Tools

LEADER 14220cam 2200733 a 4500

001 ocn456181272;

003 OCoLC;

005 20141212080930.0;

008 110614s2011 enka b 001 0 eng ;

010 a| 2011282480;

015 a| GBB0274782| bnb;

016 7 a| 0154890412| Uk;

019 a| 707589888;

020 a| 9780199288373 (pbk.);

020 a| 0199288372 (pbk.);

029 1 a| DEBBGb| BV035837361;

029 1 a| HEBISb| 221544836;

029 1 a| AU@b| 000046733153;

029 1 a| NZ1b| 13525619;

035 a| (Sirsi) 99947273531;

035 a| (OCoLC)456181272;

035 a| 99947273531;

042 a| pcc;

049 a| EREE;

050 00 a| QP623b| .E45 2011;

060 14 a| QU 58.7 E46m 2011;

082 04 a| 572.882| 22;

084 a| WD 53552| rvk;

100 1 a| Elliott, David,d| 1965-=| ^A1092870;

245 10 a| Molecular biology of RNA /c| David Elliott, Michael Ladomery.;

300 a| ix, 441 pages :b| illustrations ;c| 27 cm;

336 a| text2| rdacontent;

337 a| unmediated2| rdamedia;

338 a| volume2| rdacarrier;

504 a| Includes bibliographical references and index.;

505 00 g| Machine generated contents note:g| 1.t| Introduction to Molecular Biology of RNA --g| 1.1.t| Aims of this book --g| 2.t| RNA can form versatile structures --g| 2.1.t| DNA and RNA are composed of slightly different building blocks --g| 2.2.t| Nucleotides are joined together through a phosphodiester backbone to give nucleotidec hains --g| 2.3.t| RNA secondary structure hydrogen bonding between bases holds nucleotide chains together in double helices --g| 2.4.t| Nucleic acids have primary, secondary, and, in the case of RNA, tertiary structure --g| 2.5.t| Five common secondary structure motifs are found within RNA molecules --g| 2.6.t| Secondary structure motifs form through base pairing in RNA molecules --g| 2.7.t| The formation of RNA duplexes is stimulated and particularly charged molecules and particularly metal ions --g| 2.8.t| RNAs form tertiary structures --g| 2.9.t| Complex folded RNAs which bind to target molecules can be selected --g| 2.10.t| Riboswitches are shape-changing RNAs which can flip gene expression patterns on binding specific target molecules;

505 00 g| 2.11.t| RNA helices can connect different molecules of RNA together --g| 2.12.t| RNA is a versatile molecule --g| 3.t| Catalytic RNAs --g| 3.1.t| RNA is inherently chemically unstable because of its 2'-OH group --g| 3.2.t| The protein enzyme RNAse A uses acid-base catalysis to carry out RNA strand cleavage --g| 3.3.t| Three properties of RNA enable the catalytic function of ribozymes --g| 3.4.t| Ribozymes are widespread in nature and fall into large and small groups --g| 3.5.t| Small ribonucleolytic ribozymes catalyse their own cleavage --g| 3.6.t| The hammerhead ribozyme --g| 3.7.t| The HDV ribozyme --g| 3.8.t| RNA-cutting ribozymes are used to control gene expression in both bacteria and eukaryotes --g| 3.9.t| The large ribozymes --g| 3.10.t| Group I introns are spliced through a two-step mechanism which uses metal ions in their active sites --g| 3.11.t| Group II introns are also spliced through a two-step mechanism --g| 3.12.t| RNAse P is an essential ribozyme which processes the 5' end of tRNA --g| 3.13.t| Catalysis in the ribosome is RNA based --g| 3.14.t| Are ribozymes true catalysts? --g| 3.15.t| The RNA World hypothesis: a time when RNA was used as a genetic material;

