Study of Interaction of the Cyclin-Dependent Kinase 5 With Its Activator, P25 and With the P25-Derived Inhibitor, CIP PDF Download
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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: 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: nist
Publisher:
ISBN: 9781493765515
Category :
Languages : en
Pages : 64
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Book Description
A high-affinity inhibitor protein called CIP, which canbe 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 specificneuronal proteins. This typically occurs in the case ofneurodegenerative diseases such as Alzheimer s. In this paper we 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. We use a geometry-based technique to verify the following hypothesis: p25 s truncation providesincreased 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. Our in silico study is based on a geometry-based alignment algorithm. The algorithm is capable of efficiently aligningtwo 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. Our results indicate the validity of the flexibility hypothesis. They could be used, along with some observations we made on cdk5 activation, as basis for a set of verytargeted and therefore more efficient molecular dynamics simulations.
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: Lingyan Zhang
Publisher:
ISBN: 9781124218359
Category :
Languages : en
Pages : 182
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Book Description
Cylcine-dependent kinase 5 (Cdk5) is a member of the CDK family, but, distinct from other CDKs, it does not participate in cell cycle regulation. Instead, its activation requires association with its neuron-specific regulator p35 or p39 and, thus, Cdk5's activity has mainly been associated with the central nervous system (CNS). Cdk5-p35 complex has been found to be critical for post mitotic neuronal activities such as neurite outgrowth, axon guidance, neuronal migration and neuronal survival. Under pathological conditions, however, the p35 regulatory subunit can undergo proteolysis to form CDK5/p25 and a 10 kDa amino-terminal fragment, p10. While CDK5/p35 is essential for normal brain development and function, CDK5/p25 causes neuron death associated with Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and other human neurodegenerative disorders. While all studies have placed p25 at the center of attention, we have discovered that p10 may serve an important role in protecting neurons from toxicity associated with CDK5/p25. Our studies confirm the common wisdom that CDK5/p25 is inherently neurotoxic, but we herein propose that cell death per se is directly attributable to the rapid degradation of p10. Our research demonstrated the protective effect of p10 against toxicity induced by Cdk5-p25 complex in different cell types. We also showed that p10 can protect neurons from MPP+ induced toxicity and block neurons from cell cycle re-entry induced by aberrant CDK5/p25 activity. Interestingly, although p10 can reduce CDK5/p25 activity in cells, it doesn't directly inhibit CDK5/p25 kinase activity in vitro. This leads us to propose that p10 might associate with other proteins in cells to form protein complex, which is required for its protective effects against CDK5/p25.
Author:
Publisher:
ISBN:
Category : Cells
Languages : en
Pages : 652
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Book Description
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:
Publisher:
ISBN:
Category : Medicine
Languages : en
Pages : 1828
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Book Description
Author: Felipe Sierra
Publisher: Springer
ISBN: 3319232460
Category : Medical
Languages : en
Pages : 637
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Book Description
This book provides the first comprehensive overview of a new scientific discipline termed Geroscience. Geroscience examines the molecular and cellular mechanisms that might explain why aging is the main risk factor for most chronic diseases affecting the elderly population. Over the past few decades, researchers have made impressive progress in understanding the genetics, biology and physiology of aging. This book presents vital research that can help readers to better understand how aging is a critical malleable risk factor in most chronic diseases, which, in turn, could lead to interventions that can help increase a healthy lifespan, or ‘healthspan.’ The book begins with an analysis of the Geroscience hypothesis, as well as the epidemiological underpinnings that define aging as a candidate main risk factor for most chronic diseases. Next, each chapter focuses on one particular disease, or group of diseases, with an emphasis on how basic molecular and cellular biology might explain why aging is a major risk factor for it. Coverage in the book includes: cancer, cardiovascular disease, dementias, stroke, Parkinson's and Alzheimer’s diseases, osteoporosis, arthritis, diabetes asthma, emphysema, kidney disease, vision impairment, and AIDS/HIV. It finishes with a chapter on pain in the elderly and an overview of future steps needed to bring the newly acquired knowledge into the clinic and the public at large.
Author: Lorenzo Galluzzi
Publisher: Humana Press
ISBN: 9781627032384
Category : Science
Languages : en
Pages : 0
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Book Description
Cell senescence is the process whereby cells permanently lose the possibility to proliferate without undergoing cell death, and occurs in a plethora of distinct model organisms. In Cell Senescence: Methods and Protocols, expert researchers in the field detail the methods that are now commonly used to study cell senescence, in model organisms encompassing bacteria, fungi, worms, flies, zebrafish, and mammalian cells. These techniques cover the study of all the morphological, biochemical and functional manifestations of senescence at the cellular level and include protocols for population analyses and high-throughput approaches in suitable model organisms. Written in the highly successful Methods in Molecular BiologyTM series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls.
Author: Renato Paro
Publisher: Springer Nature
ISBN: 3030686701
Category : Science
Languages : en
Pages : 215
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Book Description
This open access textbook leads the reader from basic concepts of chromatin structure and function and RNA mechanisms to the understanding of epigenetics, imprinting, regeneration and reprogramming. The textbook treats epigenetic phenomena in animals, as well as plants. Written by four internationally known experts and senior lecturers in this field, it provides a valuable tool for Master- and PhD- students who need to comprehend the principles of epigenetics, or wish to gain a deeper knowledge in this field. After reading this book, the student will: Have an understanding of the basic toolbox of epigenetic regulation Know how genetic and epigenetic information layers are interconnected Be able to explain complex epigenetic phenomena by understanding the structures and principles of the underlying molecular mechanisms Understand how misregulated epigenetic mechanisms can lead to disease
