why receptors are good drug target?
436441
Because the drug binds to it. When the drug binds to the receptor, the drug begins to work.
869334
Since caffeine and other methyxanthines act as competitive antagonists to adenosine.  This means that they bond to the same receptor site but fail to activate it.  As they are bound to the receptor, the true agonist is unable to bind and activate that receptor.   Similar to carbon monoxide, caffeine could have a higher affinity to the receptor thus attaching to the receptor longer and/or displacing adenosine from the receptor to attach.\n\nAs for the role of adenosine in dilation of blood vessels, I have only found that it dilates coronary arteries and constricts the the afferent arterioles of the glomerulus.
863141
Yes it is. There are drugs that target the microtubule structure as well as those that act on the actin based microfilament structure.
410312
check out the link for the whole article..\n\nResearchers have identified a molecule that appears to play a critical part in how cancers spread to bones.\n\nAlthough the experiments were done in mice, the Austrian researchers hope the finding will lead to new treatments that can keep cancers such as breast, prostate and skin cancer from spreading to bone.\n\nThey found that a protein in bone called RANKL communicates with a receptor in breast, prostate and skin cancer cells, telling them to migrate.
402542
There are a number of theories, but the short answer is "nobody knows".  Could be establishment of new synapses, could be changes in receptor sensitivity, could even be new neurons stimulated to develop, but at this point, we dont have any real idea.
391224
There are two classes of acetylcholine receptors, muscarinic and nicotinic (see Molecular Biology, Pharmacology, and Brain Distribution of Subtypes of the Muscarinic Receptor). These receptors play major roles in the function of the body. In brain, evidence suggests a role for muscarinic receptors in memory function (28, 71) and in the pathophysiology of affective illness (46, 47, 79) and schizophrenia (24, 50, 85, 86). Because of their putative role in cognitive function, muscarinic receptors have been a focus of research in Alzheimer's disease (see Experimental Therapeutics).\n\nResearchers defined the two classes of cholinergic receptors early in this century on the basis of tissue responses to certain agonists and antagonists (22). A response caused by muscarine, an alkaloid derived from a poisonous mushroom (Amanita muscaria), and antagonism of a response caused by atropine, an alkaloid from the deadly nightshade (Atropa belladonna—a favorite of poisoners in past centuries), defined muscarinic receptors in a tissue. On the other hand, response to nicotine and blockade by d-tubocurarine (one of the alkaloids from the South American arrow poisons) defined nicotinic receptors. These definitions for the two types of cholinergic receptors are still used today.\n\nMuscarinic receptors are widely distributed throughout the body. They mediate various types of responses in many different tissues—such as cardiac tissue, smooth muscle, and exocrine glands—and in cells throughout the peripheral and central nervous system. Within the nervous system, muscarinic receptors are present on some axon endings (heteroreceptors and autoreceptors), regulating neurotransmitter release (1, 67, 68, 90). These receptors are also on the soma and dendrites of many types of neurons, including cholinergic and noncholinergic neurons (67, 95).\n\nIn the past several years, discoveries by molecular biologists have made the field of muscarinic receptors immensely interesting and complex. At a time when pharmacologists could identify at most three subtypes of muscarinic receptors, molecular biologists showed that at least five different muscarinic receptors exist on the basis of molecular cloning experiments (15, 16, 54, 55, 63). Much knowledge about these receptors has come from the use of transfected cell lines that have incorporated into their genome and express the gene encoding the specific muscarinic receptor.\n\nThis chapter will focus mainly on the biochemical events associated with activation of muscarinic receptors. The concepts of receptors, their effectors, and second messengers will be presented along with a general discussion of the types of membrane-bound receptors. Specific aspects of transduction at cholinergic receptors will be presented along with a brief discussion of the neuropsychopharmacology of muscarinic receptors.\n\nRECEPTORS\n\nThe concept of a receptor was put forth in the latter part of the nineteenth century and the early part of this century by Professors J. N. Langley and Paul Ehrlich. Professor Ehrlich has stated "the toxin must unite . . . with `receptors' in order for the toxin to have its effects" (30). Professor Langley used the term "receptive substance" (56).\n\nA receptor is a highly specialized protein, which, in most cases, is a transmembrane spanning protein on the cellular surface (receptors for steroid hormones are intracellular). This receptor protein has the unique ability to recognize (bind) specific molecules. All neurotransmitters, neuromodulators, and hormones have specific receptors. Many neurotransmitters are known to have more than one type of receptor to which they bind.\n\nCurrently, receptors may be classified into four groups based upon their signal transduction mechanisms: (i) receptors that are ligand-gated ion channels [e.g., the nicotinic acetylcholine (21, 65) and gamma-aminobutyric acid (GABA) receptors (13, 75)]; (ii) receptors that are enzymes [e.g., the ins
511563
Immune cells have special receptor proteins on their plasma membrane that recognize the corresponding proteins on the microorganisms.
