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10 - Progress in achieving proof of concept for p38 kinase inhibitors

Target Validation in Drug Discovery, 2007, p.179-198

2007 Elsevier Inc. ;ISBN: 0123693934 ;ISBN: 9780123693938 ;DOI: 10.1016/B978-012369393-8/50011-0

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  • Title:
    10 - Progress in achieving proof of concept for p38 kinase inhibitors
  • Author: Adams, Jerry L ; Lee, John C.
  • Is Part Of: Target Validation in Drug Discovery, 2007, p.179-198
  • Description: The availability of selective p38 inhibitors provides the critical tools required to delineate the role that protein kinases play in signaling pathways. Activation of p38 has been observed in various organisms as a response to many stimuli. The p38α orthologs in yeast, worm, and frog have been implicated in osmoregulation, stress responses, and cell-cycle regulation. Downstream substrates of p38 MAP kinases are MAPKAPK2 and MAPKAPK3, which phosphorylate various substrates—including small heat shock protein 27 (HSP27), lymphocyte-specific protein 1(LSP1), cAMP response element-binding protein (CREB), transcription factor (ATF1), SRF, and tyrosine hydroxylase. The mechanism by which p38 MAP kinase inhibitors suppress expression of inflammatory cytokines has been elusive. The initial focus on p38 inhibitors as potential disease-modifying agents to treat rheumatoid arthritis has expanded to the exploration of psoriasis, Crohn's disease, inflammatory bowel disease, chronic obstructive pulmonary disease, cardiovascular disease, stroke, cardiac hypertrophy, Alzheimer's disease, and vascular injury. The role of MAPKAPK-2 in p38-induced inflammatory cytokine synthesis has been validated in a knock-out mouse.
  • Publisher: Elsevier Inc
  • Language: English
  • Identifier: ISBN: 0123693934
    ISBN: 9780123693938
    DOI: 10.1016/B978-012369393-8/50011-0
  • Source: Ebook Central Academic Complete
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