Useful Materials for Chapter 9

Click here to see a useful animation on signal amplification. It explains how signal transduction pathways, while they may seem unnecessarily complex, amplify a cell's response to a single signal molecule. If each signal only caused a reaction in one particular protein, for example, this would not be a very effective response. This animation uses the hormone epinephrine as an example. Although it only activates a single molecule of adenylyl cyclase, the cellular response is amplified through the pathway. I suggest keeping an eye on amplification count on the right of the screen while moving through the animation.

This video walks you through the fight-or-flight response of the body. I found it useful for making a real-life connection involving the three-stage process of the cells' response to signal molecules. It also included some extra information on the role of nerve signals in the process. I enjoyed the graphics in this video, as they zoomed in and out of the cells and display exactly how the response takes place.

Also, if you are looking for an online flashcard site, I suggest studyblue.com. It's really simple to use and I may share some flashcards that I create on there in the future.

Cancer-Causing Bacteria Induces Apoptosis

Barry Marshall discovered that stomach ulcers are caused by bacteria after he drank a petri-dish containing Helicobacter pylori, a bacteria. He subsequently developed gastritis as a result, then cleared this through the use of antibiotics. The discovery that stomach ulcers could be treated with antibiotics was significant for the medical community as they could lead to stomach cancer and duodenal ulcers.

Helicobacter pylori Micrograph

Researchers have recently identified a bacterial toxin, called vacuolating cytotoxin A or VacA, that plays a role in apoptosis. Apoptosis is a process of programmed cell death. VacA had previously been shown to cause cell death, which is important to the development of gastric cancers. Instead of attacking the cells lining the stomach, Helicobacter pylori causes the cells to undergo apoptosis. Too little or too much apoptosis can lead to several conditions, such as neurodegenerative diseases, cancers, and autoimmune disorders. Apoptosis can occur naturally for several reasons such as well cell population needs to be regulated or as a defense mechanism. Cell death can also be induced due to damage in the cell caused by disease or noxious substances.


VacA is a product of Helicobacter pylori. In order apoptosis to occur, the mitochondria are targeted by VacA, since these parts of the cell are responsible for energy production. VacA makes the outer membrane of the mitochondria permeable,disrupting its electron gradient. This electron gradient is needed for oxidative phosphorylation during cellular respiration. Thus, the mitochondria is unable to produce adequate amounts of usable energy for the cell. In addition, VacA disrupts the structure of mitochondria by preventing them from forming a network and effectively isolating them. Since having functioning mitochondria is essential to cell life, the VacA results in the cell killing itself through apoptosis. Through these mechanisms, Helicobacter pylori causes cell death of stomach cells in small areas, which can then results in gastric cancer and, in less severe cases, peptic ulcers.


Click here to access the article on the cancer-causing bacteria and here to access the article that I got my general information on apoptosis from.

Drug Discovery Opportunities through Allosteric Modulators of G Protein-Coupled Receptors

This article is about the new opportunities for drugs to be discovered through the identification of allosteric ligands. These have generally not been the main focus of GPCR, or G-Protein Couple Receptors. GPCR are located in cell membrane surfaces and respond to a variety of extracellular signaling. They have been investigated for the discovery of several drugs that moderate specific GPCRs. When GPCRs are stimulated by the proper ligand, intracellular signal transduction is initiated. Activation of  β-arrestin pathways and activation of G-proteins are the two mechanisms of signal transduction. The binding of the lingand stabilizes the receptor, allowing it's C-terminal domain to interact with protein complex and its Gα portion to hydrolyse GTP and interact with adenylate cyclase and/or phospholipase C. The receptor is phosphorylated when it reacts with G-protein-coupled receptor kinases and is able to bind β-arrestins. This prevents more G-protein signaling from occurring and also begins a series of intracellular events that are independent from G-proteins.

GPCRs have been pharmacological targets. However, only certain classes of GPCRs are able to be targeted with drugs. The article is proposing that idenitfying allosteric ligands that bind to different sites other than the orthosteric site will provide new opportunities for drugs to be produced. Allosteric modulators allow for enhanced saturability as well as selectivity. Because they cause conformational changes in their receptors, allosteric modulators can alter affinity and capability. Therfore, allosteric modulators can impact how receptors relate and respond to their binding partners, producing selective responses. The article then describes different techniques that can be used to identify allosteric modulators.

For more information, click here to access the article that I got my information from.

Useful Materials for Chapter 7

So cellular respiration can seem complicated, but I have found that animations can help you to understand the various steps of it. You can click here to get a very quick visual of the entire process. I liked this animation because it gives you a quick idea of how the energy intermediates as well as waste products are produced. I also like how it keeps track of the carbon molecules of the glucose. However, I also wanted to look at something that was more detailed. Click here for a link to a much more detailed cellular respiration animation. This one kept track of all the energy intermediates produced during the various steps, counting them up as the animation proceeds. It didn't confuse me with all the names of the complexes in the electron transport chain. Instead, it just labeled them "Complex I", "Complex 2", and so on, also indicating how the electrons move due to how strong an electron acceptor each complex was. There is another part aftewards that includes all the names of the complexes in the chain, if you wish to know them. There are also several "pop-up questions" that test your understanding of the material presented in the animation.