505 00 g| 3.16.t| Experiments have been carried out to model the early steps that might have occurred during the evolution of life --g| 4.t| The RNA-binding proteins --g| 4.1.t| The RNA recognition motif (RRM) --g| 4.2.t| The K-homology (KH) domain --g| 4.3.t| The cold-shock domain --g| 4.4.t| Double-stranded RNA-binding proteins --g| 4.5.t| The zinc-finger domain --g| 4.6.t| Other RNA-binding domains --g| 4.7.t| Investigating protein-RNA interactions --g| 5.t| Co-transcriptional pre-mRNA processing --g| 5.1.t| Transcription and the RNA polymerases --g| 5.2.t| Formation of the ends of an mRNA --g| 5.3.t| The C-terminal domain (CTD) of RNA polymerase II --g| 5.4.t| The link between splicing and transcription --g| 5.5.t| The spatial organization of pre-mRNA processing --g| 5.6.t| Histone mRNA 3' end formation --g| 6.t| Pre-mRNA splicing by the spliceosome --g| 6.1.t| RNA splicing was discovered in a virus --g| 6.2.t| Spliceosomal introns play a critical role in efficient eukaryotic gene expression --g| 6.3.t| Introns enhance a eukaryotic gene expression at several levels --g| 6.4.t| Pre-mRNAs are punctuated by splice sites at intron-exon junctions --g| 6.5.t| Splice sites are complementary to a group of small nuclear RNAs;

505 00 g| 6.6.t| snRNAs are associated with proteins to give snRNPs --g| 6.7.t| Splicing follows a two-step reaction pathway --g| 6.8.t| Splicing happens in a series of spliceosomal protein complexes --g| 6.9.t| The spliceosome cycle --g| 6.10.t| Spliceosome assembly and disassembly are cyclical --g| 6.11.t| A minor class of eukaryotic spliceosomal introns have different splice sites --g| 6.12.t| Major and minor spliceosomes coexist in most eukaryotes --g| 6.13.t| Trans-splicing is common in trypanosome parasites and in the nematode C, elegans, where it enables efficient translation --g| 6.14.t| Pre-mRNA splicing is thought to have evolved from parasitic DNA elements --g| 6.15.t| Introns evolved early in eukaryotes --g| 6.16.t| Introns and exons can both appear and disappear in evolution --g| 7.t| How pre-mRNAs are decoded by the splicing machinery --g| 7.1.t| Introns and exon definition --g| 7.2.t| A splicing code helps exon recognition and so controls splicing --g| 7.3.t| Discovery of the splicing code --g| 7.4.t| The splicing code comprises binding sites for nuclear RNA-binding proteins embedded in transcribed sequences --g| 7.5.t| The cis-splicing code is read by nuclear RNA-binding proteins;

505 00 g| 8.6.t| Changes in the splicing code can regulate alternative splicing patterns --g| 8.7.t| Signal transduction pathways can regulate alternative splicing by changing the function and location of splicing factors --g| 8.8.t| Protein phosphorylation --g| 8.9.t| Stimulation of cells with growth factors switches the splicing of the cell surface molecule CD44 --g| 8.10.t| The splicing repressor hnRNP A1 relocalizes to the cytoplasm in response to cellular stress --g| 8.11.t| Splicing decisions can be regulated by dephosphorylation of splicing factors --g| 8.12.t| Transcription elongation speeds can regulate alternative splicing choices --g| 8.13.t| Rates of elongation of RNA polymerase II can be regulated to affect alternative splicing --g| 8.14.t| Transcription can also modulate splicing pathways via the recruitment of cofactors --g| 8.15.t| Alternative splicing in action: alternative splicing pathways can control complex developmental pathways in metazoans --g| 9.t| Pre-mRNA splicing defects in development and disease --g| 9.1.t| Splicing mutations are very frequent causes of human genetic disease --g| 9.2.t| Mutations in splicing control sequences frequently cause exon skipping in humans;

