Answer: depolarization; hyperpolarization
Explanation:
At resting potential (absence of stimulus), the cell membrane of a neuron is said to be polarized with a net negative charge within due to more potassium (K+) ions present than sodium (Na+) ions.
However, an impressed stimuli reverses the ions content as K+ ions flows out and quickly replaced by Na+ ions, resulting in a decrease in membrane potential and a more positive cell membrane. Thus, depolarization occurs.
An increase in the membrane potential (so that it becomes more negative) is called hyperpolarization.
Answer:
The prolonged electrical depolarization of cardiac muscle cells -that occurs during contraction- is due primarily to the persistent influx of calcium ion
Explanation:
The action potential of the heart muscle is longer with respect to skeletal muscle (around 300 milliseconds), and this is due to the activity of calcium (Ca⁺⁺ ) in the intracellular compartment.
The initial depolarization of cardiac muscle fiber depends on the entry of sodium (Na⁺) into the cell. However, for the action potential to occur and be maintained, Ca⁺⁺ must increase its cytoplasmic levels, which depends on:
- The increase in intracellular sodium induces the release of Ca⁺⁺ from the sarcoplasmic reticulum.
- Calcium entry from the extracellular space through the voltage dependent Ca⁺⁺ channels.
- The entry of extracellular Ca⁺⁺ causes the release of more Ca⁺⁺ ions by the sarcoplasmic reticulum, further increasing its intracellular concentration.
This is how the ion that guarantees the duration of the action potential of the cardiac muscle cell is the Ca⁺⁺.
Learn more:
Calcium, sodium and cardiac muscle cells brainly.com/question/4473795
Answer:
PFFT this might help? sorry if not mate
Explanation:
Cell cycle checkpoint controls play a major role in preventing the development of cancer [see Sherr, 1994, for a more detailed discussion]. Major checkpoints occur at the G1 to S phase transition and at the G2 to M phase transitions. Cancer is a genetic disease that arises from defects in growth-promoting oncogenes and growth-suppressing tumor suppressor genes. The p53 tumor suppressor protein plays a role in both the G1/S phase and G2/M phase checkpoints. The mechanism for this activity at the G1/S phase checkpoint is well understood, but its mechanism of action at the G2/M phase checkpoint remains to be elucidated. The p53 protein is thought to prevent chromosomal replication specifically during the cell cycle if DNA damage is present. In addition, p53 can induce a type of programmed cell death, or apoptosis, under certain circumstances. The general goal of p53 appears to be the prevention of cell propagation if mutations are present. The p53 protein acts as a transcription factor by binding to certain specific genes and regulating their expression. One of these, WAF1 or Cip1, is activated by p53 and is an essential downstream mediator of p53-dependent G1/S phase checkpoint control. The function of p53 can be suppressed by another gene, MDM2, which is overexpressed in certain tumorigenic mouse cells and binds to p53 protein, thus inhibiting its transcriptional activation function. Other cellular proteins have been found to bind to p53, but the significance of the associations is not completely understood in all cases. The large number of human cancers in which the p53 gene is altered makes this gene a good candidate for cancer screening approaches.
