Answer:
true
Explanation:
pa brainliest po please
<u><em>#carryonlearning</em></u>
Answer
Option C - Skeletal Muscles
Explanation
Antagonistic pairs are the muscles that are functionally opposite, if one produces flexion, then the other's primary action is an extension. Skeletal muscles work in pairs to move a bone so that the muscles can function properly. They contract the bone making nerves deliver a message to the brain. For example. Biceps and triceps. The lower arm is moved upwards when the biceps muscle contracts and the triceps muscle is relaxed and vice versa.
Answer: it’s distant objects shift in frequency toward red on the electromagnetic spectrum, which tells us objects are moving away from us!
Explanation: This is correct because I got this one right on my quiz and I took notes on it!
Answer:
skull tropper
Explanation:
I got it from the guy from fortnite
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.
