If you have a, lets say, a 60bp (GTCx20) restriction enzyme, which will cut out 20 triplet codons CAG (huntington disease), will the person be cured if given to all cells?
209325
Sure it WOULD work if there were means to deliver it to each cell, ensure 100% restriction efficiency & specificity, and ligate the DNA nick afterwards. So far it is sci-fi; prenatal diagnostics is the way to go for now.
294464
maybe its bcoz of the genetic factor \n\nyoga is the best option \n\nit doesnot have side effects
471390
B, that's it. The idea is to stall for time until a cure is found. \n\nOh, and it can still be transferred. Be careful kids.
486096
Hi Andrea, Here is some comforting news but not to the specific question . I have advanced emphysema myself and will be searching for more information myself.Tulane University's Center for Gene Therapy has received a $9.5 million federal grant to develop treatments using adult stem cells for emphysema, cystic fibrosis and asbestos-related lung disease. \nThe AMA does not recognize this treatment for COPD/emphysema. The FDA does not approve nor disapprove, as it is a treatment. The FDA does not regulate treatments.\nLive Cell Therapy Treatments have been practiced in Europe for more than 50 years successfully and in Mexico for 20 years.
554039
Finding out the function of each gene is a complex procedure. But once a gene is identified and singled out, silencing it by means of RNA interference is a great way to find out how it works, yes.\n\nI just wanted to add some comments.\nThere is some confusion with respect to what knowing the entire genome can and cannot do. \nA gene is defined as a portion of DNA that codes for a protein.\nHowever, differences during the translation from DNA to protein can result in different proteins with quite different properties. In the past, when genes were first discovered and studied, it was believed that each gene coded for a protein, and each protein determined a character. Many people still believe that there is a "blue eye gene" or a "intelligence gene". This is not so. \nWith some exceptions, each character that we perceive as such (for instance, curly hair, large flowers) is the result of the interaction of several alleles (the "versions" of each gene that we carry), as well as other processes and phenomena that occur between the translation of a protein and the full development of a living being (called epigenetic factors). \n\nThat being said, RNA interference is a great tool to learn more about the effects of specific genes, yes. Hopefully people will understand that in the case of complex systems such as living beings, and humans specifically, the separate study of each part is not enough to understand the whole.
363888
K.C.'s answer works if you have a selective media that will work. Also (or in addition to that) you may want to plate out colonies and then PCR out a unique sequence or two.\n\nThis wouldn't be definitive but if you design your primers right it may work, but also may be very time consuming.\n\nAlso you may want to try restriction digests to remap your gene. This would work well, if you have a good map.\n\nGood luck, what a bummer
314834
I'm very skeptical of a "god" gene.  A "gullibility" gene seems much more likely.\n\nYes, it is unfair to those who have been saddled with such a gene.  They'll have to work extra hard to overcome their disability.
89031
Scientists have reported that they've found an "extremely unusual" trait in the cells of some mothers with two or more gay sons, providing more evidence to suggest that homosexuality might be inherited.\n\n\nMothers of multiple gay sons were about six times more likely than other women to process their X chromosomes in a certain way, researchers discovered.\n\n\nResearchers aren't entirely sure what the findings mean, said study co-author Sven Bocklandt, a postdoctoral researcher at UCLA. Making things more complicated, about 75 percent of mothers of multiple gay sons don't have the trait.\n\n\nStill, the study, released Tuesday in the journal Human Genetics, raises plenty of questions, Bocklandt said, especially as researchers try to figure out whether homosexuality has genetic roots and if there truly is a "gay gene" -- or genes.\n\n\n"What everybody wants is the gene, and we don’t have it yet," Bocklandt said. "But this is an independent confirmation that the X chromosome is involved."\n\n\nBocklandt and colleagues looked at a phenomenon known as X-chromosome inactivation, in which cells inside the bodies of females automatically turn off -- or inactivate -- one of their two X chromosomes. That leaves them with one working X chromosome -- just like males, who have a single X and a single Y chromosome.\n\n\nNormally, each cell in a female's body randomly turns off one or the other X chromosome. In some cases, such as when families share a genetic disease, there is "extreme skewing" -- one X chromosome is more likely to be turned off than the other, Bocklandt said.\n\n\nIn the new study, the researchers looked at 97 mothers of one or more gay sons and 103 women with no gay sons to see what their blood cells did with their X chromosomes. The researchers recruited many of the women with the help of PFLAG.\n\n\nThey found that nearly a quarter of the mothers of multiple gay sons inactivated the same X chromosome -- in other words, nonrandomly -- compared to just 4 percent of the women without gay sons. Of those with one gay son, 13 percent inactivated the same X chromosome.\n\n\nDr. Ionel Sandovici, a genetics researcher at the Babraham Institute in Cambridge, England, who is familiar with the research findings, cautioned that the study is small, with just 44 mothers of multiple gay sons being examined. More research in larger groups must be done to confirm the results, Sandovici said.\n\n\nThe research does provide "circumstantial evidence" that the X chromosome contributes to the development of male sexuality, Sandovici said. But "we still understand very little about molecular mechanisms of sexual orientation, and this seems to be rather a complicated biological puzzle."\n\nBut of course its Nature vs. Nurture and its possible that the person could just become gay because of his environment/experiences or just be born that way.
