<h2>GPCRs and RTKs</h2>
Explanation:
1) Phosphorylation of receptor can terminate signal or desensitize receptor: GPCRs because when signal persists a protein kinase receptor is activated,this further catalyse the phosphorylation of several serine residue at cytosolic phase of 7 transmembrane
Phosphorylated transmembrane recognized by arrestin protein blocks interaction between trimeric G protein and receptor thus blocks signal transduction
2) Autophosphorylation of receptor can initiate signal: RTKs because receptor dimerization activates intrinsic tyrosine kinase activity by which they phosphorylate its own tyrosine residue on cytosolic phase
3) Structure contains seven transmembrane helices: GPCRs because it consists of single polypeptide and spans the membrane 7 times hence called 7 transmembrane;it recognizes external signal and activates trimeric G protein
4) Ligand binding induces conformational change in receptor: RTKs because normally RTK exist in monomeric form in absence of any ligand molecule but when any ligand molecule binds receptor starts to dimerize
5) Receptor activation causes phosphorylation of its cytosolic subunits: RTKs because when receptor gets activates the intrinsic tyrosine kinase activity by which they phosphorylate its cytosolic subunits
6) An example is the insulin receptor: Insulin receptor is present on plasma membrane and belongs to RTK family and always exist in dimeric form
7) Transports some ligands through the membrane: Neither GPCR nor RTK;ligand gets transported through the membrane through ligand gated channel
8) An example is the epinephrine receptor: Epinephrine is an endocrine hormone produced by adrenal glands in stress condition and prepare body for fight and flight;Epinephrine uses GPCR signalling pathway by four different types of membrane receptors in different tissues
9) Activate heterotrimeric G proteins directly: Transmembrane protein of GPCR recognizes the external signal and activates G protein,activated G protein binds with effector enzyme and activate it which further produce or destroy secondary messenger that carry message from cell surface to cell interior
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