Are you looking for read ebook online? Search for your book and save it on your Kindle device, PC, phones or tablets. Download JAK-STAT Pathway in Disease PDF full book. Access full book title JAK-STAT Pathway in Disease by Jr., Richard H. Bell. Download full books in PDF and EPUB format.
Author: Jr., Richard H. Bell Publisher: CRC Press ISBN: 1498713769 Category : Medical Languages : en Pages : 191
Book Description
This book reviews current understanding of the biological roles of the signal transducer and activator of transcription (STAT) proteins and their dysregulation in diseases. STAT proteins were named after their role as signal transducers and activators of transcription. STAT proteins are highly conserved among species, thus reflecting the importance
Author: Jr., Richard H. Bell Publisher: CRC Press ISBN: 1498713769 Category : Medical Languages : en Pages : 191
Book Description
This book reviews current understanding of the biological roles of the signal transducer and activator of transcription (STAT) proteins and their dysregulation in diseases. STAT proteins were named after their role as signal transducers and activators of transcription. STAT proteins are highly conserved among species, thus reflecting the importance
Author: Alister C. Ward Publisher: Springer Science & Business Media ISBN: 9780306474248 Category : Science Languages : en Pages : 154
Book Description
This book for the first time comprehensively surveys the research investigating the Jak-Stat pathway and its role in normal blood development as well as its perturbation in disease. It draws on the expertise of world-renowned medical researchers to take the reader from basic biology through to recent therapeutic advances.
Author: Ritobrata Goswami Publisher: CRC Press ISBN: 1351042440 Category : Medical Languages : en Pages : 339
Book Description
JAK-STAT pathway is one of the few signal transduction pathways that transduce signals involved in multiple homeostatic biological processes including cell differentiation and proliferation, cell death, hematopoiesis and immune responses. JAK-STAT is an elegant pathway that is relatively simple and evolutionary conserved as gene expression is regulated by external parameters. Activated by growth factors or cytokines, this signal transduction cascade regulates the transcription of genes at the nucleus. Mutations and polymorphisms in JAK-STAT pathway are associated with inflammatory diseases and cancers that could impede regular homeostasis. Features: Details activation and microRNA-mediated regulation of JAK-STAT pathway Provides exclusive information about the association of the pathway in various diseases including allergic inflammation, neuro-inflammatory disorder, atopic dermatitis hematopoietic malignancies, cardiovascular disorder, renal disorder, immunodeficiency, liver fibrosis, diabetes and obesity that affect individuals across the globe Clinical relevance of the signaling cascade has been discussed in context of novel class of therapeutics that targets this pathway. An overview of JAK-STAT signaling pathway and the structure-function relationship of different domains of the cascade are discussed. This book provides detailed information on various diseases that are associated with JAK-STAT pathway. It will act as a very good reference book for basic science researchers, academicians, industry professionals involved in translational research leading to product development. This book will excite future professionals towards better understanding of the regulation of this pathway, its association with other signaling cascades to design novel therapeutics.
Author: Thomas Decker Publisher: Springer Science & Business Media ISBN: 3709108918 Category : Science Languages : en Pages : 451
Book Description
JAK tyrosine kinases and STAT transcription factors constitute a signaling pathway, which is activated by cytokines. By activating gene transcription it regulates essential biological responses to environmental cues. The Jak-Stat pathway is involved in the regulation of cell development, differentiation, proliferation and apoptosis. Improper function may contribute to hematopoietic malignancies and cancer. This book provides comprehensive insights into the latest basic and clinical developments in the field. The first part reviews recent findings and new technologies pertaining to basics of Jak-Stat function. The second part describes the evolution of Jak-Stat signaling and the role of the pathway in invertebrate organisms. The third part focuses on Jak-Stat signaling in hematopoietic cells under both physiological and pathophysiological conditions. Finally, chapters in the fourth section describe the relationship of Jak-Stat signaling to various states of disease, particularly infection, leukemias and solid cancers. The book is intended for all scientists in molecular biology, biochemistry and cell biology dealing with biomedical issues.
Author: Richard H. Bell, Jr. Publisher: CRC Press ISBN: Category : Medical Languages : en Pages : 348
Book Description
Performing a surgical operation must be one of the most complex motor tasks undertaken by humans. To the student rotating on a third-year clerkship, or to the resident beginning a surgical career, the complexity can no doubt be daunting. It is the goal of this handbook to try to bring some degree of order to the complexity, focusing on many of the common operations in general, plastic, thoracic, and vascular surgery, and in organ transplantation. We have done so by dividing each procedure into specific and well-defined steps.
