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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.
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.
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
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.
This Methods in Molecular Biology volume covers JAK and STAT specific approaches, the negative regulators of the pathway, and production and crystallization of JAK and STAT proteins, and more.Includes protocols, materials lists, tips and troubleshooting advice."
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.
Background: Stem cells have been identified within proliferating infantile haemangioma (IH), the most common tumour of infancy, and have been demonstrated to play a critical role in the rapid proliferation and gradual involution of this tumour. There is accumulating evidence showing that IH is caused by aberrant proliferation and differentiation of a haemogenic endothelium (HE). This HE possesses a functional capacity to undergo primitive erythropoiesis in vitro. Short chain fatty acid (SCFA) derivatives have been shown to stimulate cell proliferation and induce STAT-5 activation in various haematopoietic cell lines. Aims: The aims of this study were to investigate (1) the activity of the components of JAK-STAT pathway within the three phases of IH development; (2) the haematopoietic capacity of IH in vitro; and (3) the effects of SCFAs, butyric acid and propionic acid, to induce erythroid differentiation of explant-derived cells (IHEDCs) in culture. Methods: The presence of pSTAT proteins in proliferating, involuted and involuting IH were investigated using 3,3'-diaminobenzidine (DAB) and immunofluorescent (IF) immunohistochemical (IHC) staining, 1-DE Western Blotting, and NanoString analysis. Proliferating IH explants were cultured using an in vitro model and the IHEDCs emanating from the explants were harvested. Cell suspension of volume equivalent to 5x105 live cells was plated on Matrigel and incubated in 0.05-1mM butyric acid, RPMI and 0.05-1mM propionic acid, and 0.05M DMSO (positive control) in each of RPMI media only, RPMI enriched with iron and MCDB media. Media was changed daily and cells were extracted and quantified following 24-72 hours in culture. Differentiated IHEDCs were characterised by IF immunocytochemical (ICC) staining with glycophorin-A. Results: Protein and genomic data reveal the expression of STATs 1, 3 and 5 which are activated in IH, particularly in the proliferative phase, with expression tapering as the lesion involutes. pSTAT3 is expressed most abundantly with pSTAT5 the least abundant. Low concentrations of both butyric acid and propionic acid significantly increased proliferation and differentiation of IHEDCs into blast colonies and the production of bi-concave cells within 72 hours in culture. These enucleated bi-concave cells expressed the erythrocyte-specific marker, glycophorin-A. Conclusion: The findings of SCFAs promoting proliferation and differentiation of IHEDCs into blast colonies and differentiated erythrocytes reveal a novel role for SCFAs in human haematopoietic differentiation, possibly via pSTAT-5 signalling. IH offers a simple and novel in vitro model for generating haematopoietic precursors and production of human erythrocytes.
This book focuses on three of the main categories of myeloproliferative neoplasm: polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Relevant laboratory and clinical advances are comprehensively covered, and great emphasis is placed on the practical issues that challenge physicians in their daily practice. The main topics considered thus include contemporary diagnostic approaches, the value and limitations of mutation screening for diagnostic and prognostic purposes, risk stratification in terms of both survival and other disease complications such as leukemic transformation and thrombosis, and modern therapeutic strategies, including conventional drugs, allogeneic stem cell transplantation, and experimental drugs still under study. The reader will find Critical Concepts and Management Recommendations in Myeloproliferative Neoplasms to be an invaluable and up-to-date source of information from leading authorities in the field.