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Pamela S Ohashi - One of the best experts on this subject based on the ideXlab platform.
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lps tlr4 Signal Transduction Pathway
Cytokine, 2008Co-Authors: Yongchen Lu, Pamela S OhashiAbstract:The stimulation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) induces the release of critical proinflammatory cytokines that are necessary to activate potent immune responses. LPS/TLR4 Signaling has been intensively studied in the past few years. Here we review molecules involved in TLR4-mediated Signaling, including players that are involved in the negative regulation of this important Pathway.
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LPS/TLR4 Signal Transduction Pathway
Cytokine, 2008Co-Authors: Yongchen Lu, Pamela S OhashiAbstract:The stimulation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) induces the release of critical proinflammatory cytokines that are necessary to activate potent immune responses. LPS/TLR4 Signaling has been intensively studied in the past few years. Here we review molecules involved in TLR4-mediated Signaling, including players that are involved in the negative regulation of this important Pathway.
Roger J Davis - One of the best experts on this subject based on the ideXlab platform.
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the jnk Signal Transduction Pathway
Current Opinion in Cell Biology, 2007Co-Authors: Claire R Weston, Roger J DavisAbstract:The c-Jun NH 2 -terminal kinases (JNKs) are an evolutionarily conserved sub-group of mitogen-activated protein (MAP) kinases. Recent studies have improved our understanding of the physiological function of the JNK Pathway. Roles of novel molecules that participate in the JNK Pathway have been defined and new insight into the role of JNK in survival Signaling, cell death, cancer and diabetes has been achieved.
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jund mediates survival Signaling by the jnk Signal Transduction Pathway
Molecular Cell, 2003Co-Authors: Jennifer A Lamb, Juanjose Ventura, Patricia M Hess, Richard A Flavell, Roger J DavisAbstract:Abstract The c-Jun NH 2 -terminal kinase (JNK) can cause cell death by activating the mitochondrial apoptosis Pathway. However, JNK is also capable of Signaling cell survival. The mechanism that accounts for the dual role of JNK in apoptosis and survival Signaling has not been established. Here we demonstrate that JNK-stimulated survival Signaling can be mediated by JunD. The JNK/JunD Pathway can collaborate with NF-κB to increase antiapoptotic gene expression. This observation accounts for the ability of JNK to cause either survival or apoptosis in different cellular contexts. Furthermore, these data illustrate the general principal that Signal Transduction Pathway integration is critical for the ability of cells to mount an appropriate biological response to a specific challenge.
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the jnk Signal Transduction Pathway
Current Opinion in Genetics & Development, 2002Co-Authors: Claire R Weston, Roger J DavisAbstract:The c-Jun NH(2)-terminal kinase (JNK) is a member of an evolutionarily conserved sub-family of mitogen-activated protein (MAP) kinases. Recent studies have led to progress towards understanding the physiological function of the JNK Signaling Pathway, including the analysis of the phenotype of knockout mice. An important role for JNK in the non-canonical Wnt-Signaling Pathway has been established. Insight into the role of scaffold proteins that may assemble functional JNK modules has been achieved. In addition, a small molecule pharmacological inhibitor of JNK has been described and it is likely that this drug will facilitate future studies of JNK function.
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nuclear accumulation of nfat4 opposed by the jnk Signal Transduction Pathway
Science, 1997Co-Authors: Chiwing Chow, Julie Cavanagh, Martin Dickens, Mercedes Rincon, Roger J DavisAbstract:The nuclear factor of activated T cells (NFAT) group of transcription factors is retained in the cytoplasm of quiescent cells. NFAT activation is mediated in part by induced nuclear import. This process requires calcium-dependent dephosphorylation of NFAT caused by the phosphatase calcineurin. The c-Jun amino-terminal kinase (JNK) phosphorylates NFAT4 on two sites. Mutational removal of the JNK phosphorylation sites caused constitutive nuclear localization of NFAT4. In contrast, JNK activation in calcineurin-stimulated cells caused nuclear exclusion of NFAT4. These findings show that the nuclear accumulation of NFAT4 promoted by calcineurin is opposed by the JNK Signal Transduction Pathway.
