Answer:
Starch: Carbohydrate
Polysaccharide: Carbohydrate
Cholesterol: Lipid
Phospholipid: Lipid
Glycerol: Lipid
Glycogen: Carbohydrate
Monosaccharide: Carbohydrate
Nucleotide: Nucleic Acid
Cellulose: Carbohydrate
RNA: Nucleic Acid
Amino Acid: Protein
Polypeptide chain: Protein
Enzyme: Protein
Glucose: Carbohydrate
Saturated Fat: Lipid
Unsaturated Fatty Acid: Lipid
DNA: Nucleic Acid
<em>(I am unsure for</em><em> </em><em>Polypeptide chain</em>, <em>Saturated Fat, and Unsaturated Fatty Acid)</em>
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<u><em>Hope this helps!</em></u>
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<em>-Isa</em>
Answer:
. A euglena survives on its own because it completes all life functions. A white blood cell cannot survive on its own because it is just one cell.
Explanation:
. A euglena survives on its own because it completes all life functions. A white blood cell cannot survive on its own because it is just one cell because A Euglena is a unicellular organism that can perform photosynthesis and complete cell activities. They live in fresh water, have eyespot, can excrete and have flagella for movement which are cellular activities
But a white blood cell cannot survive because it is one cell because it is produce from bone marrow and is a part of the immune system and work with other networks in the body system to fight against body infections.
Answer: Read explanation
Explanation: there’s actually no similarity at all. A cell membrane is made of phospholipids, globular proteins, glycolipids, glycoproteins, and cholesterol, and has passages that serve explicitly for passive and active transport of materials through it.
The skin is made of cells and dead keratin and serves as much as possible to prevent most substances from moving through it. It’s “designed” for toughness and distensibility, not for selective permeability.
All in all, the difference is that a cell membrane is explicitly and only for the passing and transport of materials through it, and the skin in the skin is made to be tough and durable, almost the opposite of a cell membrane.
The correct answer is the last statement.
If the regulatory serine is mutated to alanine, then acetyl-CoA carboxylase will get activated spontaneously and will produce malonyl-CoA. The increased concentrations of malonyl-CoA will obstruct the oxidation of fatty acids by preventing the entry of fatty acids into the mitochondria.
It is because the AMP-activated protein kinase phosphorylates the serine residues of acetyl-CoA carboxylase to inactivate it. If a mutation occurs in such residues, then the AMPL cannot phosphorylate acetyl-CoA carboxylase and this enzyme will get activated spontaneously.
In such a situation, there will be more than sufficient production of malonyl-CoA, which will inhibit the admittance of more fatty acid getting inside the mitochondria; this will indirectly prevent the oxidation of fatty acids.
