Answer:
- GLYCOLYSIS :- Glycolysis is the metabolic pathway that converts glucose C₆H₁₂O₆, into pyruvic acid, CH₃COCOOH. The free energy released in this process is used to form the high-energy molecules adenosine triphosphate and reduced nicotinamide adenine dinucleotide
- PRODUCTS :- Glycolysis produces 2 ATP, 2 NADH, and 2 pyruvate molecules: Glycolysis, or the aerobic catabolic breakdown of glucose, produces energy in the form of ATP, NADH, and pyruvate, which itself enters the citric acid cycle to produce more energy.
- INPUT:- Glycolysis is the first step in cellular respiration, occurring in all living cells. Overall, the input for glycolysis is one glucose, two ATP and two NAD+ molecules giving rise to two pyruvate molecules, four ATP and two NADH.
- BREAKDOWN:- During glycolysis, glucose ultimately breaks down into pyruvate and energy; a total of 2 ATP is derived in the process (Glucose + 2 NAD+ + 2 ADP + 2 Pi --> 2 Pyruvate + 2 NADH + 2 H+ + 2 ATP + 2 H2O). The hydroxyl groups allow for phosphorylation. The specific form of glucose used in glycolysis is glucose 6-phosphate
- STAGES:-
- Reaction 1: glucose phosphorylation to glucose 6-phosphate.
- Reaction 2: isomerization of glucose 6-phosphate to fructose 6-phosphate
- Reaction 3: phosphorylation of fructose 6-phosphate to fructose 1,6-bisphosphate
- Reaction 4: cleavage of fructose 1,6-bisphosphate into two three-carbon fragments.
Explanation:
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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.
A. Become cancer because in the process of mitosis (cell replication) idlf the cell replication does not work properly and keep going on and on it will begin creating mutations to help it replicate causing cancer to happen.
Ex: let's say you have a paper cut. Your blood cells must replicate in order to close that gap in your body. They begin replication but if they get out of control and begin creating mutations it will turn into cancer.