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Showing 1 to 20 of 30 for “"c-jun N-terminal kinase"”.

  1. The role of c-Jun N-terminal kinase one and two in motoneuron maturation and maintenance

    … ). Subgroups of the mitogen activated protein kinases (MAPK) family have been implicated in neuronal differentiation, death, regeneration, and survival (Bogoyevitch and Kobe, 2006; Frebel and Wiese, 2006). The c-Jun N-terminal kinases (JNKs) are stress-activated members of the MAPK family, …

    wfu Repository record for The role of c-Jun N-terminal kinase one and two in motoneuron maturation and maintenance (opens in a new tab)

  2. Elevated temperature alters cytokine output and c-Jun N-terminal kinase signaling downstream of toll-like receptor activation

    Fever is a fundamental and important response to infection. Previous studies have shown that alterations in temperature can alter the phenotype of innate immune cells, such as phagocytic ability, but the effects of elevated temperature on the molecular mechanisms that underlie these differences …

    utmb Repository record for Elevated temperature alters cytokine output and c-Jun N-terminal kinase signaling downstream of toll-like receptor activation (opens in a new tab)

  3. The <i>Drosophila</i> T-box Transcription Factor Midline Functions within the Insulin/AKT and c-Jun-N-terminal Kinase Signaling Pathways to Regulate Interomatidial Bristle Formation and Cell Survival

    … </em>within the insulin receptor (InR) and the c-Jun-N-terminal kinase (JNK) signaling pathways to regulate interommatidial bristle (IOB) formation. Previous studies have identified <em>mid</em>’s role in cell fate specification of sensory organ precursor cells in conjunction with the Notch-Delta …

    usm Repository record for The <i>Drosophila</i> T-box Transcription Factor Midline Functions within the Insulin/AKT and c-Jun-N-terminal Kinase Signaling Pathways to Regulate Interomatidial Bristle Formation and Cell Survival (opens in a new tab)

  4. Notch Signaling Is Important in the Survival, Proliferation, and Self-Renewal of the Putative Breast Cancer Stem Cell Population

    … a RT-qPCR based approach as well as several kinase inhibitors including those that inhibit c-Jun N-terminal kinase and the p38 mitogen activated kinase.</p><p>The CSCs possessed elevated levels of Notch activation compared to the non-CSCs regardless of breast cancer phenotype, sample origin …

    loyola-thes Repository record for Notch Signaling Is Important in the Survival, Proliferation, and Self-Renewal of the Putative Breast Cancer Stem Cell Population (opens in a new tab)

  5. A TOLL-LIKE RECEPTOR-INDUCIBLE AND B CELL-SPECIFIC ENHANCER REGULATES MURINE GAMMAHERPESVIRUS 68 LATENCY AND REACTIVATION

    … was blocked by inhibitors of NF-kB or c-Jun N-terminal kinase (JNK). Overall, we determined the molecular and genetic mechanisms of M2 regulation by TLR signaling.

    wfu Repository record for A TOLL-LIKE RECEPTOR-INDUCIBLE AND B CELL-SPECIFIC ENHANCER REGULATES MURINE GAMMAHERPESVIRUS 68 LATENCY AND REACTIVATION (opens in a new tab)

  6. Regulatory role of phosphatidylinositol 4-phosphate 5-kinases in brain inflammation

    … by the type I phosphatidylinositol 4-phosphate 5-kinase (PIP5KI) family members, PIP5KIα, PIP5KIβ and PIP5KIγ, is an important regulator of diverse cellular processes at the cell surface, such as cell survival, cell proliferation, phagocytosis, macropinocytosis membraned ruffles, ion channels …

    ajou Repository record for Regulatory role of phosphatidylinositol 4-phosphate 5-kinases in brain inflammation (opens in a new tab)

