Anergic T cells are defective in both jun NH2-terminal kinase and mitogen-activated protein kinase signaling pathways

Journal of Experimental Medicine

Volumn 183, Issue 5, 1996, Pages 2017-2023

  DeSilva, Dimuthu R ^a   Feeser, Wendi S ^a   Tancula, Elizabeth J ^a   Scherle, Peggy A ^a  

^a DUPONT COMPANY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

INTERLEUKIN 2; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN KINASE; T LYMPHOCYTE RECEPTOR; TRANSCRIPTION FACTOR AP 1;

ANIMAL CELL; ARTICLE; CLONAL ANERGY; CONTROLLED STUDY; ENZYME ACTIVATION; HELPER CELL; MOUSE; NONHUMAN; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; TRANSACTIVATION; TRANSCRIPTION REGULATION;

ANIMALS; ANTIBODIES; ANTIGENS, CD3; CA(2+)-CALMODULIN DEPENDENT PROTEIN KINASE; CELLS, CULTURED; CLONAL ANERGY; CYCLOHEXIMIDE; INFLUENZA A VIRUS; INTERLEUKIN-2; IONOMYCIN; JNK MITOGEN-ACTIVATED PROTEIN KINASES; LYMPHOCYTE ACTIVATION; MICE; MICE, INBRED BALB C; MICE, INBRED STRAINS; MITOGEN-ACTIVATED PROTEIN KINASE 3; MITOGEN-ACTIVATED PROTEIN KINASES; PHOSPHORYLATION; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-RAF; SIGNAL TRANSDUCTION; SPLEEN; T-LYMPHOCYTES; TETRADECANOYLPHORBOL ACETATE; TRANSCRIPTION FACTOR AP-1;

EID: 0029952223     PISSN: 00221007     EISSN: None     Source Type: Journal    
DOI: 10.1084/jem.183.5.2017     Document Type: Article

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