The interesting thing about ligand-receptor interactions is the sheer number of different ligands and corresponding receptors. Each cell type has different receptors attached to its membrane and thus, many different ligands that can bind it. Each ligand-receptor complex sets in motion a series of chemical reactions in order to fulfill its specific role in the cell. A good example of this epinephrine (adrenaline) because it can interact with many different cell types and correspondingly receptors, but have much different effects from cell to cell.
This is really cool, but I'm not sure I totally understand the concept. Does the biofilm encompass multiple bacterial cells? Perhaps if each bacterial cell is producing the material necessary for the biofilm, this acts as a form of quorum sensing and results in the local bacteria to begin production.
So when this specific type kinase receives the phosphate group addition, it becomes capable of catalyzing reactions. So as I understand, they are like enzymes that need an external energy source in the form of a phosphate group.
This fact highlights the importance of G-protein coupled receptors in the cell. Because G-protein coupled receptors are so critical in cell signaling, this makes sense. In addition, cellular signaling is a crucial and fundamental component of cellular function, furthering the importance of G-protein coupled receptors.
Are there situations in which the phosphate is removed from kinase A so that the active site is blocked? If the kinase A receives this phosphate group when it is synthesized, then does it have it all of the time? This section states that the subsequent activation by the secondary messenger is key to making the kinase really function, but it seems weird that it kinase A would always be in the primed state.
This reminds me of the way the neurotransmitters are released into the synaptic cleft. When calcium ions interact with specific channels on the terminal end of a neuron, a series of events occurs in which results in the membrane surrounding a given neurotransmitter and releasing into to the extracellular environment. In this case calcium elicits a change membrane rather than the calmodulin.
In tumorous cells, processes completed by RAS and other oncogenes are disrupted in a way that favors the tumors growth. Specific pathways in the cell are victims of this process and they become fundamentally altered as a result. Many drugs have been designed to target specific pathways and specific oncogene. Some of these drugs include bevacizumab and metformin. Although these drugs may have a beneficial effect at first, the cancerous cell soon finds a way to utilize another pathway for the same purpose. This is known as oncogene addiction. The mechanism of this phenomenon is rooted in the rapid evolution and resultant mutation that occurs in cancer cells. Therefore, targeting specific pathways or oncogenes has proven to be ineffective in that long-run. That's why current cancer treatment is focusing on the immune system instead.