Defects in actin dynamics lead to an autoinflammatory condition through the upregulation of CXCL5

PLoS ONE

Volumn 3, Issue 7, 2008, Pages

  Verdoni, Angela M ^a   Smith, Richard S ^b   Ikeda, Akihiro ^a   Ikeda, Sakae ^a  

^a UNIVERSITY OF WISCONSIN MADISON   (United States)

^b JACKSON LABORATORY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ACTIN; ACTIN DEPOLYMERIZING FACTOR; EPITHELIAL DERIVED NEUTROPHIL ACTIVATING FACTOR 78; CXCL5 PROTEIN, HUMAN; DSTN PROTEIN, HUMAN;

ALLELE; ANIMAL CELL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; CORNEA; CORNEA EPITHELIUM; EPITHELIUM CELL; IMMUNOFLUORESCENCE; INFLAMMATION; INNATE IMMUNITY; MACROPHAGE; MOLECULAR MECHANICS; MOUSE; MOUSE MUTANT; NEUTROPHIL; NONHUMAN; NUCLEOTIDE SEQUENCE; PROTEIN ANALYSIS; PROTEIN DEFECT; PROTEIN DEPLETION; PROTEIN EXPRESSION; PROTEIN FUNCTION; PROTEIN TARGETING; UPREGULATION; ANIMAL; BIOLOGICAL MODEL; BIOSYNTHESIS; C57BL MOUSE; CHEMISTRY; GENE EXPRESSION REGULATION; GENOTYPE; HUMAN; LEUKOCYTE; METABOLISM; PHENOTYPE; TRANSGENIC MOUSE;

ANIMALIA; MUS;

ACTINS; ANIMALS; CHEMOKINE CXCL5; DESTRIN; GENE EXPRESSION REGULATION; GENOTYPE; HUMANS; INFLAMMATION; LEUKOCYTES; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MODELS, BIOLOGICAL; NEUTROPHILS; PHENOTYPE;

EID: 50549097734     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0002701     Document Type: Article

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