Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.1.17 (ornithine decarboxylase)
 6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 180 strains of Haemophilus influenzae and 119 strains of Haemophilus parainfluenzae were characterized with respect to biotype (i.e., production of indole, urease, and ornithine decarboxylase) using conventional biochemical methods and two commercially available biotyping systems: Trio-Tube Haemophilus system (Carr Microbiologicals) and the Rapid NH System (Inovative Diagnostic Systems). Concordance between the results of the Trio-Tube system and conventional biochemicals was achieved with 294 of the 299 test organisms (98.3%). With the Rapid NH System, concordance with the results of conventional biochemical tests was observed with 275 of the 299 tests strains (92.0%). One previously unrecognized biotype of H. parainfluenzae, designated biotype VIII, is described. Typical reactions of this biotype include indole production but no production of urease or ornithine decarboxylase.
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PMID:Determination of biotypes of Haemophilus influenzae and Haemophilus parainfluenzae a comparison of methods and a description of a new biotype (VIII) of H. parainfluenzae. 350 12

Polyamine depletion with the ornithine decarboxylase inhibitor alpha-difluoromethyl ornithine (DFMO), prevents Rac1 activation causing the formation of a thick actin cortex at the cell periphery and inhibits migration of intestinal epithelial cells. In the present study, we demonstrate that MEK activation by EGF increased Rac1 activation, dissociation of intercellular contacts, and migration in both control and polyamine-depleted cells, while U0126, a specific inhibitor of MEK1, prevented disruption of junctions as well as EGF-induced Rac1 activation. Constitutively active MEK1 (CA-MEK) expression altered cell-cell contacts in control and polyamine depleted cells. The expression of constitutively active Rac1 (CA-Rac1) restored beta-catenin to the cell periphery and prevented the formation of actin cortex and caused the appearance of F-actin stress fibers in polyamine-depleted cells. Inhibition of Rac activation by NSC23766, a specific inhibitor of Tiam1, an upstream guanidine nucleotide exchange factor for Rac1, reproduced the beta-catenin localization and actin structure of polyamine-depleted cells. Tiam1 localized more extensively with beta-catenin at the cell periphery in CA-Rac1 cells compared to vector cells. Polyamine depletion decreased the expression of E-cadherin to a greater extent compared to beta-catenin. Subcellular fractionation further confirmed our immuno-localization and western blotting observations. These data suggest that EGF acting through MEK1/ERK to activate Rac1 regulates cell-cell contacts. Thus, decreased migration in polyamine depleted cells may be due to the inhibition of Tiam1 activation of Rac1 and the subsequent decreased expression of beta-catenin and E-cadherin leading to reduced cell-cell contacts.
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PMID:MEK/ERK regulates adherens junctions and migration through Rac1. 1718 46