Search Results: Knockout gene technology (neuroscience)

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Figure 1.Conditional knockout can be produced using the cre-loxP system. The cre gene (white box) is controlled by a cell-type specific promoter or by a conditional promoter that can be turned on or off by the experimenter (top of figure). When and/or where the cre is expressed then controls recombination at the loxP sites (triangles, middle of figure), inserted purposely by the experimenter to flank an essential component of the gene to be knocked out. The result is a gene with a gap in it (bottom of figure) and, consequently, a functionless protein.

From update 'Knockout gene technology (neuroscience)'

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Figure 2.Signaling pathways controlling synaptic plasticity. The calcium-calmodulin-type II kinase (CaMKII) pathway is shown on the left. Calcium entering through NMDA receptors or voltage-gated ion channels (not shown) binds to calmodulin, which binds to CaMKII. CaMKII is a multimeric protein composed of two six-member rings (only one ring shown here). By autophosphorylating (circles) at the T286A site (see text), the enzyme becomes active in the absence of calcium/calmodulin and can phosphorylate substrates, including AMPA channels. The protein kinase A (PKA) pathway is shown on the right. Activation of a metabotropic receptor (which is not an ion channel and thus affects neurotransmission indirectly, for example, a glutamate receptor or perhaps a catecholamine receptor) causes adenyl cyclase activity to increase (ACI). The result is an increase in cyclic AMP (cAMP) and hence PKA activity. PKA is a four-member kinase composed of two regulatory domains (circles) and two catalytic domains (bars). Once activated, the kinase can phosphorylate substrates such as the AMPA channel.

From update 'Knockout gene technology (neuroscience)'