Trinucleotide Diseases and Instability - 14 Angebote vergleichen

Von Händler/Antiquariat, Cambridge Rare Books [545787], Cambridge, GLOUC, United Kingdom.
1998. Springer. Hard Cover. Book-VG+, integral colour cover. 9.5x6.5. 169pp. Profuse b/w illus in text. The discovery that human diseases can be caused by large scale expansions of highly unstable trinucleotide repeats has elucidated a new mutation mechanism: heritbal unstable DNA. Three out of the 10 have been identified to be involved in human diseases. This book gives an overview of the different types of repeat instability in genes and describes how this knowledge can be used diagnostically. Books.

Von Händler/Antiquariat, AmazingBookDeals [55216202], CHICAGO, IL, U.S.A.
Used book in GOOD condition. Good enough to read. Binding in GOOD shape with no missing pages. Cover has visible wear. Markings, writings and highligtings inside the book. Text ONLY. Does NOT include accessories such as CD, DVD, access code etc. Fast Shipping. Prompt Customer Service. Satisfaction guaranteed.

Lieferung aus: Vereinigte Staaten von Amerika, Frais de port à: FRA.
Von Händler/Antiquariat, Tiber Books.
Springer, Berlin / New York, 1998. Hardcover. Very Good. 8vo, hardcover. No dj. Vg+ condition. Non-circulating ex-lib copy w/ endpaper label & rear cover label neatly removed (only markings); contents bright, crisp & clean, unread. ix, 169 p., illus.

Lieferung aus: Vereinigte Staaten von Amerika, frais de port, Zone d’expédition: DOM.
Von Händler/Antiquariat, Tiber Books, MD, Cockeysville, [RE:3].
8vo, hardcover. No dj. Vg+ condition. Non-circulating ex-lib copy w/ endpaper label & rear cover label neatly removed (only markings); contents bright, crisp & clean, unread. ix, 169 p., illus. Hardcover.

Von Händler/Antiquariat, Tiber Books [15035], Cockeysville, MD, U.S.A.
8vo, hardcover. No dj. Vg+ condition. Non-circulating ex-lib copy w/ endpaper label & rear cover label neatly removed (only markings); contents bright, crisp & clean, unread. ix, 169 p., illus. Books.

Lieferung aus: Deutschland, En Stock, frais de port.
Till recently, mutations in genes were described in textbooks as deletions or point mutations. These mutations can be inherited from a parent or they are de novo alterations. The discovery in 1991 that human disease can be caused by large-scale ex­ pansion of highly unstable trinucleotide repeats has elucidated a new mutation mechanism, heritable unstable DNA. In the subsequent years more then 10 such disease genes have been identified. All dynamic mutations have been iden­ tified in neurological disorders. There are ten possible trinucleotide repeats at the DNA level, but only 3 have been identified as being involved in human dis­ eases. The rather frequent occurence of triplet repeats in the human genome indicates that other loci subject to unstable expansions may be discovered. The identification of repeat instability and the identification of disease genes containing trinucleotide repeats has helped to answer intriguing questions. The diseases share the unusual characteristic of inheritance with increased disease severity in successive gernerations, a phenomenon called anticipation. Trinu­ cleotide repeat diseases are ideal subjects for direct testing because the muta­ tion is almost exclusively of the same type and there is an extremely low occur­ ance of new mutations in these diseases. The anticipation can now be explained by the correlation of increasing repeat length with increased disease serverity. It can be speculated that other neurological disorders showing anticipation will be caused by unstable repeats as well. eBook.

