«The two forms
of calmodulin are both powerful, each imposing opposing actions that together maintain exquisite control, akin to the «yin - yang» balance in Chinese philosophy,» Yue says.
Not exact matches
Protein immunoblot and histochemical analysis with antiserum to type I NO synthase suggest that the formation
of NO in pancreatic B cells is catalyzed by an NADPH -(reduced form
of nicotinamide adenine dinucleotide phosphate), Ca2 + /
calmodulin - dependent type I NO synthase
of about 150 kilodaltons.
They found that, as with calcium channels, increasing calcium concentrations caused
calmodulin to bind within the resemblance element
of sodium channels and prevent their opening, just as in calcium channels.
Calmodulin (CaM) is a major effector for the intracellular actions
of Ca2 + in nearly all cell types.
The new study revises this viewpoint by devising ways to deliver surges
of calcium - free
calmodulin to channels.
In so doing, «it can be seen that calcium - free
calmodulin is in no way dormant, but instead markedly boosts the opening
of calcium and sodium channels to begin with,» Yue says.
In the current model, explains David Yue, M.D., Ph.D., a professor
of biomedical engineering and neuroscience at the Johns Hopkins University School
of Medicine,
calmodulin can do little until it binds to calcium, which changes its shape and snaps it into action.
In the course
of screening over 180 mutant mouse strains with a systematic battery
of behavioral tests, Dr. Tsuyoshi Miyakawa and his colleagues found that mice with heterozygous knockout
of the alpha - isoform
of calcium /
calmodulin - dependent protein kinase II (αCaMKII) exhibit behavioral deficits and other brain features consistent with bipolar disorder.
Among the most interesting ones identified were those associated with 1) the large category
of transport, and the more specific categories
of carbohydrate transport and cation: amino acid symport; 2) several related to calcium, including calcium ion binding,
calmodulin binding, and voltage gated calcium channel activity; 3) DNA damage response and signal transduction; 4) response to oxidative stress; and 5) oxygen and reactive oxygen species metabolism.
Now, Dong et al. have investigated the consequences
of Dab2 downregulation in a new STEM CELLS Translational Medicine study, demonstrating a novel role for calcium /
calmodulin - dependent protein kinase kinase - 1 (CAMKK1) in the modulation
of MSC secreted factors and a potential exciting means to enhance MSC - based cardiac repair [2].
Inactivation
of the myocyte enhancer factor - 2 repressor histone deacetylase - 5 by endogenous ca2 / /
calmodulin - dependent kinase ii promotes depolarization - mediated cerebellar granule neuron survival.
Quantitative Measurement
of Ca2 + and
Calmodulin - Target Bindings by Fura - 2 and CFP / YFP FRET Imaging in Living Cells.
Molecular interaction and functional regulation
of ClC - 3 by Ca2 + /
calmodulin - dependent protein kinase II (CaMKII) in human malignant glioma.
Neuron 2013) show that increase in intracellular calcium [Ca2 +] i induced by NMDA receptor activation or membrane depolarization strongly activates AMPK through activatoin
of Calcium /
Calmodulin - Activated Kinase Kinase 2 (CAMKK2).
NSP2 functions downstream
of Nod - factor - induced calcium spiking and a calcium /
calmodulin - dependent protein kinase.
Once the cell reaches its destination — the site
of inflammation — the
calmodulin protein enters the equation to shed the L - selectin protein, allowing it to enter the inflamed tissue.