505 00 g| 9.3.t| Molecular diagnosis of splicing mutations --g| 9.4.t| Mutation of an exonic splicing enhancer in a DNA damage control gene leads to breast cancer --g| 9.5.t| Genetic mutations create a new splice site in a premature ageing disease --g| 9.6.t| Mutations which affect splicing can deregulate the ratio of alternatively spliced mRNAs --g| 9.7.t| Mutations affecting splicing signals can be particularly severe since they change the structure of mRNAs --g| 9.8.t| Manipulating pre-mRNA splicing offers a route to treating muscular dystrophy --g| 9.9.t| Diseases caused by mutations in the transacting machinery which recognizes and splices together exons in the nucleus --g| 9.10.t| The genes which encode important spliceosomal proteins are mutated in patients with retinitis pigmentosa (RP) --g| 9.11.t| A protein important for snRNP assembly is affected by mutations causing spinal muscular atrophy (SMA) --g| 9.12.t| There is scientific controversy about why exon 7 of the SMN2 is inefficiently spliced --g| 9.13.t| Molecular therapy for SMA is targeted at correcting the splicing of SMN2 exon 7 --g| 9.14.t| Diseases caused by mis-expression of levels of splicing factor;

505 00 g| 10.11.t| Hijacking of the mRNA export machinery: the constitutive transport element sequence directs the nuclear export of unspliced transcripts from the MPMV virus --g| 10.12.t| Movement of mRMPS through the nuclear pore --g| 11.t| Nucleocytoplasmic traffic of non-coding RNA --g| 11.1.t| Compartment-specific transport complexes --g| 11.2.t| Nuclear transport of rRNA, tRNA, snRNAs, and microRNAs is dependent on the RAN GTPase protein --g| 11.3.t| Different forms of RAN are found in the nucleus and cytoplasm --g| 11.4.t| Non-coding RNA nuclear export complexes contain adaptors and receptors;

505 00 a| Note continued:g| 11.5.t| Nuclear export of ncRNA is dependent on nuclear export adaptor and receptor proteins --g| 11.6.t| Karyopherins are an important group of nuclear export receptors which respond to positional information provided by RAN --g| 11.7.t| CRM1 is the nuclear export receptor (karyopherin) for rRNAs and snRNAs --g| 11.8.t| Different karyopherins act as export receptors for tRNA and microRNAs --g| 11.9.t| After releasing their loads in the cytoplasm nuclear RNA export components are moved back into the nucleus --g| 11.10.t| Nuclear export of snRNAs --g| 11.11.t| Mature snRNPs are re-imported into the nucleus using the nuclear protein import machinery --g| 11.12.t| Mature U6 snRMP is made exclusively in the nucleus --g| 11.13.t| Retroviruses have hijacked the RNA export machinery to assist in the export of partially processed mRNAs --g| 12.t| Messenger RNA localization;

505 00 g| 12.1.t| The need for mRNA localization --g| 12.2.t| The machinery of mRNA localization --g| 12.3.t| Classical examples of mRNA localization in development --g| 12.4.t| Localization of mRNA in differentiated somatic cells --g| 12.5.t| Localization of mRNA in plants --g| 13.t| Translation of messenger RNA --g| 13.1.t| What is translation? --g| 13.2.t| The structure of the ribosome --g| 13.3.t| Deciphering the genetic code --g| 13.4.t| Three key steps in translation --g| 13.5.t| Regulation of mRNA translation --g| 13.6.t| The masked messages --g| 13.7.t| Manipulating translation --g| 14.t| Stability and degradation of mRNA --g| 14.1.t| Messenger RNAs have a half-life --g| 14.2.t| Sites and mechanisms of mRNA degradation --g| 14.3.t| The process of mRNA degradation --g| 14.4.t| Extracellular stimuli influence te stability of mRNA --g| 14.5.t| Nonsense-mediated mRNA decay --g| 14.6.t| Degradation of mRNA in bacteria and plants --g| 15.t| RNA editing --g| 15.1.t| Why edit RNA?;

