Answer: <em>The reaction is an example of a metathesis reaction, which involves the exchange of ions between the Pb(NO3)2 and KI. The Pb+2 ends up going after the I- resulting in the formation of PbI2, and the K+ ends up combining with the NO3- forming KNO3.</em>
Explanation:
Answer:d.are eventually replaced by electrons from photosytem 11
Explanation:there are two photosystems in the photosynthetic process.PSI and PS II. PS I has a reaction center called P700 because it's chlorophyll has a maximum absorption of 700nm wavelength.PSII has a reaction center called P680nm for similar reason.when an excited electron is transferred to P700,it becomes excited.this electron is passed down from from acceptor to another, until it is used to reduce NADP+ to NADPH.this electron is replaced when P680 gets excited by a photo of light and splits water to release electrons , protons and Oxygen
They are plants without a vascular system
<span>less nutrient rich than the A horizon</span>
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.
