where can i find information on cloning of the hunters syndrome gene?
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Proc Natl Acad Sci U S A. 1990 November; 87(21): 8531–8535. \n\nHunter syndrome: isolation of an iduronate-2-sulfatase cDNA clone and analysis of patient DNA.\nP J Wilson, C P Morris, D S Anson, T Occhiodoro, J Bielicki, P R Clements, and J J Hopwood\n\nIduronate 2-sulfatase (IDS, EC 3.1.6.13) is required for the lysosomal degradation of heparan sulfate and dermatan sulfate. Mutations causing IDS deficiency in humans result in the lysosomal storage of these glycosaminoglycans and Hunter syndrome, an X chromosome-linked disease. We have isolated and sequenced a 2.3-kilobase cDNA clone coding for the entire sequence of human IDS. Analysis of the deduced 550-amino acid IDS precursor sequence indicates that IDS has a 25-amino acid amino-terminal signal sequence, followed by 8 amino acids that are removed from the proprotein. An internal proteolytic cleavage occurs to produce the mature IDS present in human liver shown to contain a 42-kDa polypeptide N-terminal to a 14-kDa polypeptide. The IDS sequence has strong sequence homology with other sulfatases (such as sea urchin arylsulfatase, human arylsulfatases A, B, and C, and human glucosamine 6-sulfatase), suggesting that the sulfatases comprise an evolutionarily related family of genes that arose by gene duplication and divergent evolution. The arylsulfatases have a greater homology with each other than with the non-arylsulfatases (IDS and glucosamine 6-sulfatase). The IDS cDNA detected RNA species of 5.7, 5.4, 2.1, and 1.4 kilobases in human placental RNA and revealed structural alterations and gross deletions of the IDS gene in many of the clinically severe Hunter syndrome patients studied.
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Try these two links:\nhttp://www.scienceaid.co.uk/endocrinesystem.html\nhttp://www.scienceaid.co.uk/nervoussystem.html
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try:\n\nwww.ncbi.nlm.nih.gov\n\nnot yahoo answers
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Good God man you are on the net, you have more information than you know what to do with right at your finger tips. Go to Yahoo's main page and type genetics into the search bar.
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You could try to create a felixin knockout mouse in the mouse orthologue to human felixin to determine if the lack of expression in the mouse produced cat eyes syndrome.  If so, then you could test if subcloning the mouse felixin into an expression vector (for gene therapy-viral delivery), is therapeutically effective in the mouse.  Such animal work would be necessary before performing a similar experiment in human clinical trials.
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REFER TYHIS WEB ADDERESS\nhttp://www.genwaybio.com
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Here are good sites, with some general and specic information (follow the links for your favorite disease).  \n\nGenetests, NCBI and OMIM.  You will have to navigate the sites to mine for info.\n\nThese sites were provideded by a Yale professor who specialized in DNA diagnostics. \n\nI got an "A" in the class, and you will look very bright in your upcoming seminar by reviewing this material too.  These  are superb resources.\n\nPass on this great Karma.\n\nBest Wishes!
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Yes, try to this!\n\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=3906008
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http://www.bic.org.my/\n\nthis is the website of the Malaysian Biotechnology Information Centre.
