Titlebook: Apoptosis, Cell Signaling, and Human Diseases; Molecular Mechanisms Rakesh Srivastava Book 2007 Humana Press 2007 DNA.HIV.gene expression.g

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Protein Kinase C and Apoptosisproliferation and survival and their expression or activity is altered in some human diseases, particularly cancer. The development and utilization of PKC isoform specific tools, including dominant inhibitory kinases, mouse models in which specific PKC isoforms have been disrupted, and PKC isoform s

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MAPK Signaling in Human Diseasesng cell proliferation, differentiation, motility, and survival. Three subfamilies of MAPK have been extensively studied: extracellular signal-regulated kinases (ERK), p38-MAPK, and c-Jun N-terminal kinase (JNK). The ERKs play roles in cell proliferation, survival, and motility, and inhibitors of thi

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Serine/Threonine Protein Phosphatases in Apoptosis, myosin light chain, lamin B, some caspases and their inhibitors, as well as transcriptions factors like CREB and NF-kB/I-kB. Most is known about the protein phosphatases (PPs) PP1, PP2A, PP2B/calcineurin, PP4/PPX, and PP5. With the possible exception of PP5, which so far appears to mainly promote

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Urokinase/Urokinase Receptor-Mediated Signaling in Cancerits receptor (uPAR), and its major inhibitor plasminogen activator inhibtor-1 (PAI-1) or -2 (PAI-2) are activated by common signaling mechanisms. In tumor cells of mesenchymal or epithelial origin uPA, uPAR, and PAIs or metallo-proteinases (MMPs) are overexpressed and these molecules are implicated

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Signaling Pathways That Protect the Heart Against Apoptosis Induced by Ischemia and Reperfusionly regulated. Two mechanisms of apoptosis involve the extrinsic death receptor pathway and the intrinsic mitochondrial pathway. Both pathways lead to the activation of effector caspases, resulting in cell death. The mitochondrial pathway plays a key role in initiating apoptosis after ischemia and re

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