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Author: Nancy Y. Ip
Publisher: Springer Science & Business Media
ISBN: 0387788875
Category : Medical
Languages : en
Pages : 326
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Book Description
Cyclin Dependent Kinase 5 provides a comprehensive and up-to-date collection of reviews on the discovery, signaling mechanisms and functions of Cdk5, as well as the potential implication of Cdk5 in the treatment of neurodegenerative diseases. Since the identification of this unique member of the Cdk family, Cdk5 has emerged as one of the most important signal transduction mediators in the development, maintenance and fine-tuning of neuronal functions and networking. Further studies have revealed that Cdk5 is also associated with the regulation of neuronal survival during both developmental stages and in neurodegenerative diseases. These observations indicate that precise control of Cdk5 is essential for the regulation of neuronal survival. The pivotal role Cdk5 appears to play in both the regulation of neuronal survival and synaptic functions thus raises the interesting possibility that Cdk5 inhibitors may serve as therapeutic treatment for a number of neurodegenerative diseases.
Author: Nancy Y. Ip
Publisher: Springer Science & Business Media
ISBN: 0387788875
Category : Medical
Languages : en
Pages : 326
Get Book
Book Description
Cyclin Dependent Kinase 5 provides a comprehensive and up-to-date collection of reviews on the discovery, signaling mechanisms and functions of Cdk5, as well as the potential implication of Cdk5 in the treatment of neurodegenerative diseases. Since the identification of this unique member of the Cdk family, Cdk5 has emerged as one of the most important signal transduction mediators in the development, maintenance and fine-tuning of neuronal functions and networking. Further studies have revealed that Cdk5 is also associated with the regulation of neuronal survival during both developmental stages and in neurodegenerative diseases. These observations indicate that precise control of Cdk5 is essential for the regulation of neuronal survival. The pivotal role Cdk5 appears to play in both the regulation of neuronal survival and synaptic functions thus raises the interesting possibility that Cdk5 inhibitors may serve as therapeutic treatment for a number of neurodegenerative diseases.
Author: Nancy Y. Ip
Publisher: Springer
ISBN: 9780387570440
Category : Medical
Languages : en
Pages : 0
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Book Description
Cyclin Dependent Kinase 5 provides a comprehensive and up-to-date collection of reviews on the discovery, signaling mechanisms and functions of Cdk5, as well as the potential implication of Cdk5 in the treatment of neurodegenerative diseases. Since the identification of this unique member of the Cdk family, Cdk5 has emerged as one of the most important signal transduction mediators in the development, maintenance and fine-tuning of neuronal functions and networking. Further studies have revealed that Cdk5 is also associated with the regulation of neuronal survival during both developmental stages and in neurodegenerative diseases. These observations indicate that precise control of Cdk5 is essential for the regulation of neuronal survival. The pivotal role Cdk5 appears to play in both the regulation of neuronal survival and synaptic functions thus raises the interesting possibility that Cdk5 inhibitors may serve as therapeutic treatment for a number of neurodegenerative diseases.
Author: Antonio Cardone
Publisher: CreateSpace
ISBN: 9781496016584
Category : Medical
Languages : en
Pages : 62
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Book Description
A high-affinity inhibitor protein called CIP, which can be produced by small truncations of p35, was earlier identified by Amin, Albers, and Pant. P35 is one of the physiological activators of cdk5, a member of the cyclin-dependent kinase family. These proteins are known to be associated with the hyperphosphorylation of specific neuronal proteins. This typically occurs in the case of neurodegenerative diseases such as Alzheimer s. In this paper the authors study in silico the binding mechanism of cdk5-p25 and cdk5-CIP complexes more in detail. This provides a better understanding of the inhibitory activity of the protein CIP. The authors use a geometry-based technique to verify the following hypothesis: p25 s truncation provides increased flexibility to CIP, and hence CIP is able to conform better to cdk5 interface than p25 is. Therefore CIP is expected to bind to cdk5 more easily than p25 and prevent it from reaching its active conformation. The authors' in silico study is based on a geometry-based alignment algorithm. The algorithm is capable of efficiently aligning two protein conformations with respect to their interfaces, which are represented as point sets. The algorithm is based on biochemical criteria as well as geometrical ones.
