P-TEFb, a Cyclin-dependent Kinase Controlling Elongation by RNA Polymerase II PDF Download
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Author: Junmin Peng
Publisher:
ISBN:
Category : Cyclin-dependent kinases
Languages : en
Pages : 246
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Author: Junmin Peng
Publisher:
ISBN:
Category : Cyclin-dependent kinases
Languages : en
Pages : 246
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Book Description
Author: Giuliana Napolitano
Publisher:
ISBN:
Category :
Languages : en
Pages : 66
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Author: Zhiyuan Yang
Publisher:
ISBN:
Category :
Languages : en
Pages : 302
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Book Description
Author: Guido Silvestri
Publisher: Springer
ISBN: 303002816X
Category : Medical
Languages : en
Pages : 253
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Book Description
This volume summarizes recent advances in understanding the mechanisms of HIV-1 latency, in characterizing residual viral reservoirs, and in developing targeted interventions to reduce HIV-1 persistence during antiretroviral therapy. Specific chapters address the molecular mechanisms that govern and regulate HIV-1 transcription and latency; assays and technical approaches to quantify viral reservoirs in humans and animal models; the complex interchange between viral reservoirs and the host immune system; computational strategies to model viral reservoir dynamics; and the development of therapeutic approaches that target viral reservoir cells. With contributions from an interdisciplinary group of investigators that cover a broad spectrum of subjects, from molecular virology to proof-of-principle clinical trials, this book is a valuable resource for basic scientists, translational investigators, infectious-disease physicians, individuals living with HIV/AIDS and the general public.
Author: Torben Heick Jensen
Publisher: Springer Science & Business Media
ISBN: 1441978410
Category : Medical
Languages : en
Pages : 161
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Book Description
The diversity of RNAs inside living cells is amazing. We have known of the more “classic” RNA species: mRNA, tRNA, rRNA, snRNA and snoRNA for some time now, but in a steady stream new types of molecules are being described as it is becoming clear that most of the genomic information of cells ends up in RNA. To deal with the enormous load of resulting RNA processing and degradation reactions, cells need adequate and efficient molecular machines. The RNA exosome is arising as a major facilitator to this effect. Structural and functional data gathered over the last decade have illustrated the biochemical importance of this multimeric complex and its many co-factors, revealing its enormous regulatory power. By gathering some of the most prominent researchers in the exosome field, it is the aim of this volume to introduce this fascinating protein complex as well as to give a timely and rich account of its many functions. The exosome was discovered more than a decade ago by Phil Mitchell and David Tollervey by its ability to trim the 3’end of yeast, S. cerevisiae, 5. 8S rRNA. In a historic account they laid out the events surrounding this identification and the subsequent birth of the research field. In the chapter by Kurt Januszyk and Christopher Lima the structural organization of eukaryotic exosomes and their evolutionary counterparts in bacteria and archaea are discussed in large part through presentation of structures.
Author: Nicholas James Fuda
Publisher:
ISBN:
Category :
Languages : en
Pages : 202
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Most gene expression is regulated at the level of transcription, and the transition from initiation to productive elongation is a key point of regulation. This transition is accompanied by pausing of transcriptionally engaged polymerase in the promoter-proximal region of several heat shock genes. Although this mechanism of regulation was long thought to be limited to a few genes, recent evidence has indicated that pausing is wide-spread in higher eukaryotes. Therefore, it is increasingly important to understand the mechanisms controlling the paused polymerase. I have investigated how the site of pausing on Hsp70 is specified using highresolution mapping of polymerase on reporter genes with shifted pausing site sequences. The results indicate that the downstream sequence dictates pause position and the overall level of pausing. I have also used RNAi knock-down in Drosophila cell culture to study the roles of several factors in establishing, maintaining, and releasing the paused polymerase. These experiments have shown GAGA factor is required for pausing on many of its target genes, and the knock-down effects indicate it is involved in establishing the pause. In contrast, Spt5, a protein previously shown to enhance pausing in vitro, reduces pausing genome-wide by increasing levels of elongating polymerase. Two kinases, P-TEFb and CDK12, function in productive elongation. Previously our lab showed that P-TEFb inhibition prevented the transition into elongation, limiting the polymerase to the 5' end of the heat shock-induced Hsp70 gene. I mapped these polymerases in high resolution to show they occupied sites further downstream than the normal pause sites, suggesting P-TEFb activity may not solely release the paused polymerase. I also determined the localization of CDK12 on active genes. Its localization downstream of P-TEFb suggests that these kinases may have distinct functions. Finally, I have examined the role of Fcp1 in Hsp70 transcription. Our lab previously showed the CTD phosphatase Fcp1 was required for optimum expression of Hsp70 mRNA. Fcp1 knock-down reduced the heat shock levels of Pol II and increased phosphorylation of nonchromatin bound Pol II, indicating that Fcp1 recycling of RNA polymerase II to an initiationcompetent form is required for optimal Hsp70 heat shock transcription.