505 00 g| 15.2.t| A-->I editing takes place by modification of adenosine through removal of an amino group --g| 15.3.t| A-->I editing affects RNA hydrogen bonding between bases since inosine forms stable base pairs with cytosine --g| 15.4.t| A-->I editing was discovered because it destabilized dsRNAs --g| 15.5.t| Alu elements are the main targets of A-->I editing in humans --g| 15.6.t| Selective A-->I RNA editing by ADAR enzymes modifies mRNAs that contain short regions of dsRNA --g| 15.7.t| The four known biological functions of A-->I mRNA editing in the cell --g| 15.8.t| ADAR proteins are essential for normal nervous system development, but also play roles elsewhere in the body --g| 15.9.t| A-->I editing plays an important role in the function of trRNAs --g| 15.10.t| C-->U RNA editing takes place through base deamination (removal of an amino group from cytidine) --g| 15.11.t| C-->U RNA editing makes two different forms of the APOB mRNA in different tissues, and was the first RNA editing reaction to be discovered in animals;

505 00 g| 17.1.t| Introduction to epigenetic regulatory ncRNAs --g| 17.2.t| Transcriptionally active and inactive DNA is created by tagging chromatin with simple chemical groups --g| 17.3.t| Long ncRNAs help epigenetically programme important developmental control genes --g| 17.4.t| A difference in size of the sex chromosomes means there is a requirement for dosage compensation --g| 17.5.t| Dosage compensation in female mammals uses non-coding RNAs to inactivate one female X chromosome --g| 17.6.t| Dosage compensation in fruit flies uses a dosage compensation complex including a long ncRNA to up-regulate expression from a single male X chromosome --g| 17.7.t| Similarities and differences between mechanisms of dosage compensation in fruit flies and mammals --g| 17.8.t| Genetic imprinting controls gene expression depending on the parent of origin of the gene or chromosome --g| 17.9.t| Parentally imprinted gene clusters often include long ncRNAs --g| 17.10.t| The ncRNA AIR epigenetically represses IGF2R gene expression by directing epigenetic chromatin modification;

505 00 g| 17.11.t| Transcription of H19 ncRNA acts as a decoy for transcription of the IGF2 gene --g| 18.t| The short non-coding RNAs and gene silencing --g| 18.1.t| Key concepts and common pathways --g| 18.2.t| Discovery and mechanism of RNA interference --g| 18.3.t| The uses of RNA interference --g| 18.4.t| Discovery, biogenesis, and developmental role of microRNAs --g| 18.5.t| Transcriptional silencing by non-coding RNAs in the centromere --g| 18.6.t| RNA-induced transcriptional silencing of transposons.;

650 0 a| RNA.=| ^A4131;

650 0 a| Molecular biology.=| ^A1446;

700 1 a| Ladomery, Michael.=| ^A1092871;

856 u| http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=018695756&line_number=0001&func_code=DB_RECORDS&service_type=MEDIAz| Inhaltsverzeichnis;

938 a| Baker and Taylorb| BTCPn| BK0008582065;

938 a| YBP Library Servicesb| YANKn| 3205293;

938 a| Blackwell Book Serviceb| BBUSn| 3205293;

938 a| Coutts Information Servicesb| COUTn| 10680617;

938 a| Midwest Library Servicesb| MWSTn| 02340192010;

949 a| QP623 .E45 2011h| Joyner48i| 30372013856064o| jjlm;

910 a| PromptCat;

994 a| 92b| ERE;

596 a| 1;

998 a| 2702710;

999 a| QP623 .E45 2011w| LCc| 1i| 30372013856064d| 1/28/2022e| 4/16/2012f| 7/25/2012g| 1l| JGESm| JOYNERn| 1q| 1r| Ys| Yt| JGESBKu| 4/11/2012x| BOOKz| JSTACKSo| .STAFF. jjlm;

Molecular biology of RNA / David Elliott, Michael Ladomery.

Author/creator	Elliott, David, 1965-
Other author	Ladomery, Michael.
Format	Book
Publication Info	Oxford ; New York : Oxford University Press, ©2011.
Description	ix, 441 pages : illustrations ; 27 cm
Electronic Location	Inhaltsverzeichnis
Subjects	RNA. Molecular biology.