451876
There are 3,000,000,000 base pairs in the human genome, in EVERY SINGLE CELL.  There are 10^14 cells in the human body, and many of them divide.  Many of them divide MANY times.  So for every cell that divides, 3,000,000,000 base pairs of DNA need to be replicated.  Replication is not a computer, it is molecules, and mistakes are made all the time.  We have mechanisms that repair mistakes, but sometimes mistakes fall through the cracks.\n\nNow, of the 3,000,000,000 base pairs, only 3% of that falls into coding regions (of 25,000-30,000 genes).  A huge majority of DNA serves little function, and this might be explained by simple probabilities by evolution.  If such a small portion of DNA is in coding regions, then there is only a 3/100 chance that a mutation will occur within a coding region.  Of course there are other regions of DNA that are important, but still, mutations in a huge portion of DNA will show no effect.
295140
Yes, you can use it for over expression.  Make sure your plasmid has the proper self cloning sequences, one plasmid per cell won't do you much good.  \n\nPrecautions?  \n\nMake sure your gene is pure, as in not having anything that might ruin your experiment. Test culture your target bacterium first to weed out the non functionals and then cultivate the good ones, the ones that produce your targe protein.  You might need to assay for this stuff though, unless there's one of the specialized agars that will detect your target protein.
249729
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).
457696
I would say that there is danger. Huntingtons disease, for example, is a genetic disorder with autosomal dominant inheritance patterns, it usually is late onset, late thirties or later. If an insurance company, for example, knew a person would have Huntingtons later in life, they would probably be less likely to insure him. \n\nThe only way I know to prevent this type of discrimination absolutely is to prevent the insurance companies from knowing that man's genetic make-up, but that doesn't really seem fair, either.
185755
Generally the idea is that the DNA does not necessarily have to be introduced into every cell of the human body to cure a disease because not every cell in the body may be affected by the disease. \n\nCurrently the main idea is using viruses which are made harmless to humans. Viruses can insert DNA into their host. They can infect either only a certain cell type or a wide variety. \n\nRead up more detail about viruses used and non-viral options using the link provided or do further research using a search engine. \n\nIf it is a genetically inheritable disease I assume that the best option is if there is a very high risk for the children to have a genetic disease they would try to manipulate the DNA in a fertilized egg, so probably techniques from in-vitro fertilization would be used. Don't know if that works yet, but I am sure there is a website out there which explains that.
