Zobrazeno 1 - 10
of 24
pro vyhledávání: '"Nikolai Otmakhov"'
Publikováno v:
Frontiers in Neural Circuits, Vol 12 (2018)
Externí odkaz:
https://doaj.org/article/02b8ac629cb043fa9f6cbed9ccaf980a
Publikováno v:
PLoS ONE, Vol 10, Iss 6, p e0130457 (2015)
Because CaMKII is the critical Ca(2+) sensor that triggers long-term potentiation (LTP), understanding its activation and deactivation is important. A major advance has been the development of a FRET indicator of the conformational state of CaMKII ca
Externí odkaz:
https://doaj.org/article/e5e468eeee1645e5aa52d7410bc90d3c
Publikováno v:
PLoS ONE, Vol 10, Iss 3, p e0120881 (2015)
Over-activation of excitatory NMDA receptors and the resulting Ca2+ overload is the main cause of neuronal toxicity during stroke. CaMKII becomes misregulated during such events. Biochemical studies show either a dramatic loss of CaMKII activity or i
Externí odkaz:
https://doaj.org/article/1a95d161e13f44d2bbbb7555a0014ba9
Publikováno v:
Frontiers in Neural Circuits, Vol 12 (2018)
Frontiers in Neural Circuits
Frontiers in Neural Circuits
Autor:
Nikolai Otmakhov, John E. Lisman
Publikováno v:
Journal of Neuroscience Methods. 203:106-114
Here, we present a method for measuring the concentration of endogenous protein in cellular compartments. Importantly, the method is applicable to compartments such as dendritic spines with dimensions often close to the resolution limit of optical mi
Autor:
John E. Lisman, Farida El Gaamouch, Paul De Koninck, David Lemelin, Hyun Jae Pi, Nikolai Otmakhov
Publikováno v:
Proceedings of the National Academy of Sciences. 107:14437-14442
CaMKII is an abundant synaptic protein strongly implicated in plasticity. Overexpression of autonomous (T286D) CaMKII in CA1 hippocampal cells enhances synaptic strength if T305/T306 sites are not phosphorylated, but decreases synaptic strength if th
Autor:
Shaurav Regmi, Andy Hudmon, John E. Lisman, Ryohei Yasuda, Elena V. Gorbacheva, Nikolai Otmakhov
Publikováno v:
PLoS ONE, Vol 10, Iss 3, p e0120881 (2015)
PLoS ONE
PLoS ONE
Over-activation of excitatory NMDA receptors and the resulting Ca2+ overload is the main cause of neuronal toxicity during stroke. CaMKII becomes misregulated during such events. Biochemical studies show either a dramatic loss of CaMKII activity or i
Autor:
Ayse Dosemeci, Brent Asrican, Jung-Hwa Tao-Cheng, Thomas S. Reese, Stephen M. Carpenter, Nikolai Otmakhov, John E. Lisman
Publikováno v:
The Journal of Neuroscience. 24:9324-9331
Calcium/calmodulin-dependent protein kinase II (CaMKII) is a leading candidate for a synaptic memory molecule because it is persistently activated after long-term potentiation (LTP) induction and because mutations that block this persistent activity
Publikováno v:
Proceedings of the National Academy of Sciences. 91:8170-8174
Fura-2 and imaging technology were used to detect intracellular Ca2+ changes in CA1 pyramidal cells in hippocampal slices. During focal synaptic stimulation, one or more highly localized regions of Ca2+ elevation (hot spots) were detected in the dend
Autor:
Magdalena Sanhueza, P. Zhang, Ivar S. Stein, K. U. Bayer, G. Fernandez-Villalobos, John E. Lisman, Gyulnara G. Kasumova, Nikolai Otmakhov, Johannes W. Hell
Publikováno v:
JOURNAL OF NEUROSCIENCE
Artículos CONICYT
CONICYT Chile
instacron:CONICYT
Artículos CONICYT
CONICYT Chile
instacron:CONICYT
During long-term potentiation (LTP), synapses undergo stable changes in synaptic strength. The molecular memory processes that maintain strength have not been identified. One hypothesis is that the complex formed by the Ca(2+)/calmodulin-dependent pr