JNK inhibition and inflammation after cerebral ischemia

Brain, Behavior, and Immunity

Volumn 24, Issue 5, 2010, Pages 800-811

  Benakis, Corinne ^a   Bonny, Christophe ^b   Hirt, Lorenz ^a  

^a LAUSANNE UNIVERSITY HOSPITAL   (Switzerland)

^b Xigen Pharmaceuticals   (Switzerland)

Author keywords

C Jun N terminal kinase; Inflammation; Microglia; Middle cerebral artery occlusion; Neuroprotection; Oxygen and glucose deprivation

Indexed keywords

CD11B ANTIGEN; D JNKI1; GLUCOSE; ISOLECTIN B4; NEURON SPECIFIC NUCLEAR PROTEIN; OXYGEN; SODIUM CHLORIDE; STRESS ACTIVATED PROTEIN KINASE 1; STRESS ACTIVATED PROTEIN KINASE INHIBITOR; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIINFLAMMATORY ACTIVITY; ARTICLE; BRAIN ISCHEMIA; CELL ACTIVATION; CONTROLLED STUDY; ENZYME ACTIVATION; ENZYME INHIBITION; HIPPOCAMPUS; IN VITRO STUDY; MALE; MICROGLIA; MIDDLE CEREBRAL ARTERY OCCLUSION; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; RAT; SIGNAL TRANSDUCTION;

ANIMALS; BRAIN ISCHEMIA; HIPPOCAMPUS; IMMUNOHISTOCHEMISTRY; INFLAMMATION; JNK MITOGEN-ACTIVATED PROTEIN KINASES; MALE; MICE; MICROGLIA; NEURONS; ORGAN CULTURE TECHNIQUES; PEPTIDES; PHOSPHORYLATION; RATS; RATS, SPRAGUE-DAWLEY;

EID: 77953608972     PISSN: 08891591     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.bbi.2009.11.001     Document Type: Article

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