Contents	Machine generated contents note: 1. Introduction to Molecular Biology of RNA -- 1.1. Aims of this book -- 2. RNA can form versatile structures -- 2.1. DNA and RNA are composed of slightly different building blocks -- 2.2. Nucleotides are joined together through a phosphodiester backbone to give nucleotidec hains -- 2.3. RNA secondary structure hydrogen bonding between bases holds nucleotide chains together in double helices -- 2.4. Nucleic acids have primary, secondary, and, in the case of RNA, tertiary structure -- 2.5. Five common secondary structure motifs are found within RNA molecules -- 2.6. Secondary structure motifs form through base pairing in RNA molecules -- 2.7. The formation of RNA duplexes is stimulated and particularly charged molecules and particularly metal ions -- 2.8. RNAs form tertiary structures -- 2.9. Complex folded RNAs which bind to target molecules can be selected -- 2.10. Riboswitches are shape-changing RNAs which can flip gene expression patterns on binding specific target molecules
Contents	2.11. RNA helices can connect different molecules of RNA together -- 2.12. RNA is a versatile molecule -- 3. Catalytic RNAs -- 3.1. RNA is inherently chemically unstable because of its 2'-OH group -- 3.2. The protein enzyme RNAse A uses acid-base catalysis to carry out RNA strand cleavage -- 3.3. Three properties of RNA enable the catalytic function of ribozymes -- 3.4. Ribozymes are widespread in nature and fall into large and small groups -- 3.5. Small ribonucleolytic ribozymes catalyse their own cleavage -- 3.6. The hammerhead ribozyme -- 3.7. The HDV ribozyme -- 3.8. RNA-cutting ribozymes are used to control gene expression in both bacteria and eukaryotes -- 3.9. The large ribozymes -- 3.10. Group I introns are spliced through a two-step mechanism which uses metal ions in their active sites -- 3.11. Group II introns are also spliced through a two-step mechanism -- 3.12. RNAse P is an essential ribozyme which processes the 5' end of tRNA -- 3.13. Catalysis in the ribosome is RNA based -- 3.14. Are ribozymes true catalysts? -- 3.15. The RNA World hypothesis: a time when RNA was used as a genetic material
Contents	3.16. Experiments have been carried out to model the early steps that might have occurred during the evolution of life -- 4. The RNA-binding proteins -- 4.1. The RNA recognition motif (RRM) -- 4.2. The K-homology (KH) domain -- 4.3. The cold-shock domain -- 4.4. Double-stranded RNA-binding proteins -- 4.5. The zinc-finger domain -- 4.6. Other RNA-binding domains -- 4.7. Investigating protein-RNA interactions -- 5. Co-transcriptional pre-mRNA processing -- 5.1. Transcription and the RNA polymerases -- 5.2. Formation of the ends of an mRNA -- 5.3. The C-terminal domain (CTD) of RNA polymerase II -- 5.4. The link between splicing and transcription -- 5.5. The spatial organization of pre-mRNA processing -- 5.6. Histone mRNA 3' end formation -- 6. Pre-mRNA splicing by the spliceosome -- 6.1. RNA splicing was discovered in a virus -- 6.2. Spliceosomal introns play a critical role in efficient eukaryotic gene expression -- 6.3. Introns enhance a eukaryotic gene expression at several levels -- 6.4. Pre-mRNAs are punctuated by splice sites at intron-exon junctions -- 6.5. Splice sites are complementary to a group of small nuclear RNAs
Contents	6.6. snRNAs are associated with proteins to give snRNPs -- 6.7. Splicing follows a two-step reaction pathway -- 6.8. Splicing happens in a series of spliceosomal protein complexes -- 6.9. The spliceosome cycle -- 6.10. Spliceosome assembly and disassembly are cyclical -- 6.11. A minor class of eukaryotic spliceosomal introns have different splice sites -- 6.12. Major and minor spliceosomes coexist in most eukaryotes -- 6.13. Trans-splicing is common in trypanosome parasites and in the nematode C, elegans, where it enables efficient translation -- 6.14. Pre-mRNA splicing is thought to have evolved from parasitic DNA elements -- 6.15. Introns evolved early in eukaryotes -- 6.16. Introns and exons can both appear and disappear in evolution -- 7. How pre-mRNAs are decoded by the splicing machinery -- 7.1. Introns and exon definition -- 7.2. A splicing code helps exon recognition and so controls splicing -- 7.3. Discovery of the splicing code -- 7.4. The splicing code comprises binding sites for nuclear RNA-binding proteins embedded in transcribed sequences -- 7.5. The cis-splicing code is read by nuclear RNA-binding proteins