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a cytoplasmic inhibitor of the jnk Signal Transduction Pathway
Science, 1997Co-Authors: Martin Dickens, Jeffrey Scott Rogers, Julie Cavanagh, Art Raitano, Zhengui Xia, Jocelyn R Halpern, Michael E Greenberg, Charles L Sawyers, Roger J DavisAbstract:The c-Jun amino-terminal kinase (JNK) is a member of the stress-activated group of mitogen-activated protein (MAP) kinases that are implicated in the control of cell growth. A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned. JIP-1 caused cytoplasmic retention of JNK and inhibition of JNK-regulated gene expression. In addition, JIP-1 suppressed the effects of the JNK Signaling Pathway on cellular proliferation, including transformation by the Bcr-Abl oncogene. This analysis identifies JIP-1 as a specific inhibitor of the JNK Signal Transduction Pathway and establishes protein targeting as a mechanism that regulates Signaling by stress-activated MAP kinases.
Tarek Msadek - One of the best experts on this subject based on the ideXlab platform.
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A matter of life and death: cell wall homeostasis and the WalKR (YycGF) essential Signal Transduction Pathway
Molecular Microbiology, 2008Co-Authors: Sarah Dubrac, Paola Bisicchia, Kevin Devine, Tarek MsadekAbstract:The WalK/WalR (aka YycG/YycF) two-component system (TCS), originally identified in Bacillus subtilis, is very highly conserved and specific to low G+C Gram-positive bacteria, including a number of important pathogens. An unusual feature is that this system is essential for viability in most of these bacteria. Recent studies have revealed conserved functions for this system, defining this Signal Transduction Pathway as a crucial regulatory system for cell wall metabolism, that we have accordingly renamed WalK/WalR. Here we review the cellular role of the WalK/WalR TCS in different bacterial species, focusing on the function of genes in its regulon, as well as variations in walRK operon structure and the composition of its regulon. We also discuss the nature of its essentiality and the potential type of Signal being sensed. The WalK histidine kinase of B. subtilis has been shown to localize to the divisome and we suggest that the WalKR system acts as an information conduit between extracytoplasmic cellular structures and intracellular processes required for their synthesis, playing a vital role in effectively co-ordinating peptidoglycan plasticity with the cell division process.
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Signal Transduction Pathway controlling synthesis of a class of degradative enzymes in bacillus subtilis expression of the regulatory genes and analysis of mutations in degs and degu
Journal of Bacteriology, 1990Co-Authors: Tarek Msadek, D Henner, A Klier, Georges Rapoport, Frank Kunst, Raymond DedonderAbstract:The rates of synthesis of a class of both secreted and intracellular degradative enzymes in Bacillus subtilis are controlled by a Signal Transduction Pathway defined by at least four regulatory genes: degS, degU, degQ (formerly sacQ), and degR (formerly prtR). The DegS-DegU proteins show amino acid similarities with two-component procaryotic modulator-effector pairs such as NtrB-NtrC, CheA-CheY, and EnvZ-OmpR. By analogy with these systems, it is possible that DegS is a protein kinase which could catalyze the transfer of a phosphoryl moiety to DegU, which acts as a positive regulator. DegR and DegQ correspond to polypeptides of 60 and 46 amino acids, respectively, which also activate the synthesis of degradative enzymes. We show that the degS and degU genes are organized in an operon. The putative sigma A promoter of the operon was mapped upstream from degS. Mutations in degS and degU were characterized at the molecular level, and their effects on transformability and cell motility were studied. The expression of degQ was shown to be subject both to catabolite repression and DegS-DegU-mediated control, allowing an increase in the rate of synthesis of degQ under conditions of nitrogen starvation. These results are consistent with the hypothesis that this control system responds to an environmental Signal such as limitations of nitrogen, carbon, or phosphate sources. Images
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Signal Transduction Pathway controlling synthesis of a class of degradative enzymes in Bacillus subtilis: expression of the regulatory genes and analysis of mutations in degS and degU.
