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Taschenbuch. Zustand: Neu. Regulation of RBP1/BCAA transcriptional repression activities | Olivier Binda | Taschenbuch | 284 S. | Englisch | 2013 | LAP LAMBERT Academic Publishing | EAN 9783659350894 | Verantwortliche Person für die EU: BoD - Books on Demand, In de Tarpen 42, 22848 Norderstedt, info[at]bod[dot]de | Anbieter: preigu.
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In den WarenkorbHardback. Zustand: New. Chromatin Signaling and Diseases covers the molecular mechanisms that regulate gene expression, which govern everything from embryonic development, growth, and human pathologies associated with aging, such as cancer. This book helps researchers learn about or keep up with the quickly expanding field of chromatin signaling. After reading this book, clinicians will be more capable of explaining the mechanisms of gene expression regulation to their patients to reassure them about new drug developments that target chromatin signaling mechanisms. For example, several epigenetic drugs that act on chromatin signaling factors are in clinical trials or even approved for usage in cancer treatments, Alzheimer's, and Huntington's diseases. Other epigenetic drugs are in development to regulate various class of chromatin signaling factors. To keep up with this changing landscape, clinicians and doctors will need to stay familiar with genetic advances that translate to clinical practice, such as chromatin signaling. Although sequencing of the human genome was completed over a decade ago and its structure investigated for nearly half a century, molecular mechanisms that regulate gene expression remain largely misunderstood. An emerging concept called chromatin signaling proposes that small protein domains recognize chemical modifications on the genome scaffolding histone proteins, facilitating the nucleation of enzymatic complexes at specific loci that then open up or shut down the access to genetic information, thereby regulating gene expression. The addition and removal of chemical modifications on histones, as well as the proteins that specifically recognize these, is reviewed in Chromatin Signaling and Diseases. Finally, the impact of gene expression defects associated with malfunctioning chromatin signaling is also explored.
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Zustand: New. Examines specific chromatin signaling factors that regulate spinal muscular atrophy, ulbospinal muscular atrophy, amyotrophic lateral sclerosis, Parkinson s disease, Huntington s disease, multiple sclerosis, Angelman syndrome, Rader-Willi syndrome,.
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In den WarenkorbZustand: New. Explains molecular mechanisms that regulate gene expression, which governs everything from embryonic development, growth, and human pathologies associated with aging Educates clinicians and researchers about chromatin signaling, a molecula.
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In den WarenkorbHardback. Zustand: New. Chromatin Signaling and Diseases covers the molecular mechanisms that regulate gene expression, which govern everything from embryonic development, growth, and human pathologies associated with aging, such as cancer. This book helps researchers learn about or keep up with the quickly expanding field of chromatin signaling. After reading this book, clinicians will be more capable of explaining the mechanisms of gene expression regulation to their patients to reassure them about new drug developments that target chromatin signaling mechanisms. For example, several epigenetic drugs that act on chromatin signaling factors are in clinical trials or even approved for usage in cancer treatments, Alzheimer's, and Huntington's diseases. Other epigenetic drugs are in development to regulate various class of chromatin signaling factors. To keep up with this changing landscape, clinicians and doctors will need to stay familiar with genetic advances that translate to clinical practice, such as chromatin signaling. Although sequencing of the human genome was completed over a decade ago and its structure investigated for nearly half a century, molecular mechanisms that regulate gene expression remain largely misunderstood. An emerging concept called chromatin signaling proposes that small protein domains recognize chemical modifications on the genome scaffolding histone proteins, facilitating the nucleation of enzymatic complexes at specific loci that then open up or shut down the access to genetic information, thereby regulating gene expression. The addition and removal of chemical modifications on histones, as well as the proteins that specifically recognize these, is reviewed in Chromatin Signaling and Diseases. Finally, the impact of gene expression defects associated with malfunctioning chromatin signaling is also explored.
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Buch. Zustand: Neu. Neuware.
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Taschenbuch. Zustand: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -RBP1 and BCAA repress transcription in both HDAC-independent (R1) and HDAC-dependent (R2) manners. Like RBP1, BCAA can associate with the mSIN3A/HDAC complex via the SAP30 subunit. The region responsible for this interaction (R2) mediates HDAC-dependent transcriptional repression. The latter is regulated by the NAD+-dependent enzymatic activity of the class III histone deacetylase SIRT1, which is recruited to the mSIN3A/HDAC complex via the tumour suppressors ING1b and ING2. The HDAC-independent repression activity of both RBP1 and BCAA is regulated by post-translational modifications. The R1 repression activity can be further dissected into a domain that targets basal transcription (R1 ) and one that represses both basal and activated transcription (R1s). SUMOylation of the R1s region is essential for its repression activities. SUMOylation of R1s is itself regulated by the overall local amino acids charge. The biological relevance of RBP1 and BCAA transcriptional repression activities is highlighted by their requirement for induction of cell growth arrest and terminal cell cycle withdrawal or cellular senescence. 284 pp. Englisch.
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In den WarenkorbHardcover. Zustand: Brand New. 1st edition. 448 pages. 11.00x8.75x1.25 inches. In Stock. This item is printed on demand.
Sprache: Englisch
Verlag: LAP LAMBERT Academic Publishing Sep 2013, 2013
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Taschenbuch. Zustand: Neu. This item is printed on demand - Print on Demand Titel. Neuware -RBP1 and BCAA repress transcription in both HDAC-independent (R1) and HDAC-dependent (R2) manners. Like RBP1, BCAA can associate with the mSIN3A/HDAC complex via the SAP30 subunit. The region responsible for this interaction (R2) mediates HDAC-dependent transcriptional repression. The latter is regulated by the NAD+-dependent enzymatic activity of the class III histone deacetylase SIRT1, which is recruited to the mSIN3A/HDAC complex via the tumour suppressors ING1b and ING2. The HDAC-independent repression activity of both RBP1 and BCAA is regulated by post-translational modifications. The R1 repression activity can be further dissected into a domain that targets basal transcription (R1¿) and one that represses both basal and activated transcription (R1¿). SUMOylation of the R1¿ region is essential for its repression activities. SUMOylation of R1¿ is itself regulated by the overall local amino acids charge. The biological relevance of RBP1 and BCAA transcriptional repression activities is highlighted by their requirement for induction of cell growth arrest and terminal cell cycle withdrawal or cellular senescence.VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 284 pp. Englisch.