Compared and contrast intracellular signaling by receptor tyrosine kinase and G-

Question

Compared and contrast intracellular signaling by receptor tyrosine kinase and G- protein receptor. Discuss how these receptors are activated respectively and name at least 2 downstream targets for each kind of receptor. Also name one example for each kind of receptor of a physiological process is activated via these receptor. (10 pts) Discuss the role of calcium in the contraction of striated skeletal muscle contraction and smooth muscle. Clearly discuss how Ca2 release is triggered and the effects of the Ca2+ inside the cell in each case. Also discuss why sometimes a person may experience some involuntary "twitching" of skeletal muscle after consuming large amounts of caffeinated drinks (10 pts).

Explanation / Answer

Part-1

Receptor tyrosine kinase & G-protein receptor

Activation Method: -

G protein-coupled receptors play many different roles in the human body, and disruption of GPCR signaling can cause disease. In Tyrosine Kinase, a selection of proteins comprises those domains, and while any such proteins bind, it is able to initiate a downstream signaling cascade that leads to a cellular reaction.

Part-2

Calcium and its role in Muscle Contraction

Action potential that travels down the motor neuron and reaches neuron terminal causes the release of calcium from the sarcoplasmic reticulum. this released calcium will screen binding sites on actin, consequently exposing them and making ready to bind with myosin. myosin heads then bind to the binding sites on actin. this binding lets in actin to be pushed inwards, closer to the middle of the sarcomere, causing shortening of the sarcomere and consequently muscle contraction.

      Ca2+ triggering: -

Smooth muscle contraction is activated by phosphorylation of the 20-kDa light chains of myosin catalyzed by Ca2+/calmodulin (CaM)-dependent myosin light chain kinase (MLCK). The mechanism of activation of smooth muscle contraction is fundamentally different from that of skeletal and cardiac (striated) muscles, although both are triggered by an increase in cytosolic free Ca2+ concentration [Ca2+]. In striated muscles, Ca2+binds to troponin C, inducing a conformational change in proteins of the contractile machinery, ultimately enabling actin-myosin interaction and cross-bridge cycling. Smooth muscle cells do not express troponin. Instead, Ca2+binds to CaM, a homolog of troponin C.

      Caffeine and Muscle twitching: -

caffeine causes a dose-dependent increase in force of contraction and duration of contraction of skeletal muscle by causing increased release of calcium ions from the sarcoplasmic reticulum through a physical coupling and conformational changes in the voltage sensitive di-hydro pyridine receptor.

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