Answer:
the concentration of misfolded proteins would be higher than normal.
Explanation:
Chaperones proteins are required for the correct protein folding of proteins. These proteins were first discovered in bacteria. The level of chaperones is increased under thermic stress conditions, it is for that reason that they are also known as heat shock proteins (Hsp). For example, Hsp70 is a chaperon protein constitutively expressed under stress conditions that is involved in the folding of protein precursors and the refolding of misfolded proteins. In humans, Hsp70 is encoded by the HSPA1A gene, and its increased expression level is related to different health problems including neurodegenerative diseases, cerebral ischemia and epilepsy.
Thank you for posting your question here at brainly. I hope my answer here will help you. To answer the question, t<span>he membrane protein thermogenin disrupts the H+ gradient in fat cell mitochondria and this results in the release of heat.</span>
Answer:
1.The pleural cavity aids optimal functioning of the lugs during breathing. It transmits movements of the chest wall to the lungs, particularly during heavy breathing. The closely approved chest wall transmits pressures to the visceral pleural surface and hence to the lung (10-19.
2.The diaphragm, located below the lungs, is the major muscle of respiration. It is a large, dome-shaped muscle that contracts rhythmically and continually, and most of the time, involuntarily. Upon inhalation, the diaphragm contracts and flattens and the chest cavity enlarge.
Explanation:
The silica content affects the type of explosion in a volcano: explosive or quiet. depending on hte explosion the lava can take more time to harden. in that time the igneous rock can trap several things in the lava and those things can affect the color.
When looking at a Neuromuscular Junction (NMJ), we know that neurotransmitters (NT) are released from the presynaptic cell and they then bind to the receptors that are located on the postsynaptic cell - this causes the effect of the NT being released.
So we are told that NT are still being released, however they are not having an effect. This would mean that they are probably being blocked by something - in this case, it seems that the neurotoxin is the culprit in the blocking of these receptors.
Therefore, if the NT cannot bind to the receptors on the postsynaptic cell, they are not going to have any effect, no matter how much NT is being released.
So the answer in this case is: The neurotoxin is most likely C) Blocking the receptors on the postsynaptic cell.