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*Shaking my shaggy skull* Sadly no as it is a chromosomal disorder, modern science has not advanced that far.\n:c(\nWolf-Hirschhorn syndrome is an extremely rare chromosomal disorder caused by a partial deletion (monosomy) of the short arm ("p") of chromosome 4. Major symptoms may include extremely wide-set eyes (ocular hypertelorism) with a broad or beaked nose, a small head (microcephaly), low-set malformed ears, mental and growth deficiency, heart (cardiac) defects, and seizures. Because the amount of genetic material deleted varies, the symptoms of this syndrome vary from case to case.\nTreatment is cosmetic mostly in nature. Treatment of Wolf-Hirschhorn Syndrome may include surgical repair of malformations. For example, surgery may be performed to correct cleft lip and palate. Other treatment is symptomatic and supportive. A team approach may be helpful in ensuring that affected individuals reach their fullest potential. Such a team approach may include special remedial education, physical therapy, and other medical, social, or vocational services. Genetic counseling will also be of benefit for families of children with Wolf-Hirschhorn Syndrome.\nIn the future with the advance of genetic sciences perhaps we can find cures that will do things like repair DNA and chromosomal disorders. http://www.hhm.k12.nf.ca/parsonsbio/bioproject/cure.html\nStem Cell research was making interesting progress along those lines until recently.\nThere are currently 26 labs in the US alone studying WHS\nSome resource links are as follows\nhttp://www.madisonsfoundation.org/content/3/1/display.asp?did=230\nhttp://www.webmd.com/hw/raising_a_family/nord622.asp\nhttp://hw.healthdialog.com/kbase/nord/nord622.htm\nhttp://www.rarediseases.org/search/rdbdetail_abstract.html?disname=Wolf+Hirschhorn+Syndrome#\nhttp://www.hhm.k12.nf.ca/parsonsbio/bioproject/WolfHome.html
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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8163284&dopt=Citation
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Here is some basic info. Follow the link to the Lowe Syndrome Association website for more info.\n\n\nLowe Syndrome (LS) is a rare genetic condition that causes physical and mental handicaps, and medical problems. It was first described in 1952 by Drs. Lowe, Terrey, and MacLachlan at the Massachusetts General Hospital in Boston. \n\nThe condition became known as "Lowe syndrome" named after Dr. Charles Lowe, the senior member of the group that described it. Because of the three major organ systems involved (eyes, brain, and kidney), it is also known as OCRL (oculo-cerebro-renal) syndrome.\n\nBoys with Lowe Syndrome are born with cataracts in both eyes, which are usually removed at a few months of age. Most boys are fitted with glasses, contacts, or a combination of the two. Glaucoma is present in about 50% of the boys with Lowe syndrome, though usually not at birth. Prescription eye drop and/or surgery is required to maintain appropriate eye pressure in these cases.\n\nWhile not present at birth, many Lowe Syndrome boys develop kidney problems at approximately one year of age. This is characterized by the abnormal loss of certain substances into the urine, including bicarbonate, sodium, potassium, amino acids, organic acids, albumin and other small proteins, calcium, phosphate, glucose, and L-carnitine. This problem is known as Fanconi-type renal tubular dysfunction and can also be seen in certain other diseases and syndromes. In Lowe syndrome, the Fanconi syndrome may be mild and involve only a few substances or may be severe and involve large losses of many substances. Medications can be prescribed to replace the lost substances. \n\nThe Cause \nLowe syndrome is a hereditary condition that affects only males. It is caused by a single defective gene (an alteration or "mutation") in a gene called OCRL1. Because of this defective gene, an essential enzyme called PIP2-5-phosphatase is not produced. This is the underlying cause of Lowe syndrome. Much research has taken place in the last few years. The gene has been mapped and the defecient enzyme has been identified, although its role is not fully understood.
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I searched the ultimate source of all the stuff on net and here's what came out-\n\nhttp://scholar.google.com/scholar?q=humans%20and%20shark%20dna&hl=en&lr=&oi=scholart\nhttp://www.google.com/search?hl=en&q=humans+and+shark+dna\n\nGood luck
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Here are a few sites that have good ones :\nhttp://ghr.nlm.nih.gov/handbook/basics/dna\nhttp://www.elmhurst.edu/~chm/vchembook/582dnadoublehelix.html (more a ball and stick model)\nhttp://www.envirohealthtech.com/images/DNA.jpg (this one is just pretty)
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Try:\nhttp://www.nlm.nih.gov/medlineplus/ency/article/003058.htm
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Please visit the sites\nhttp://www.RESEARCH.GS \nhttp://www.RESEARCH.TC \nhttp://www.research.gs/?q=research+paper\nhttp://www.research.gs/?q=stock+research\nhttp://www.research.gs/?q=medical+research\nhttp://www.research.gs/?q=legal+research\nhttp://www.research.gs/?q=patent+research\nhttp://www.research.gs/?q=cancer+research
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Try this one: \n\nhttp://www.kendall-bioresearch.co.uk/class.htm