Author: Publisher: ISBN: Category : Languages : en Pages : 188
Book Description
Dysregulation of the Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway is critically involved in the pathogenesis of multiple sclerosis (MS)/experimental autoimmune encephalomyelitis (EAE). Suppressor Of Cytokine Signaling (SOCS) proteins are the negative regulators of the JAK/STAT pathway. To determine the role of SOCS3 in myeloid cells in EAE, mice with conditional SOCS3 deletion in myeloid cells (LysMCre-SOCS3fl/fl) were created and tested. LysMCre-SOCS3fl/fl mice develop a severe, non-resolving atypical form of disease, characterized by lesions and extensive neutrophil and other inflammatory cell infiltrates in the cerebellum and brainstem, elevated STAT activation, elevated cytokine, chemokine and iNOS expression, and prominent axonal damage. Mechanistically, loss of SOCS3 leads to a pronounced polarization to the pro-inflammatory macrophage (M1) phenotype, which promotes T-cell proliferation and polarization to Th1 and Th17 phenotypes, and has functional consequences for neurons. Cerebellum- and brainstem-infiltrating SOCS3-deficient neutrophils play a critical role in mediating atypical EAE development. Antibody-mediated depletion of neutrophils and blocking CXCR2 signaling ameliorates atypical EAE development. Functionally, SOCS3-deficient neutrophils produce high levels of CXCL2, CCL2, CXCL10, nitric oxide (NO), TNF-a and IL-1b, recruiting themselves and other inflammatory infiltrates into the cerebellum and brainstem and creating a pro-inflammatory environment. Importantly, neutrophils may have a direct pathogenic role in driving axonal damage by local production of NO. As dysregulation of the JAK/STAT pathway has been implicated in MS/EAE, we utilized AZD1480, a JAK1/2 small molecule inhibitor, to investigate its therapeutic potential in models of EAE. Inhibition of JAK1/2 restrains pro-inflammatory responses in both T cells and myeloid cells. AZD1480 treatment suppresses differentiation of Th1 and Th17 cells and exerts an inhibitory effect on M1 polarization. Using AZD1480 for proof-of-principle, we demonstrate that inhibiting the JAK/STAT pathway has striking clinical efficacy in five EAE models: classical EAE, atypical EAE, relapsing-remitting (RR)-EAE, Th1 cell-mediated EAE, and Th17 cell-mediated EAE. In conclusion, these studies reveal a role for SOCS3 in myeloid cells to provide protection against detrimental inflammatory responses in the central nervous system. In addition, our data suggest the feasibility of the JAK/STAT pathway as a therapeutic target for neuroinflammatory diseases.
Author: Paul S. Yamauchi Publisher: Springer ISBN: 3319668846 Category : Medical Languages : en Pages : 567
Book Description
Written by leading experts in the field and designed for dermatologists and residents, this book includes evidence-based medicine that underscores the clinical data, as well as practical tips on how to use both biologic and systemic agents in the field of dermatology. In the past decade, there have been several groundbreaking advances in medical dermatology. Novel biologic and systemic agents have been developed to treat inflammatory disorders, including psoriasis and atopic dermatitis, as well as skin malignancies such as melanoma. Biologic and Systemic Agents in Dermatology encompasses these developments by describing the mechanism of action of these various agents and the clinical efficacy and safety to treating these respective disorders. The utilization of biologic and systemic agents in other dermatologic conditions, pharmacoeconomics, pharmacovigilance, and clinical trials outcomes are discussed as well as topics including tumor necrosis, conventional systemic agents for psoriatic disease, and oral agents for atopic dermatitis.
Author: Todd Leff Publisher: John Wiley & Sons ISBN: 9783527629534 Category : Science Languages : en Pages : 530
Book Description
This timely and most comprehensive reference available on the topic covers all the different aspects vital in the fight against the global obesity epidemic. Following a look at adipose tissue development and morphology, the authors go on to examine its metabolic and endocrine functions and its role in disease. The final section deals with comparative and evolutionary aspects of the tissue. The result is an essential resource for cell and molecular biologists, physiologists, biochemists, pharmacologists, and those working in the pharmaceutical industry.
Author: Jr., Richard H. Bell
Author: Jr., Richard H. Bell
Author: Alister C. Ward
Author: Ritobrata Goswami
Author: Thomas Decker
Author: Alister C. Ward
Author: 
Author: Richard H. Bell, Jr.
Author: 
Author: Paul S. Yamauchi
Author: Todd Leff