000 04400nam a22005055i 4500
001 978-0-387-98173-4
003 DE-He213
005 20251006084433.0
007 cr nn 008mamaa
008 100301s2009 xxu| s |||| 0|eng d
020 _a9780387981734
020 _a99780387981734
024 7 _a10.1007/978-0-387-98173-4
_2doi
082 0 4 _a571.4
_223
100 1 _aBeckerman, Martin.
_eauthor.
245 1 0 _aCellular Signaling in Health and Disease
_h[electronic resource] /
_cby Martin Beckerman.
264 1 _aNew York, NY :
_bSpringer US,
_c2009.
300 _bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
490 1 _aBiological and Medical Physics, Biomedical Engineering,
_x1618-7210
505 0 _aMetabolic Syndromes -- Energy Balance -- Insulin Signaling and Type 2 Diabetes -- Metabolic Program Execution and Switching -- Cholesterol -- Atherosclerosis -- Chronic Inflammation -- Redox Signaling -- Cancer -- The Cell Cycle -- Cell Cycle Checkpoints and DNA Damage Repair -- Apoptosis and Senescence -- Epigenetics -- Tumor Growth -- Tumor Metabolism -- Metastasis -- Neurodegeneration -- Protein Folding, Misfolding, and Aggregation -- Alzheimer's Disease -- Chaperones, Endoplasmic Reticulum Stress, and the Unfolded Protein Response -- Parkinson's Disease -- Huntington's Disease and Amyotrophic Lateral Sclerosis.
520 _aIn today's world, three great classes of non-infectious diseases - the metabolic syndromes (such as type 2 diabetes and atherosclerosis), the cancers, and the neurodegenerative disorders - have risen to the fore. These diseases, all associated with increasing age of an individual, have proven to be remarkably complex and difficult to treat. This is because, in large measure, when the cellular signaling pathways responsible for maintaining homeostasis and health of the body become dysregulated, they generate equally stable disease states. As a result the body may respond positively to a drug, but only for a while and then revert back to the disease state. Cellular Signaling in Health and Disease summarizes our current understanding of these regulatory networks in the healthy and diseased states, showing which molecular components might be prime targets for drug interventions. This is accomplished by presenting models that explain in mechanistic, molecular detail how a particular part of the cellular signaling web operates properly in health and improperly in disease. The stability of the health- and disease-associated states is dynamic and supported by multiple feedback loops acting positively and negatively along with linkages between pathways. During the past few years an ongoing series of important discoveries have been made that advance our understanding of how the body works and may guide us on how to better deal with these diseases. These include the discovery of chronic inflammation as a causal factor in all of these disease classes, the appearance of reactive oxygen species as a messenger molecule that can act both positively and negatively, the propensity of proteins to misfold into aggregation- and disease-prone forms, and the rise of epigenetics including the emergence of small non-coding RNA with important regulatory functions out of the so-called junk RNA. Chapters are devoted to each of these classes of findings with additional details integrated into the chapters dealing directly with the diseases. The connections responsible for maintaining stability are explored in depth.
650 0 _aPHYSICS.
650 0 _aMEDICINE.
650 0 _aBIOCHEMISTRY.
650 0 _aCYTOLOGY.
650 0 _aBIOMEDICAL ENGINEERING.
650 1 4 _aPHYSICS.
650 2 4 _aBIOPHYSICS AND BIOLOGICAL PHYSICS.
650 2 4 _aCELL BIOLOGY.
650 2 4 _aMOLECULAR MEDICINE.
650 2 4 _aBIOMEDICAL ENGINEERING.
650 2 4 _aBIOCHEMISTRY, GENERAL.
710 2 _aSpringerLink (Online service)
773 0 _tSpringer eBooks
776 0 8 _iPrinted edition:
_z9780387981727
830 0 _aBiological and Medical Physics, Biomedical Engineering,
_x1618-7210
856 4 0 _uhttp://dx.doi.org/10.1007/978-0-387-98173-4
_zVer el texto completo en las instalaciones del CICY
912 _aZDB-2-PHA
942 _2ddc
_cER
999 _c59599
_d59599