Once you think you know respiration pretty well, you can click here to take a self-test! I know, I know, tests in school are enough, but this could help prepare you for the rapidly approaching bio exam, so why not? This test was useful because it is graded online, which can help you target which topics you may need to study more. You should try this link as well, and click on "begin problem set" on the bottom of the page. It includes helpful tutorials for questions that you don't know the answers to. Not all the questions pertain to this chapter, so just skip those. With that, have fun studying!

Salmonella Uses Human Intestines to Foster Growth

The bacteria Salmonella enterica, which is a common cause of food poisoning, takes advantage of the body's immune response to enhance its production of energy. Bacteria have to produce energy in order to survive, either by respiration or fermentation. However, oxygen is sparse in human intestines, so bacteria use fermentation in order to survive. Respiration is much more energy efficient than fermentation is, producing a higher number of ATP.

When Salmonella is injested, it invades the intestine's surface, causing the immune system to produce oxygen radicals that kill of the bacteria. Some bacteria are killed by this process, but many others benefit from a sulfur compound that the oxygen radicals create. This sulfur compound is called tetrathionate, which Salmonella can use instead of oxygen to carry out respiration. As we learned in class, oxygen is needed to act as the final electron recpetor in the elctron transport chain. Tetrathionate acts as the final electron acceptor for Salmonella, which is what allows it to produce energy through respiration rather than the less energetically productive process of fermentation. Tetrathionate had previously been by researchers to promote Salmonella growth in samples, but it was throught that this sulfur compound was not found in living human beings. Stimulating the immune response gives Salmonella an advantage, as it allows them to carry out respiration and thus produce more energy than the other bacteria in the intestine. When this response is stimulated, it also allows Salmonella to spread to other hosts, as the body induces diarrhea and vomiting in an attempt to rid itself of this bacteria.

The symptoms of Salmonella infection include vomiting, fever, abdominal cramps, and diarrhea. While most people recover quickly, it can be fatal in people with suppressed immune systems. Antibiotic treatment is ineffective, as it also ihibits the growth of beneficial bacteria in the body. Researchers are hopeful that targeting sulfur compounds will help stop the bacteria from establishing itself in the intestine.

You can click here for the article that I got my information from or you can click here for a shorter article that basically talks about the same thing.

Approved Drugs that Shift Cellular Energy Metabolism toward Glycolysis Identified

This article discusses the discovery of several drugs that affect cellular energy metabolism in animals. Changes in energy production pathways in cells can occur naturally, such as in development or in response to energetically demanding activities, but can also occur due to disease. The goal of the team that discovered these drugs was to identify compounds that can induce this shift in a safe manner, and research how the therapeutic value of this shift. Cancer cells produce energy predominantly through glycolysis, so a mechanism that would switch energy production from this may suppress tumor growth.

Previous studies show that mitochondrial respiration could mimic ischemic preconditioning. This is when there is a brief decrease in blood supply to a tissue, which can protect it from future damage if blood supplies are completely cut off. A new screening strategy was created by the team, in which there were two environments: one that had glucose (glycolysis and respiration), and another that had galactose (respiration). A drug that would be able to redirect metabolism from respiration to glycolysis would would stop the growth of cells in the galactose while it would have minimal effect on the cells in the glucose. Several drugs were identified to cause a shift in energy metabolism, including anticancer drugs that inhibit rapidly proliferating cell growth.

Most drugs that mimic ischemic preconditioning are too toxic for human cells, but the researchers were able to identify eight drugs that produced a less intense, but significant, shift from respiration to glycolysis. One of these drugs was meclizine, which is an over-the-counter drug that is used for treating nausea and vertigo. This drug was tested on and it was discovered that pretreatment with meclizine reduced ischemic damage in cardiac cell in the case of a heart attack. It also reduced damage to brain cells when tested on a stroke model. A lot of testing is still needed before this type of drug can be used on human cases.

Click here to see the article that I got my information from.

Autophagy: Finding the Line Between Normal and Diseased

Autophagy is when a cell gets rid of intracellular components, such as organelles and proteins. The inability of autophagosomes to do work can lead to several diseases, including cancer, inflammatory diseases, and neurodegeneration. Autophagosomes are membrane-bound organelles that transport cellular components to lysosomes, fusing to become autolysosomes. Enzymes in the autolysosome then degrade the enveloped material, converting it to basic materials that can be reused in the cell.

As more research has been conducted on autophagy, it has been observed that there are several links between autophagy and human diseases. Some autophagic proteins, such as beclin-1, have tumor suppressing properties. Mice that lack the Beclin-1autophagy protein have shown more formation of tumors than those who have Beclin-1. Mutations in the genes of autophagosomes can lead to the accumulation of damaged DNA as well as genome instability. Observing autophagic pathways can be tricky because it can be difficult to distinguish them from normal pathways.

Autophagosomes are biologically important molecules because they function in homeostatic processes. These homeostatic mechanisms include helping the cell signal its homeostatic condition to the outside environment and modifying the cell's metabolic state to more effectively counter harmful external stimuli. Their activity is regulated by external conditions, such as nutrients and stress, and mTOR, which supervises cell signaling pathways involved in cellular metabolism. Researchers are looking to determine what function autophagosomes have on developmental processes in the hopes of producing disease therapies through their research. For more information, click here to access my article.