  7. Effect of Anti-fibrotic Drug (Pirfenidone) on TGF-β Signaling Pathway in Ocular Fibrotic Disorders

    … (Smad) 2/3, p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, and extracellular signal related kinase expression were conducted to elucidate the cell signaling networks that contribute to the anti-fibrotic effect of pirfenidone. Results: Treatment with TGF-β1 induced typical …

    ajou Repository record for Effect of Anti-fibrotic Drug (Pirfenidone) on TGF-β Signaling Pathway in Ocular Fibrotic Disorders (opens in a new tab)

  8. ROS regulation of axonal mitochondrial transport

    … effects, we examined Ca2+ levels and the JNK (c-Jun N-terminal Kinase) pathway, which have been shown to regulate mitochondrial transport and general fast axonal transport, respectively. We found that elevated ROS increased Ca 2+levels, and that the Ca2+ chelator EGTA rescued ROS-induced defects …

    purdue-thes Repository record for ROS regulation of axonal mitochondrial transport (opens in a new tab)

  9. Gain And Loss Of Progranulin Have Opposite Effects On Autophagy

    … TNF receptor (TNFR) over-stimulation and C-Jun N-terminal kinase (JNK) activation. Excessive activation of brain autophagy is associated to neurodegeneration and either JNK or autophagy inhibition improve neuronal viability and dysfunction in PGRN deficient neurons and PGRN null C. elegans. …

    the-open-u Repository record for Gain And Loss Of Progranulin Have Opposite Effects On Autophagy (opens in a new tab)

  10. The GluK4 Kainate Receptor Subunit Regulates Mood, Memory and Excitotoxic Neurodegeneration

    … tissue revealed that GluK4 may act through the c-Jun N-terminal Kinase (JNK) pathway to regulate the molecular cascades that lead to excitotoxicity. Finally, I found preliminary evidence to suggest that GluK4 may regulate hippocampal seizure activity following intraperitoneal injection of kainate. …

    rockefeller Repository record for The GluK4 Kainate Receptor Subunit Regulates Mood, Memory and Excitotoxic Neurodegeneration (opens in a new tab)

  11. Molecular mechanisms mediating the induction of apoptosis by chemopreventive selenium compounds

    … in inhibition of apoptosis. Activities of stress kinases INK (c-jun N-terminal kinase) and p38 were also induced on selenium treatment and intervention studies using specific chemical inhibitors and/or dominant negative mutants suggested that INK, but not p38, was functionally important for the …

    glasgow Repository record for Molecular mechanisms mediating the induction of apoptosis by chemopreventive selenium compounds (opens in a new tab)

  12. Phosphatidylinositol 4-phosphate 5-kinase Involved in Neuroglial Toll-like Receptor Signaling

    … by the type I phosphatidylinositol 4-phosphate 5-kinase (PIP5K) family members, was necessary for TLR4 signaling. However, details of the PIP5K-mediated PIP2 production pathway and its direct regulatory effect on TLR4 signaling remain not well understood. Thus, in the present study, I have …

    ajou Repository record for Phosphatidylinositol 4-phosphate 5-kinase Involved in Neuroglial Toll-like Receptor Signaling (opens in a new tab)

  13. PLASMA JNK3 AS A NOVEL PERIPHERAL BIOMARKER IN ALZHEIMER'S AND PARKINSON'S DISEASES: EARLY DIAGNOSIS AND DISEASE MONITORING

    … This thesis investigated the potential of c-Jun N-terminal kinase 3 (JNK3), a neuron-specific stress-activated kinase, as a novel peripheral biomarker with translational value in both AD and PD. In the AD cohort, which included patients with AD, mild cognitive impairment (MCI), and controls …

    milano Repository record for PLASMA JNK3 AS A NOVEL PERIPHERAL BIOMARKER IN ALZHEIMER'S AND PARKINSON'S DISEASES: EARLY DIAGNOSIS AND DISEASE MONITORING (opens in a new tab)

