Answer:
There was no receptor for epinephrine to associate with and invigorate the sign transduction course that prompts the actuation of the compound
By and large, Earl Sutherland helped in translating and discovering the breakdown of the glycogen into glucose-1-phosphate in nearness of glycogen phosphorylase and this sign course pathway is activated by the epinephrine. The epinephrine doesn't have the correct receptor to discover and start the sign transduction process and thus glucose-1-phoshate isn't shaped. It requires CAMP which is again a second delivery person for starting the entire of the transduction procedure.
Answer:
In eukaryotes, the genome comprises several double-stranded, linear DNA molecules bound with proteins to form complexes called chromosomes
Y chromosome found in males which influence the degree of maleness
Answer:
Muscle contraction function.
Explanation:
The nerve endings possess synaptic acetylcholine vesicles ready to be released. The action potential depolarizes the presynaptic terminal and increases the concentration of axoplasmic calcium; Acetylcholine molecules are thus released, so that the concentration of the neurotransmitter at postsynaptic (nicotinic) receptors is temporarily increased. This is followed by post-synaptic membrane depolarization, muscle membrane action potential with increased rnioplasmic calcium concentration, and finally muscle contraction. Acetylcholine is hydrolyzed by acetylcholinesterase and resynaptic at the presynaptic level by cholinecetyltransferase. The etiopathogenesis of myasthenia gravis is autoimmune and there are antibodies against acetylcholine receptors that circulate in the blood, as well as a decrease in the number of receptors on the motor plates, that is, it is produced by the postsynaptic blockage of the myoneural plaque, that generates fatigue and localized or generalized muscle weakness that is characterized by the worsening of the contractile force of the muscle.
