An organism reacts to changes in its environment. this is called Behavior
Answer:
The fact that it reveals is that:
Epinephrine binds to the receptor tyrosine kinase on the cell membrane and does not act on glycogen phosphorylase.
Explanation:
In cellular respiration, epinephrine is a neurotransmitter and a plasma membrane hormone receptor. It is not a lipid-derived hormone, but rather an amino acid-derived hormone. As a result, they are unable to pass through the plasma membrane of cells. They bind to receptors on the outer surface of the plasma membrane through plasma membrane hormone receptors (receptor's tyrosine kinase of the cell membrane) because they are lipid insoluble hormones.
Unlike steroid hormones, lipid insoluble hormones (epinephrine) do not directly influence glycogen phosphorylase or the target cell because they cannot enter the cell and operate directly on DNA. The activation of a signaling pathway occurs when these hormones attach to a cell surface receptor; this activates intracellular activity and performs the hormone's specific effects. Nothing crosses through the cell membrane in this fashion; the hormone that binds at the cell's surface stays at the cell's surface, while the intracellular component stays within the cell.
I believe the answer is A
C. Are vascular is the answer
<h2>CRISPR/Cas9</h2>
Explanation:
CRISPR can be used to reintroduce dystrophin back into the KO mouse
- CRISPR stands for Clustered Regularly Interspaced Short Palindromic Repeats and is used to for gene editing
- CRISPR/Cas-mediated genome editing has been shown to permanently correct DMD mutations and restore dystrophin function in mouse models
- Germline editing by injecting zygotes with CRISPR/Cas9 editing component was first done in mdx mice by correcting the mutated exon 23
- Postnatal editing of mdx mice was then achieved using recombinant adeno-associated virus to deliver CRISPR/Cas9 genome editing components and correct the dystrophin gene by skipping or deleting the mutated exon 23 in vivo
- Germline and postnatal CRISPR/Cas9 editing approaches both successfully restored dystrophin function in the mice and same technique can be used for KO mouse model
