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Secondary antibodies targeting multiple host’s IgG are conjugated to alkaline phosphatase. Keywords: Buffers, Cell biology, Enzyme-linked immunosorbent assay, Immunohistochemistry, Immunoprecipitation, Molecular biology, Peptide synthesis, Phosphorylations.
48) Order the steps leading to glycogen breakdown resulting from the stimulation of liver cells by glucagon. 1) Activation of protein kinase A (PKA) 2) cAMP levels rise 3) Phosphorylation.
Binding of growth factors to the extracellular domain results in multimerization and trans-autophosphorylation on Tyr residues and consequent activation of the catalytic domain. Often cytosolic proteins with Src-homology 2 ([[SH2]]) domains or phosphotyrosine binding ([[PTB]]) domains bind to the autophosphorylation sites of the activated receptors. The [[SH2]]- and [[PTB]]-containing proteins may be enzymes such as phosphoinositide 3-kinase ([[PI3K]]) or phospholipase C-gamma, or they may be adaptor proteins such as Shc, IRS1, [[Grb2]] or GAB1 that recruit other enzymes involved in signal transduction.
Even though the direct activation of IRF7 through TLR7 has been demonstrated in pDC, the direct activation of other transcription factors has not been documented. Figure 5 shows a transcription network which illustrates interactions between the TLR7 signaling pathway components and transcription factors known to be activated by the TLR7 pathway in other cell types including IRF7, NFkB, IRF5, and c-Jun. The network includes protein-protein binding interactions, protein phosphorylation.
Ango et al.  suggested that Homer-3 prevents the so-called agonist (glutamate)-independent, constitutive activity specifically observed with isoform a of the mGluR1 receptor . In the cerebellum, Homer-3 co-immunoprecipitates with structurally highly related Homer-1b , which influences translocation of the mGluRs from the ER to the plasma membrane, as well as with mGluR1 and ITPR1 . Homer-3 may be regulated to some extent by the immediate-early gene product Homer-1a, its direct competitor on mGluR1a, which disrupts its binding to that receptor . The coupling function of Homer-3 and thus the postsynaptic molecular architecture in response to synaptic activity in PCs has been proposed to be regulated by calcium/calmodulin-dependent protein kinase II (CaMKII)-mediated phosphorylation.