Author:
Publisher: ScholarlyEditions
ISBN: 1481686879
Category : Medical
Languages : en
Pages : 37
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Book Description
Cyclin-Dependent Kinases—Advances in Research and Application: 2013 Edition is a ScholarlyPaper™ that delivers timely, authoritative, and intensively focused information about ZZZAdditional Research in a compact format. The editors have built Cyclin-Dependent Kinases—Advances in Research and Application: 2013 Edition on the vast information databases of ScholarlyNews.™ You can expect the information about ZZZAdditional Research in this book to be deeper than what you can access anywhere else, as well as consistently reliable, authoritative, informed, and relevant. The content of Cyclin-Dependent Kinases—Advances in Research and Application: 2013 Edition has been produced by the world’s leading scientists, engineers, analysts, research institutions, and companies. All of the content is from peer-reviewed sources, and all of it is written, assembled, and edited by the editors at ScholarlyEditions™ and available exclusively from us. You now have a source you can cite with authority, confidence, and credibility. More information is available at http://www.ScholarlyEditions.com/.
Author: Juliana Dushanova
Publisher: IntechOpen
ISBN: 9789533078762
Category : Medical
Languages : en
Pages : 606
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Book Description
Parkinson's disease (PD) results primarily from the death of dopaminergic neurons in the substantia nigra. Current PD medications treat symptoms; none halt or retard dopaminergic neuron degeneration. The main obstacle to developing neuroprotective therapies is a limited understanding of the key molecular mechanisms that provoke neurodegeneration. The discovery of PD genes has led to the hypothesis that misfolding of proteins and dysfunction of the ubiquitin-proteasome pathway are pivotal to PD pathogenesis. Previously implicated culprits in PD neurodegeneration, mitochondrial dysfunction, and oxidative stress may also act in part by causing the accumulation of misfolded proteins, in addition to producing other deleterious events in dopaminergic neurons. Neurotoxin-based models have been important in elucidating the molecular cascade of cell death in dopaminergic neurons. PD models based on the manipulation of PD genes should prove valuable in elucidating important aspects of the disease, such as selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process.
Author:
Publisher: ScholarlyEditions
ISBN: 1464934754
Category : Science
Languages : en
Pages : 70
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Book Description
Cell Cycle Proteins: Advances in Research and Application: 2011 Edition is a ScholarlyBrief™ that delivers timely, authoritative, comprehensive, and specialized information about Cell Cycle Proteins in a concise format. The editors have built Cell Cycle Proteins: Advances in Research and Application: 2011 Edition on the vast information databases of ScholarlyNews.™ You can expect the information about Cell Cycle Proteins in this eBook to be deeper than what you can access anywhere else, as well as consistently reliable, authoritative, informed, and relevant. The content of Cell Cycle Proteins: Advances in Research and Application: 2011 Edition has been produced by the world’s leading scientists, engineers, analysts, research institutions, and companies. All of the content is from peer-reviewed sources, and all of it is written, assembled, and edited by the editors at ScholarlyEditions™ and available exclusively from us. You now have a source you can cite with authority, confidence, and credibility. More information is available at http://www.ScholarlyEditions.com/.
Author: Brett Lee Roach
Publisher:
ISBN: 9781085568166
Category : Cellular immunity
Languages : en
Pages : 83
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Book Description
Abstract: Reversible protein phosphorylation serves as a key mechanism to regulate virtually every cellular process by altering the activation status, subcellular location, stability and/or protein-protein interactions of the target protein. Protein kinases, the enzymes that catalyze the phosphorylation reaction, are often themselves subject to phosphoregulation. Cyclin-dependent kinase 5 (CDK5) is a proline-directed serine/threonine kinase essential for embryonic development whose over-activation has been implicated in several pathologies including neuro-degeneration, cancer cell metastasis and type II diabetes. Therefore, it is important to investigate molecular mechanism(s) that mediate regulation of CDK5 activity. Here, we identify and characterize a novel phosphoregulatory site on CDK5. Our mass spectrometry analysis identified seven putative phosphorylation sites on CDK5. Using phosphomimetic and non-phosphorylatable mutants, we determined that phosphorylation of S47, one of the identified sites, renders the kinase catalytically inactive. The inactivation of the kinase due to the phosphomimetic change at S47 results from the inhibition of its interaction with its cognate activator, p35 as determined by co-immunoprecipitation assays. Finally, we connect the effect of this regulatory event to a cellular phenotype by showing that the S47D CDK5 mutant inhibits cell migration. Together, these results have uncovered a potential physiological mechanism to regulate CDK5 activity. The evolutionary conservation of this residue in not only CDK5, but also in other CDK family members suggests that this phosphosite may represent a shared regulatory mechanism across the CDK family.