  14. Heat shock protein 90, a potential biomarker for type I diabetes: mechanisms of release from pancreatic beta cells

    … stress and ensuing cytotoxicity mediated by c-Jun N-terminal kinase (JNK) appeared to play a role in HSP90 release. Beta cell HSP90 release was attenuated by pre-treatment with tauroursodeoxycholic acid (TUDCA), which has been shown previously to protect beta cells against JNK-mediated, …

    iupui Repository record for Heat shock protein 90, a potential biomarker for type I diabetes: mechanisms of release from pancreatic beta cells (opens in a new tab)

  15. Regulation of Insulin and CHOP Gene Expression in Pancreatic Beta Cells

    … as NF-kappaB (nuclear factor-kappaB) and JNK (c-Jun N-terminal kinase) signaling pathways. The second project focused on the mechanisms by which JNK and NF-kappaB regulate the expression of CHOP, a mediator of ER stress-induced apoptosis, upon IL-1beta stimulation. Exposure of beta cells to …

    utswmed Repository record for Regulation of Insulin and CHOP Gene Expression in Pancreatic Beta Cells (opens in a new tab)

  16. Significance of Altered Golgi Apparatus and Cell Fusion Events in Ovarian Cancer Cells

    … of cisplatin-stress induced activation of c-Jun-N-terminal kinase (JNK) significantly reduced fragmentation of the Golgi in ovarian cancer cells while extracellular signal-regulated kinase (ERK1/2) inhibition significantly increased fragmentation in A2780 cells but had no effect on other cell …

    oxford-brookes Repository record for Significance of Altered Golgi Apparatus and Cell Fusion Events in Ovarian Cancer Cells (opens in a new tab)

  17. RAR beta trans-repression of AP-1 transcription factor in HeLa cervical cancer cells : consequences on transcription of viral and cellular AP-1 controlled genes

    … consistently reduced in HeLa RARß2 clones was c-Jun, despite ongoing gene expression. In order to understand by which mechanism c-Jun is reduced, and since the phosphorylation of c-Jun is important for protein stabilization, HeLa RARß2 clones were treated with different c-Jun-N-terminal kinase

    heid-diss Repository record for RAR beta trans-repression of AP-1 transcription factor in HeLa cervical cancer cells : consequences on transcription of viral and cellular AP-1 controlled genes (opens in a new tab)

  18. Stress hormones epinephrine and corticosterone modulate herpes simplex virus 1 and 2 productive infection and reactivation primarily in sympathetic, not sensory, neurons

    … the transcription factor β-catenin, and the c-Jun N-terminal kinase (JNK). Corticosterone-induced reactivation of HSV-1 in SCG neurons required activation of glucocorticoid receptor (GCR) and transcription factors CREB and JNK. In contrast, corticosterone-induced reactivation of HSV-2 in TG and …

    vt Repository record for Stress hormones epinephrine and corticosterone modulate herpes simplex virus 1 and 2 productive infection and reactivation primarily in sympathetic, not sensory, neurons (opens in a new tab)

  19. The Role Of ROS-mediated ERK and JNK Activation In The Induction Of Autophagy And Apoptosis In Tumour Cells By A Novel Small Molecule Compound

    … via activation of extracellular regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). Inhibition of ERK and JNK virtually completely blocked drug-induced autophagy and apoptosis. Interestingly, inhibition of JNK activity reversed C1-induced increase in Atg7 expression, indicating that …

    nus Repository record for The Role Of ROS-mediated ERK and JNK Activation In The Induction Of Autophagy And Apoptosis In Tumour Cells By A Novel Small Molecule Compound (opens in a new tab)

  20. The in vitro effects of diallyl trisulfide on osteoclast formation and function in RAW 264.7 murine macrophages

    … B (NF-kappaB) and mitogen-activated protein kinase (MAPK) pathways are crucial for osteoclast differentiation and activation in a process known as osteoclastogenesis. Diallyl trisulfide (DATS) is an organosulfur compound produced in garlic which has shown powerful anti-cancer effects in vitro …

    pretoria Repository record for The in vitro effects of diallyl trisulfide on osteoclast formation and function in RAW 264.7 murine macrophages (opens in a new tab)

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