Hello. this is very simple. i know it and im in middle school. dont highschoolers know that you can just ask google and get a verified answer in just a few seconds?
sighs, well i guess older kids dont get technology as much as we do.
no offense, but seriously if you pay more attention in class you might not be asking this silly question right now.
Molecule which enzyme<span> acts on = the substrate. 5. Substrate molecule is held within the active site by bonds that temporarily form between certain amino acids of the active site and groups on the substrate molecule. ... This folds in a particular way = each </span>enzyme<span> has a </span>specific<span> tertiary </span>structure<span>.</span>
I'm not completely sure, but I'm fairly certain that the answer is B.
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.
