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.
Not exact matches
Cunningham and her postdoc at the time, Christine Kirvan, found that the antibodies literally
bind to human neurons, activating an enzyme called calcium /
calmodulin - dependent protein (CaM) kinase II.
For starters, a key protein called
calmodulin, which helps spindles form, failed to
bind to the spindles properly.
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.
Instead, it inhibits proteins related to
calmodulin, an important calcium
binding protein.
The activated
calmodulin can then
bind to a specialized control lever inside calcium and sodium channels, which closes the channels.
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.
A pollen - specific
calmodulin -
binding protein, NPG1, interacts with putative pectate lyases.
Nucleotides and phosphorylation bi-directionally modulate Ca2 + /
calmodulin - dependent protein kinase II (CaMKII)
binding to the N - methyl - D - aspartate (NMDA) receptor subunit GluN2B.
Quantitative Measurement of Ca2 + and
Calmodulin - Target
Bindings by Fura - 2 and CFP / YFP FRET Imaging in Living Cells.