Journal of Bacteriology, 1990Co-Authors: Tarek Msadek, D Henner, A Klier, Georges Rapoport, Frank Kunst, Raymond DedonderAbstract:The rates of synthesis of a class of both secreted and intracellular degradative enzymes in Bacillus subtilis are controlled by a Signal Transduction Pathway defined by at least four regulatory genes: degS, degU, degQ (formerly sacQ), and degR (formerly prtR). The DegS-DegU proteins show amino acid similarities with two-component procaryotic modulator-effector pairs such as NtrB-NtrC, CheA-CheY, and EnvZ-OmpR. By analogy with these systems, it is possible that DegS is a protein kinase which could catalyze the transfer of a phosphoryl moiety to DegU, which acts as a positive regulator. DegR and DegQ correspond to polypeptides of 60 and 46 amino acids, respectively, which also activate the synthesis of degradative enzymes. We show that the degS and degU genes are organized in an operon. The putative sigma A promoter of the operon was mapped upstream from degS. Mutations in degS and degU were characterized at the molecular level, and their effects on transformability and cell motility were studied. The expression of degQ was shown to be subject both to catabolite repression and DegS-DegU-mediated control, allowing an increase in the rate of synthesis of degQ under conditions of nitrogen starvation. These results are consistent with the hypothesis that this control system responds to an environmental Signal such as limitations of nitrogen, carbon, or phosphate sources.
Yongchen Lu - One of the best experts on this subject based on the ideXlab platform.
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lps tlr4 Signal Transduction Pathway
Cytokine, 2008Co-Authors: Yongchen Lu, Pamela S OhashiAbstract:The stimulation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) induces the release of critical proinflammatory cytokines that are necessary to activate potent immune responses. LPS/TLR4 Signaling has been intensively studied in the past few years. Here we review molecules involved in TLR4-mediated Signaling, including players that are involved in the negative regulation of this important Pathway.
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LPS/TLR4 Signal Transduction Pathway
Cytokine, 2008Co-Authors: Yongchen Lu, Pamela S OhashiAbstract:The stimulation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) induces the release of critical proinflammatory cytokines that are necessary to activate potent immune responses. LPS/TLR4 Signaling has been intensively studied in the past few years. Here we review molecules involved in TLR4-mediated Signaling, including players that are involved in the negative regulation of this important Pathway.
Amy E Mckee - One of the best experts on this subject based on the ideXlab platform.
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on trk the trkb Signal Transduction Pathway is an increasingly important target in cancer biology
Clinical Cancer Research, 2009Co-Authors: Carol J Thiele, Amy E MckeeAbstract:In the beginning, Trk was an oncogene. Yet Neurotrophin-Trk Signaling came to preeminence in the field of neurobiology. Now it is appreciated that Trks regulate important processes in nonneuronal cells and, in addition to their impact on tumors of neural origin, may contribute to the pathogenesis of carcinomas, myelomas, and prostate and lymphoid tumors. Although mutations and rearrangements of Trk are seen only sporadically in human cancers, such as medullary thyroid carcinoma, a number of recent studies indicate that expression of TrkB contributes to tumor pathology. In neuroblastoma, TrkA expression marks good prognosis which TrkB and Brain-derived neurotrophic factor (BDNF) expression marks poor prognosis. Activation of the BDNF/TrkB Signal Transduction Pathway also stimulates tumor cell survival and angiogenesis and contributes to resistance to cytotoxic drugs and anoikis, enabling cells to acquire many of the characteristic features required for tumorigenesis. Small molecule inhibitors, such as Cephalon's CEP-701, are in phase 1 and 2 clinical trials, and a series of AstraZeneca Trk inhibitors are poised to enter the clinic. As monotherapy, inhibitors may be effective only in tumors with activating Trk mutations. Important clinical follow-up will be the assessment of Trk inhibitors in combination with standard chemo- or radiotherapy or other Signal Transduction Pathway inhibitors.