Lieferung aus: Niederlande, Direct beschikbaar.
bol.com.
Till recently, mutations in genes were described in textbooks as deletions or point mutations. These mutations can be inherited from a parent or they are de novo alterations. The discovery in 1991 that human disease can be caused by large-scale ex pansion of highly unstable trinucleotide repeats has elucidated a new mutation mechanism, heritable unstable DNA. In the subsequent years more then 10 such disease genes have been identified. All dynamic mutations have been iden tified in neurological disorders. There are ten possible trinucleotide repeats at the DNA level, but only 3 have been identified as being involved in human dis eases. The rather frequent occurence of triplet repeats in the human genome indicates that other loci subject to unstable expansions may be discovered. The identification of repeat instability and the identification of disease genes containing trinucleotide repeats has helped to answer intriguing questions. The diseases share the unusual characteristic of inheritance with increased disease severity in successive gernerations, a phenomenon called anticipation. Trinu cleotide repeat diseases are ideal subjects for direct testing because the muta tion is almost exclusively of the same type and there is an extremely low occur ance of new mutations in these diseases. The anticipation can now be explained by the correlation of increasing repeat length with increased disease serverity. It can be speculated that other neurological disorders showing anticipation will be caused by unstable repeats as well. Till recently, mutations in genes were described in textbooks as deletions or point mutations. These mutations can be inherited from a parent or they are de novo alterations. The discovery in 1991 that human disease can be caused by large-scale ex­ pansion of highly unstable trinucleotide repeats has elucidated a new mutation mechanism, heritable unstable DNA. In the subsequent years more then 10 such disease genes have been identified. All dynamic mutations have been iden­ tified in neurological disorders. There are ten possible trinucleotide repeats at the DNA level, but only 3 have been identified as being involved in human dis­ eases. The rather frequent occurence of triplet repeats in the human genome indicates that other loci subject to unstable expansions may be discovered. The identification of repeat instability and the identification of disease genes containing trinucleotide repeats has helped to answer intriguing questions. The diseases share the unusual characteristic of inheritance with increased disease severity in successive gernerations, a phenomenon called anticipation. Trinu­ cleotide repeat diseases are ideal subjects for direct testing because the muta­ tion is almost exclusively of the same type and there is an extremely low occur­ ance of new mutations in these diseases. The anticipation can now be explained by the correlation of increasing repeat length with increased disease serverity. It can be speculated that other neurological disorders showing anticipation will be caused by unstable repeats as well. Inhoud:Taal: Engelstalig;EAN: 9783540696803;Bindwijze: E-book;Verschijningsdatum: 2013-06-05; Engelstalig | E-book | 1998 | 9783540696803.

Lieferung aus: Vereinigtes Königreich Großbritannien und Nordirland, frais de port, Zone d’expédition: EUR.
Von Händler/Antiquariat, Cambridge Rare Books, Cambridge, Gloucestershire, [RE:4].
1998. Springer. Hard Cover. Book-VG+, integral colour cover. 9.5x6.5. 169pp. Profuse b/w illus in text. Hard cover.

Lieferung aus: Australien, in-stock.
Till recently, mutations in genes were described in textbooks as deletions or point mutations. These mutations can be inherited from a parent or they are de novo alterations. The discovery in 1991 that human disease can be caused by large-scale ex- pansion of highly unstable trinucleotide repeats has elucidated a new mutation mechanism, heritable unstable DNA. In the subsequent years more then 10 such disease genes have been identified. All dynamic mutations have been iden- tified in neurological disorders. There are ten possible trinucleotide repeats at the DNA level, but only 3 have been identified as being involved in human dis- eases. The rather frequent occurence of triplet repeats in the human genome indicates that other loci subject to unstable expansions may be discovered. The identification of repeat instability and the identification of disease genes containing trinucleotide repeats has helped to answer intriguing questions. The diseases share the unusual characteristic of inheritance with increased disease severity in successive gernerations, a phenomenon called anticipation. Trinu- cleotide repeat diseases are ideal subjects for direct testing because the muta- tion is almost exclusively of the same type and there is an extremely low occur- ance of new mutations in these diseases. The anticipation can now be explained by the correlation of increasing repeat length with increased disease serverity. It can be speculated that other neurological disorders showing anticipation will be caused by unstable repeats as well.

Lieferung aus: Deutschland, Download sofort lieferbar.
eBooks, eBook Download (PDF), Till recently, mutations in genes were described in textbooks as deletions or point mutations. These mutations can be inherited from a parent or they are de novo alterations. The discovery in 1991 that human disease can be caused by large-scale ex- pansion of highly unstable trinucleotide repeats has elucidated a new mutation mechanism, heritable unstable DNA. In the subsequent years more then 10 such disease genes have been identified. All dynamic mutations have been iden- tified in neurological disorders. There are ten possible trinucleotide repeats at the DNA level, but only 3 have been identified as being involved in human dis- eases. The rather frequent occurence of triplet repeats in the human genome indicates that other loci subject to unstable expansions may be discovered. The identification of repeat instability and the identification of disease genes containing trinucleotide repeats has helped to answer intriguing questions. The diseases share the unusual characteristic of inheritance with increased disease severity in successive gernerations, a phenomenon called anticipation. Trinu- cleotide repeat diseases are ideal subjects for direct testing because the muta- tion is almost exclusively of the same type and there is an extremely low occur- ance of new mutations in these diseases. The anticipation can now be explained by the correlation of increasing repeat length with increased disease serverity. It can be speculated that other neurological disorders showing anticipation will be caused by unstable repeats as well.