512779
You're right, the information under Wikipedia's Growth Hormone Treatment section is very vague. However, it does tell you that the gene for the growth hormone is inserted into bacteria, which mass produce the protein.\n\nFrom that, we can surmise what you could potentially do to mass produce growth hormone.\n\nFirst, of all, you need the gene. That's simple. You get a bunch of pituitary cells and then create some primers that bind upstream and downstream of the actual gene.\n\nThese primers should consist of approximately 25 base nucleotides, and should bind before the gene and after the stop codon.\n\nYou then use PCR to amplify it up. That technique can be found in any old Molecular Biology textbook, though the Maniatis book (referenced below) is very good and detailed on this.\n\nNow the best thing to do next is to put your gene of choice into a plasmid (a circular piece of DNA) that expresses an antibiotic resistance gene, and right in front of a gene promoter that is always switched on (and obviously, one that forces the bacteria to produce vast quantities of the hormone).\n\nThat's very simple. Use a nuclease to cut your plasmid. (It's best to use two nucleases, to cut out a small section of the plasmid DNA out). Use the same nucleases to cut the ends of your extract gene (making sure the nuclease that cuts upstream of your extract DNA is also the same nuclease that cuts at the "upstream" part of your plasmid and vice versa). That means you have to find a nuclease that cuts at the right places, which may require a bit of searching.\n\nBecause both have been cut by the same enzyme, they'll have sticky ends that match. They'll anneal naturally and because you used the same enzyme to cut upstream of both plasmid and extract gene, the gene will anneal the right way round instead of backwards. (If it anneals backwards, the gene won't work). Use a DNA ligase to join up the backbone and voila, you've got a plasmid that should express antibiotic resistance and your hormone gene.\n\nTransform it into bacteria, possibly using heat shock. Select for the bacteria that express the antibiotic gene (as it should also express the growth hormone), by putting it on to an agar plate with the antibiotic in and lots of goodies and nutrients for the bacteria.\n\nOnly the ones with the plasmid will survive and they'll form little colonies on a plate. Now you've got to check that your plasmid contains the gene. After all, the insertion of your gene into the plasmid could have failed.\n\nThat's simple. All you have to do is take a little bit from a colony, break it open and use a pair of primers that bind at the 5' end and the 3' end of the gene, and do a PCR. If the gene is there, you'll get a product. If not, you won't.\n\nThen, you do a Western blot, to make sure the protein is actually being made. You could have skipped the above PCR step, but there was the chance that some rogue growth hormone could have infected your samples. Doing the PCR, shows you that any protein is there because the bacteria is making it from the gene you put into it, and not because it just happened to be on some of your apparatus.\n\nI'll refer you to the sources below, as a Western blot is a long detailed procedure that'll make this answer insanely long.\n\nAfter you've done that and proved to yourself that the bacteria has your gene and is making your protein, you grow it up in a huge vat full of nutrients. Siphon some off every now and then, and extract the protein.\n\nYou need do nothing more, except keep growing the bacteria, making sure it's always there and that the antibiotic selection is always on. If it isn't, the bacteria will eventually reject the plasmid, as it won't be of any use to it.\n\nThere you have it. It may not be the exact same protocol as what industry uses, but it will get you similar results.
652869
Not possible. Genetics give you what you have, be thankful for it.
520283
It will depend on what the doctor orders for medications and what stage of Huntingtons the patient is in.  If they are in the early stages they can probably still work and take care of themself but as the disease progresses they will need more care and eventually probably need to be in a nursing home.  If they have the disease though they will be on disability after they cannot work any more so disability will help with the cost of some meds and with care etc.
56640
Genetic engineering, genetic modification (GM), and the now-deprecated gene splicing are terms for the process of manipulating genes, usually outside the organism's normal reproductive process.\n\nIt often involves the isolation, manipulation and reintroduction of DNA into cells or model organisms, usually to express a protein. The aim is to introduce new characteristics such as making a crop resistant to a herbicide, introducing a novel trait, or producing a new protein or enzyme. Examples include the production of human insulin through the use of modified bacteria, the production of erythropoietin in Chinese Hamster Ovary cells, and the production of new types of experimental mice such as the OncoMouse (cancer mouse) for research, through genetic redesign.\n\nSince a protein is specified by a segment of DNA called a gene, future versions of that protein can be modified by changing the gene's underlying DNA. One way to do this is to isolate the piece of DNA containing the gene, precisely cut the gene out, and then reintroduce (splice) the gene into a different DNA segment. Daniel Nathans and Hamilton Smith received the 1978 Nobel Prize in physiology or medicine for their isolation of restriction endonucleases, which are able to cut DNA at specific sites. Together with ligase, which can join fragments of DNA together, restriction enzymes formed the initial basis of recombinant DNA technology.