Author: Bo Cheng
Publisher:
ISBN:
Category : RNA polymerases
Languages : en
Pages : 342
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Book Description
Author: Courtney Virginia St. Amour
Publisher:
ISBN:
Category :
Languages : en
Pages : 282
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RNA Polymerase (Pol) II transcribes protein-coding genes in eukaryotic cells. Transcription by Pol II is coordinated with processes through the carboxyl-terminal domain (CTD) of its largest subunit, Rpb1. Cyclin-dependent kinases (CDKs) phosphorylate CTD heptad repeats to influence their binding properties and thereby govern co-transcriptional mRNA processing. Transcription factor (TF) IIH-associated Cdk7 phosphorylates Ser5 residues to recruit capping enzymes, while Cdk9 promotes elongation by phosphorylating the CTD and the processivity factor Spt5. I examined the functions of these essential kinases in fission yeast in a putative mRNA quality control mechanism that could ensure that only fully capped transcripts are elongated. I found that Cdk9 forms a constitutive and stable complex with the cyclin Pch1 and the 5'-cap methyltransferase Pcm1 in vivo. Using chemical genetics, we showed that Mcs6 activity is required to recruit the Cdk9-Pch1-Pcm1 complex to a subset of CDK-dependent genes. In vitro, I showed that phosphorylation of the CTD by Mcs6 stimulates subsequent phosphorylation by Cdk9. Together, these observations support a model in which Mcs6 and Cdk9 act sequentially to coordinate elongation and capping of select pre-mRNAs. To test that model, I undertook a functional dissection of the fission yeast Cdk9-Pch1-Pcm1 complex. I show that a Cdk9 carboxyl-terminal extension, distinct from the catalytic domain, mediates binding to Pcm1 and the Pol II CTD. Removal of this segment leads to growth defects and transcriptional deficiencies. These phenotypes are suppressed by Pcm1 overproduction, suggesting that normal transcript elongation and gene expression depend on physical linkage between Cdk9 and Pcm1. The extension is dispensable, however, for recognition by Cdk9 of CTD substrates "primed" by Mcs6. Cdk9 prefers CTD peptides phosphorylated at Ser7 over unmodified repeats. In vivo, Ser7 phosphorylation depends on Mcs6 activity, suggesting a mechanism to order transcriptional CDK functions, independent of chromatin recruitment. Therefore, fission yeast Cdk9 comprises a catalytic domain sufficient for primed substrate recognition, and a multivalent recruitment module that couples transcription with capping. Together, these results support a proposed model whereby CTD phosphorylation by Mcs6 stimulates subsequent Cdk9 activity and the Cdk9/Pcm1 complex serves to coordinate capping with transcript elongation, thereby protecting mRNA quality.
Author: Nicholas F. Marshall
Publisher:
ISBN:
Category : Drosophila
Languages : en
Pages : 320
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Book Description
Author: Steven Gray
Publisher: Academic Press
ISBN: 0128002247
Category : Medical
Languages : en
Pages : 748
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Book Description
Epigenetic Cancer Therapy unites issues central to a translational audience actively seeking to understand the topic. It is ideal for cancer specialists, including oncologists and clinicians, but also provides valuable information for researchers, academics, students, governments, and decision-makers in the healthcare sector. The text covers the basic background of the epigenome, aberrant epigenetics, and its potential as a target for cancer therapy, and includes individual chapters on the state of epigenome knowledge in specific cancers (including lung, breast, prostate, liver). The book encompasses both large-scale intergovernmental initiatives as well as recent findings across cancer stem cells, rational drug design, clinical trials, and chemopreventative strategies. As a whole, the work articulates and raises the profile of epigenetics as a therapeutic option in the future management of cancer. - Concisely summarizes the therapeutic implications of recent, large-scale epigenome studies, including the cancer epigenome atlas - Discusses targeted isoform specific versus pan-specific inhibitors, a rational drug design approach to epigenetics relevant to pharmacoepigenetic clinical applications - Covers new findings in the interplay between cancer stem cells (CSCs) and drug resistance, demonstrating that epigenetic machinery is a candidate target for the eradication of these CSCs