Contents	8.6. Changes in the splicing code can regulate alternative splicing patterns -- 8.7. Signal transduction pathways can regulate alternative splicing by changing the function and location of splicing factors -- 8.8. Protein phosphorylation -- 8.9. Stimulation of cells with growth factors switches the splicing of the cell surface molecule CD44 -- 8.10. The splicing repressor hnRNP A1 relocalizes to the cytoplasm in response to cellular stress -- 8.11. Splicing decisions can be regulated by dephosphorylation of splicing factors -- 8.12. Transcription elongation speeds can regulate alternative splicing choices -- 8.13. Rates of elongation of RNA polymerase II can be regulated to affect alternative splicing -- 8.14. Transcription can also modulate splicing pathways via the recruitment of cofactors -- 8.15. Alternative splicing in action: alternative splicing pathways can control complex developmental pathways in metazoans -- 9. Pre-mRNA splicing defects in development and disease -- 9.1. Splicing mutations are very frequent causes of human genetic disease -- 9.2. Mutations in splicing control sequences frequently cause exon skipping in humans
Contents	9.3. Molecular diagnosis of splicing mutations -- 9.4. Mutation of an exonic splicing enhancer in a DNA damage control gene leads to breast cancer -- 9.5. Genetic mutations create a new splice site in a premature ageing disease -- 9.6. Mutations which affect splicing can deregulate the ratio of alternatively spliced mRNAs -- 9.7. Mutations affecting splicing signals can be particularly severe since they change the structure of mRNAs -- 9.8. Manipulating pre-mRNA splicing offers a route to treating muscular dystrophy -- 9.9. Diseases caused by mutations in the transacting machinery which recognizes and splices together exons in the nucleus -- 9.10. The genes which encode important spliceosomal proteins are mutated in patients with retinitis pigmentosa (RP) -- 9.11. A protein important for snRNP assembly is affected by mutations causing spinal muscular atrophy (SMA) -- 9.12. There is scientific controversy about why exon 7 of the SMN2 is inefficiently spliced -- 9.13. Molecular therapy for SMA is targeted at correcting the splicing of SMN2 exon 7 -- 9.14. Diseases caused by mis-expression of levels of splicing factor
Contents	10.11. Hijacking of the mRNA export machinery: the constitutive transport element sequence directs the nuclear export of unspliced transcripts from the MPMV virus -- 10.12. Movement of mRMPS through the nuclear pore -- 11. Nucleocytoplasmic traffic of non-coding RNA -- 11.1. Compartment-specific transport complexes -- 11.2. Nuclear transport of rRNA, tRNA, snRNAs, and microRNAs is dependent on the RAN GTPase protein -- 11.3. Different forms of RAN are found in the nucleus and cytoplasm -- 11.4. Non-coding RNA nuclear export complexes contain adaptors and receptors
Contents	Note continued: 11.5. Nuclear export of ncRNA is dependent on nuclear export adaptor and receptor proteins -- 11.6. Karyopherins are an important group of nuclear export receptors which respond to positional information provided by RAN -- 11.7. CRM1 is the nuclear export receptor (karyopherin) for rRNAs and snRNAs -- 11.8. Different karyopherins act as export receptors for tRNA and microRNAs -- 11.9. After releasing their loads in the cytoplasm nuclear RNA export components are moved back into the nucleus -- 11.10. Nuclear export of snRNAs -- 11.11. Mature snRNPs are re-imported into the nucleus using the nuclear protein import machinery -- 11.12. Mature U6 snRMP is made exclusively in the nucleus -- 11.13. Retroviruses have hijacked the RNA export machinery to assist in the export of partially processed mRNAs -- 12. Messenger RNA localization
