Fas-mediated neutrophil apoptosis and associated A1 protein expression during systemic inflammation are regulated independently of both tumor necrosis factor receptors.

Shock (Augusta, Ga.)

Volumn 19, Issue 3, 2003, Pages 201-207

  Kotani, Joji ^a   Avallone, Nicholas J ^a   Lin, Edward ^a   Goshima, Masahiro ^a   Gandhi, Kishor ^a   Lowry, Stephen F ^a   Calvano, Steve E ^a  

^a ROBERT WOOD JOHNSON MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BIOLOGICAL MARKER; DNA BINDING PROTEIN; FAS ANTIGEN; LEUKOCYTE ANTIGEN; LIPOPOLYSACCHARIDE; REPLICATION FACTOR C; TUMOR NECROSIS FACTOR RECEPTOR; TUMOR NECROSIS FACTOR RECEPTOR 1; TUMOR NECROSIS FACTOR RECEPTOR 2;

ANIMAL; APOPTOSIS; ARTICLE; BLOOD; BONE MARROW CELL; CYTOLOGY; DRUG EFFECT; GENE EXPRESSION REGULATION; GENETICS; IMMUNOLOGY; INFLAMMATION; MOUSE; MOUSE MUTANT; NEUTROPHIL; PHYSIOLOGY; PROTO ONCOGENE;

ANIMALS; ANTIGENS, CD; ANTIGENS, CD95; APOPTOSIS; BIOLOGICAL MARKERS; BONE MARROW CELLS; DNA-BINDING PROTEINS; GENE EXPRESSION REGULATION; GENES, BCL-2; INFLAMMATION; LIPOPOLYSACCHARIDES; MICE; MICE, KNOCKOUT; NEUTROPHILS; RECEPTORS, TUMOR NECROSIS FACTOR; RECEPTORS, TUMOR NECROSIS FACTOR, TYPE I; RECEPTORS, TUMOR NECROSIS FACTOR, TYPE II; REPLICATION PROTEIN C;

EID: 0141888170     PISSN: 10732322     EISSN: None     Source Type: Journal    
DOI: 10.1097/00024382-200303000-00002     Document Type: Article

References (0)