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phosphatidyl inositol/inflammation
Врската е зачувана во таблата со исечоци
Страница 1 од 118 резултати
Phosphatidyl-Inositol-3 Kinase Inhibitors Regulate Peptidoglycan-Induced Myeloid Leukocyte Recruitment, Inflammation, and Neurotoxicity in Mouse Brain.
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Acute brain injury leads to the recruitment and activation of immune cells including resident microglia and infiltrating peripheral myeloid cells (MC), which contribute to the inflammatory response involved in neuronal damage. We previously reported that TLR2 stimulation by peptidoglycan (PGN) from
A phosphatidyl-inositol-3-kinase-dependent anti-inflammatory pathway activated by Salmonella in epithelial cells.
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Salmonella activates the phosphatidyl-inositol-3-kinase (PI3K)/Akt pathway in epithelial cells, but its role in inflammation has not been previously elucidated. We show here that inhibition of PI3K in T84 intestinal epithelial cells results in augmentation of Salmonella-induced interleukin-8 (IL-8)
Phosphatidyl Inositol 3 Kinase-Gamma Balances Antiviral and Inflammatory Responses During Influenza A H1N1 Infection: From Murine Model to Genetic Association in Patients.
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Influenza A virus (IAV) infection causes severe pulmonary disease characterized by intense leukocyte infiltration. Phosphoinositide-3 kinases (PI3Ks) are central signaling enzymes, involved in cell growth, survival, and migration. Class IB PI3K or phosphatidyl inositol 3 kinase-gamma (PI3Kγ), mainly
Cloning of an inflammation-specific phosphatidyl inositol-linked form of murine vascular cell adhesion molecule-1.
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Vascular cell adhesion molecule-1 (VCAM1) is a member of the immunoglobulin (Ig) superfamily which interacts with the integrin very late antigen-4 (VLA4). The VCAM1/VLA4 interaction mediates both adhesion and signal transduction and is thought to play an important role in inflammatory and immune
[Inhibitory effect of oleanolic acid on inflammatory response in IL-1β-stimulated human synovial sarcoma SW982 cells].
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To study the role of oleanolic acid on interleukin (IL)-1β-stimulated expression of inflammatory cytokines, and to explore its anti-inflammatory mechanism in SW982 cells, the toxicity of oleanolic acid on SW982 cells was detected by MTT; effects of different concentrations of oleanolic acid(5, 10,
Regulation of COX-2 expression in canine prostate carcinoma: increased COX-2 expression is not related to inflammation.
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BACKGROUND
Cyclooxygenase-2 (COX-2) expression has been documented in human and canine prostate carcinoma (PCA). Canine PCA is a histologically heterogeneous tumor, sometimes including inflammatory infiltrates. However, it is unknown whether COX-2 expression in canine PCA is related to the
Deficiency of Pdk1 contributes to primordial follicle activation via the upregulation of YAP expression and the pro‑inflammatory response.
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The molecular mechanisms underlying the activation of primordial follicles are poorly understood. The serine/threonine protein kinase phosphoinositide‑dependent kinase 1 (PDK1), a pivotal downstream effector of phosphatidyl inositol‑3 kinase (PI3K) signaling, plays a vital role in cellular
The adhesiveness of monocytic U937 cells is stimulated by pro-inflammatory agents and inhibited by adenosine 3':5'-cyclic monophosphate.
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We investigated the regulation of the adhesiveness of the human promonocytic cell line U-937, differentiated along the monocytic pathway either by 1,25-(OH)2-cholecalciferol or a combination of retinoic acid and dibutyryl cAMP. Adhesion to untreated polystyrene plastic was induced by inflammatory
Oxidative stress employs phosphatidyl inositol 3-kinase and ERK signalling pathways to activate cAMP phosphodiesterase-4D3 (PDE4D3) through multi-site phosphorylation at Ser239 and Ser579.
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RAW macrophages, which express the PDE4D3 and PDE4D5 cAMP phosphodiesterase isoforms, exhibited increased PDE4 activity when challenged with H2O2 in a fashion that was negated by treatment with the cell permeant antioxidant, N-acetyl cysteine and by diphenyleneiodonium chloride, an inhibitor of
Homocysteine-induced macrophage inflammatory protein-2 production by glomerular mesangial cells is mediated by PI3 Kinase and p38 MAPK.
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BACKGROUND
Homocysteine (Hcy) and inflammatory cytokines have been linked to adverse outcomes in persons with cardiovascular and kidney diseases and recent reports suggest that cytokine-mediated inflammatory infiltrates may be an important contributor to the pathogenesis the aforementioned diseases.
Potential role of insulin signaling on vascular smooth muscle cell migration, proliferation, and inflammation pathways.
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To investigate the role of insulin signaling pathways in migration, proliferation, and inflammation of vascular smooth muscle cells (VSMCs), we examined the expression of active components of the phosphatidyl inositol 3 (PI-3) kinase (p-Akt) and mitogen-activated protein kinase (MAPK) (p-Erk) in
Chronic inflammation and pathogenesis of GI and pancreatic cancers.
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The pathogenesis of cancer represents a complex and multifactorial process requiring a number of acquired and genetic defects. It is becoming increasingly apparent that many cancers originate from a chronic inflammatory process. The topic of this review is the inflammatory response and development
Inflammatory-mediated repression of the rat ileal sodium-dependent bile acid transporter by c-fos nuclear translocation.
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OBJECTIVE
Ileal malabsorption of bile salts is observed in Crohn's ileitis. We define the transcriptional mechanisms involved in cytokine-mediated repression of the rat apical sodium-dependent bile acid transporter (ASBT).
METHODS
ASBT regulation was studied in IL-1beta-treated IEC-6 and Caco-2
Modulation of leukocyte transendothelial migration by integrin-associated glycosyl phosphatidyl inositol (GPI)-anchored proteins.
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Leukocyte transendothelial migration is an essential process in inflammation and the immune response. The mechanisms involved in leukocyte adhesion to the endothelium, forming the first step in leukocyte extravasation, have been fairly well documented. However, subsequent steps, which include
Inflammatory conditions induce IRES-dependent translation of cyp24a1.
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Rapid alterations in protein expression are commonly regulated by adjusting translation. In addition to cap-dependent translation, which is e.g. induced by pro-proliferative signaling via the mammalian target of rapamycin (mTOR)-kinase, alternative modes of translation, such as internal ribosome
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