hind limb bone in vivo and by fluid shear stress (FSS) in mouse calvarial osteoblasts in vitro both at
Synapsins are neuronal phosphoproteins that coat synaptic vesicles and are believed to function in the regulation of neurotransmitter release. The signaling mechanism for short-chain free fatty acid (SCFA)-stimulated NE release was examined using primary-cultured mouse sympathetic cervical ganglion neurons. Pharmacological and knockdown experiments showed that activation of sympathetic neurons by SCFA propionate involves SCFA receptor GPR41 linking to G??-PLC?3-ERK1/2-synapsin 2 signaling. Furth
Palmitylcarnitine, an amphiphile that accumulates in and leaks from ischemic heart tissue, affected the fast sodium ion channel and the slow calcium channel in avian ventricular muscle. In the presence of 5.4 mM external potassium ion, palmitylcarnitine reduced the maximum rate of rise of the action potential and increased action potential duration at the plateau level without changing the resting potential. Steady state inactivation of the maximum rate of rise, an index of fast sodium ion curre
Open papers in the app to read, cite, and organize with AI.
