Advanced Search
Now showing items 1-4 of 4
Characterization of a multiprotein complex involved in excitation-transcription coupling of skeletal muscle
(Biomed Central, 2016)
skeletal primary cultures and adult fibers
[19, 20]. Our studies place extracellular ATP as a master
regulator of the E-T coupling leading to muscle plasticity
(as reviewed in [21]). We demonstrated that ATP is re-
leased by physiological activity...
[20]. We can conclude that the re- leased ATP and its metabolites are fundamental mediators between electrical stimulation, slow intracellular calcium transients, and gene expression related to muscle plasticity [19]. Taken all the previous work...
[20]. We can conclude that the re- leased ATP and its metabolites are fundamental mediators between electrical stimulation, slow intracellular calcium transients, and gene expression related to muscle plasticity [19]. Taken all the previous work...
An Inositol 1,4,5-Triphosphate (IP3)-IP3 Receptor Pathway Is Required for Insulin-Stimulated Glucose Transporter 4 Translocation and Glucose Uptake in Cardiomyocytes
(ENDOCRINE SOC, 2010-10)
� by itself triggers translocation/
fusion of GLUT4 with the plasma
membrane, the IP3R-dependent re-
lease participate in specific pathways
aimed to that purpose.
Finally, the involvement of �� sub-
units of a heterotrimeric G protein in
GLUT4 translocation...
that a link exists between IP3R-dependent Ca 2� re- lease and GLUT4 translocation, but this mechanism is particular for certain stimuli. In particular, the link between IP3R-dependent Ca 2� release andmobilizationofGLUT4 is a novel contribution...
that a link exists between IP3R-dependent Ca 2� re- lease and GLUT4 translocation, but this mechanism is particular for certain stimuli. In particular, the link between IP3R-dependent Ca 2� release andmobilizationofGLUT4 is a novel contribution...
Electrical Stimuli Release ATP to Increase GLUT4 Translocation and Glucose Uptake via PI3Kg-Akt-AS160 in Skeletal Muscle Cells
(American Diabetes Association, 2013)
ryanodine-sensitive stores, whereas the slow component is
Ca2+ released through inositol-1,4,5-trisphosphate receptor
(IP3R) (21,23) and depends on ATP concomitantly re-
leased from the stimulated cells (24). ATP signals in skel-
etal muscle through P2Y...
Glucose-Dependent Insulin Secretion in Pancreatic beta-Cell Islets from Male Rats Requires Ca2+ Release via ROS-Stimulated Ryanodine Receptors
(Public Library Science, 2015)
, where addition of exogenous
H2O2 promotes RyR redox modifications and specifically stimulates RyR-mediated Ca
2+ re-
lease [30, 59].
Additionally, we found that 100 μMH2O2 disrupted GSIS, confirming previous reports in
rat islets [29] and mouse...