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Mechanism of action is different for different drugs.\nI am confusing about drug/medicine.\nIf it is the habitual use of medicine/drug often lead to muscle break down, kidney damage, liver dysfunction, nerve impairement, vision proble etc when excessive amounts are taken.
1135871
They work through signal transduction.
1118237
This is not a simple question.  Some hormones, once they activate the receptor are endocytosed with the receptor into the cell.  Therefore, these hormones can only activate the receptor one time.\n\nOther hormones activate receptors inside the cells (e.g. steroid hormones) and again, may stay attached to the receptor as it translocates to the nucleus to activate gene expression.\n\nLastly, still others may activate a surface receptor and then dissociate from the receptor, making them available to activate the receptor again.\n\nHope this was helpful.   If you go to Pubmed (enter "entrez pubmed" in your search engine), they have access to many online medical texts on cell biology.  You can search these books for their chapters and info. on hormones, receptors, etc.\n\nBest wishes.
564264
Basically, it is tagging the substance to be delivered to an incredibly tiny particle of gold; usually, there is an antibody (or other targeting substance) attached to the gold particle as well, to target a specific cell type or cellular structure.  It is the antibody that does the targeting; the gold nanoparticle is but the (essentially passive) tool used to carry the targeting molecule and the drug molecule.\n\nIt's one of the developing technologies--it's far from being routine, yet, last I heard.
1095681
it is not that either drug is stronger...it is what works for you.  A lot of my patients will tell me to give them something that is strong...it is not whether it is strong, it has to be effective\nthe otehr thing that most people do not realize is that you build up a tolerance to some medications...the more you take, the more you need....Xanax(R) / alprazolam is exactly like that...the more you take, the more you need
82949
To trigger a biological response.
720619
During the large scale manufacturing of drugs, a certain amount of drug will migrate into the solvent. By recovering the solvent and reprocessing, this drug can be sold and yields will increase. The advantage of this is higher capacity and less hazardous waste.
536417
Many of the orignal studies were based on mutations in bacteria which halt growth or have other phenotypes, where it was found that mutations could be labeled into several groups, and that if bacteria from different groups mated, then the phenotype is restored.  From this it was deduced that the mutations were in coding regions for proteins that exist in a network ie A to B to C, and usually proteins like A and B were in a complex.  Today its a large part of cell and molecular biology to figure out if proteins are in complexes, and what the complex does.  Its not necessarily important that A and B are in a complex, but what that complex does; since that is the proteni function in cells.  So if A and C are in a complex, the complex has a certain function.  if B and C are in a complex, then there is a different function.  Drug companies have been exploiting this type of knowledge for a long time, but what is more impt is the understanding of how proteins interact with other proteins, and how they regulate cellular functions.  Once this is understood, then drugs can be rationaly designed.  Even then, however, it's not possible to guarantee patient efficacy.  \n\nWe just had a great lecture by Gordon Mills, an expert in the PTEN protein pathway, and he talked about the dozens of drugs made against various members of this pathway, and noted that so far none of these drugs are effective in patients, although they work in the test tube and in mice.  So, drug discovery is a very difficult issue and takes billions of dollars for one drug to be delivered to market (and 10 years or more).
449693
because they are bloch the B receptors which are responsible for heart contractions\n\nthen heart rate and contraction decrease ,this may lead to fatigue
262510
Cells of the immune system more specifically B cells produce antibodies with shapes similar to the receptors on the foreign cells. Therefore these antibodies fit into the receptor sites on the membrane of the foreign cell and causes its membrane to break down.