Author: Van G. Wilson
Publisher: Springer
ISBN: 3319500449
Category : Medical
Languages : en
Pages : 413
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Book Description
This is the second edition of a very well received book that details how the sumoylation system functions and how it modulates numerous cellular activities. SUMO is a post-translational modifier in the ubiquitin super-family that has gained recognition over the last twenty years as an essential and prevalent regulatory molecule. Individual chapters explore the biochemistry, molecular biology, and cell biology of the sumoylation system and its substrate proteins. The book is divided into three themed parts: Molecular Functions (I), Cell Growth Regulation (II), and Diseases (III). Parts I and II focus on the contribution of sumoylation to cellular activities in both the nuclear and cytoplasmic compartments. The nuclear activities covered include nucleic acid metabolism (both RNA and DNA), chromosome structure and replication, and nucleocytoplasmic transport. Cytoplasmic processes presented include regulation of membrane ion channels, general metabolism, and apoptotic signalling. Topics in Part III include the role of sumoylation in developmental abnormalities (craniofacial and cardiovascular), diabetes, neurodegenerative diseases, cancer, and infections with viruses and bacteria. Each of the corresponding chapter authors is an active researcher who has made significant contributions to understanding sumoylation. This second edition provides updates and revisions to most of the original chapters plus adds six new chapters to address important developing areas of sumoylation research. This volume is intended for a scientific audience from undergraduates to independent researchers. The content will serve as both a solid introduction for the novice reader and an in depth treatment for the advanced scholar.
Author: Peter K. Vogt
Publisher: Springer
ISBN: 9783642719431
Category : Medical
Languages : en
Pages : 169
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Book Description
More than 10 years ago, the discovery of cyclin-dependent ki nases (Cdks) ushered in a new era in the understanding of cell proliferation and its control. Not only were both of the known cell cycle transitions, from G 1 to S phase and G2 to M phase, found to be dependent on these protein kinases, but the reg ulatory assumption intrinsic to cyclin-dependent kinases, a stable inactive catalytic subunit (the Cdk) and an unstable requisite positive regulatory activating subunit (the cyclin), led to a simple model for cell cycle control. Modulation of cyclin accumulation, and thereby Cdk activation, was proposed to be the overarching principle governing the passage through cell cycle phases. An other reality to emerge from the discovery of Cdks was the ex ceptional degree of evolutionary conservation maintained in the machinery and organization of proliferation control. Not only were Cdks shown to be structurally conserved between yeast and man, but mammalian Cdks could substitute functionally for the endogenous enzymes in a yeast cell. The problem of cell cycle control was thought to have been virtually solved. The ensuing years have provided a much more complex view of cell cycle control and the role and regulation of Cdks. The uncritical enthusiasm with which many of the ideas were em braced has required tempering. For example, although Cdks appear to be highly conserved phylogenetically, cyclins are much less so.
Author: Ekrem Dere
Publisher: Academic Press
ISBN: 0124159273
Category : Medical
Languages : en
Pages : 317
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Book Description
Gap junctions between glial cells or neurons are ubiquitously expressed in the mammalian brain and play a role in brain development including cell differentiation, cell migration and survival, and tissue homeostasis, as well as in human diseases including hearing loss, neuropathies, epilepsy, brain trauma, and cardiovascular disease. This volume provides neuroscience researchers and students with a single source for information covering the physiological, behavioral and pathophysiological roles of gap junctions in the brain. In addition, the book also discusses human disease conditions associated with mutations in single gap junction connexion genes, making it applicable to clinicians doing translational research. Finally, it includes reviews of pharmacological studies with gap junction blockers and openers, summarizing information obtained from phenotyping gap junctions mouse mutants. Serves as the most current and comprehensive reference available covering the physiological, behavioral and pathophysiological roles of gap junctions in the brain Chapters summarize knowledge of the basic physiology of gap junctions in the brain, as well as of human disease conditions associated with mutations in single gap junction connexin genes Includes reviews of pharmacological studies with gap junction blockers and openers, summarizing information obtained from phenotyping gap junctions mouse mutants