Contents	12.1. The need for mRNA localization -- 12.2. The machinery of mRNA localization -- 12.3. Classical examples of mRNA localization in development -- 12.4. Localization of mRNA in differentiated somatic cells -- 12.5. Localization of mRNA in plants -- 13. Translation of messenger RNA -- 13.1. What is translation? -- 13.2. The structure of the ribosome -- 13.3. Deciphering the genetic code -- 13.4. Three key steps in translation -- 13.5. Regulation of mRNA translation -- 13.6. The masked messages -- 13.7. Manipulating translation -- 14. Stability and degradation of mRNA -- 14.1. Messenger RNAs have a half-life -- 14.2. Sites and mechanisms of mRNA degradation -- 14.3. The process of mRNA degradation -- 14.4. Extracellular stimuli influence te stability of mRNA -- 14.5. Nonsense-mediated mRNA decay -- 14.6. Degradation of mRNA in bacteria and plants -- 15. RNA editing -- 15.1. Why edit RNA?
Contents	15.2. A-->I editing takes place by modification of adenosine through removal of an amino group -- 15.3. A-->I editing affects RNA hydrogen bonding between bases since inosine forms stable base pairs with cytosine -- 15.4. A-->I editing was discovered because it destabilized dsRNAs -- 15.5. Alu elements are the main targets of A-->I editing in humans -- 15.6. Selective A-->I RNA editing by ADAR enzymes modifies mRNAs that contain short regions of dsRNA -- 15.7. The four known biological functions of A-->I mRNA editing in the cell -- 15.8. ADAR proteins are essential for normal nervous system development, but also play roles elsewhere in the body -- 15.9. A-->I editing plays an important role in the function of trRNAs -- 15.10. C-->U RNA editing takes place through base deamination (removal of an amino group from cytidine) -- 15.11. C-->U RNA editing makes two different forms of the APOB mRNA in different tissues, and was the first RNA editing reaction to be discovered in animals
Contents	17.1. Introduction to epigenetic regulatory ncRNAs -- 17.2. Transcriptionally active and inactive DNA is created by tagging chromatin with simple chemical groups -- 17.3. Long ncRNAs help epigenetically programme important developmental control genes -- 17.4. A difference in size of the sex chromosomes means there is a requirement for dosage compensation -- 17.5. Dosage compensation in female mammals uses non-coding RNAs to inactivate one female X chromosome -- 17.6. Dosage compensation in fruit flies uses a dosage compensation complex including a long ncRNA to up-regulate expression from a single male X chromosome -- 17.7. Similarities and differences between mechanisms of dosage compensation in fruit flies and mammals -- 17.8. Genetic imprinting controls gene expression depending on the parent of origin of the gene or chromosome -- 17.9. Parentally imprinted gene clusters often include long ncRNAs -- 17.10. The ncRNA AIR epigenetically represses IGF2R gene expression by directing epigenetic chromatin modification
Contents	17.11. Transcription of H19 ncRNA acts as a decoy for transcription of the IGF2 gene -- 18. The short non-coding RNAs and gene silencing -- 18.1. Key concepts and common pathways -- 18.2. Discovery and mechanism of RNA interference -- 18.3. The uses of RNA interference -- 18.4. Discovery, biogenesis, and developmental role of microRNAs -- 18.5. Transcriptional silencing by non-coding RNAs in the centromere -- 18.6. RNA-induced transcriptional silencing of transposons.
Bibliography note	Includes bibliographical references and index.
LCCN	2011282480
ISBN	9780199288373 (pbk.)
ISBN	0199288372 (pbk.)

Availability

Library	Location	Call Number	Status	Item Actions
Joyner	General Stacks	QP623 .E45 2011	✔ Available	Place Hold

Molecular biology of RNA / David Elliott, Michael Ladomery.

Click here for more information about this title

Availability