To cut a long story short, and to explain quickly the role of the sodium
channel, let's just say that it is like a door in the membrane of the nerve
cells, which allows sodium ions to enter the cell in certain circumstances.
The diagram on the right is an animation showing an hypothesis on the functioning of the channel. It is a model.
Ions do not go through lipidic membranes, therefore the main feature of our channel is that it will have the shape of a funnel, or tunnel. Because the funnel must be closed most of the time, it will have a gate. And because it needs to be opened sometimes, there will be a device in this protein to tell if the channel should be open or closed. The channel will only let sodium ions in, and not potassium or hydrogen ions. The gate is specially designed to act as a filter for the desired ion.
Such a complex protein has several subunits. They are called , 1 and 2. is the biggest and most important unit. It is also the most studied. Usually, the bond between the subunits is weak. Some other non-protein elements are linked to the channel. Some chains of sugar residues (in pink) are attached to the external part of the protein, and can be phosphorylated.
We know most about the subunit. It is quite a big unit, 200kDa (Da = Dalton). This subunit is composed of four groups of six helices, arranged to form a pore in the membrane that the NA+ passes through. The precise way the protein is arranged is not well known, but chemical and sequence data can give us an idea.
A characteristic of the subunit is the abundance of helices in its structure. This is the main feature of the molecule. There are no - pleated sheets.
The subunit is coded for by a 6000 nucleotides long mRNA. The gene is 60, 000 bp long, which is ten times the size of the mRNA. So in the case of the sodium channel, 90% of the sequence of the gene is not coding.
The sodium channel is a highly specialised protein. Mutations in the genes of the sodium channel will affect the primary structure. In some cases, changes in the primary structure will affect the secondary, the tertiary, and the quaternary structure. Some mutations in the genes can be lethal, while some will affect only a small aspect of the function of the gene. For example, it has now been shown that some mutations in the genes of the sodium channel account for the resistance of some insects to insecticides. In humans, mutations in the sodium channel genes are responsible for some forms of myopathies.