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.