Early G1 growth arrest of hybridoma B cells by DMSO involves cyclin D2 inhibition and p21([CIP]) induction

Oncogene

Volumn 17, Issue 9, 1998, Pages 1159-1166

  Ponzio, Gilles ^a   Loubat, Agnès ^a   Rochet, Nathalie ^a   Turchi, Laurent ^a   Rezzonico, Roger ^b   Farahi Far, Dariush ^a   Dulic, Vjekoslav ^c   Rossi, Bernard ^a  

^a INSERM   (France)

^b GENEVA UNIVERSITY HOSPITALS   (Switzerland)

^c ETABLISSEMENT FRANÇAIS DU SANG   (France)

Author keywords

CDKs; Cell cycle; Cyclin D2; DMSO; p21( CIP1 ); p27( KIP1 )

Indexed keywords

CYCLIN DEPENDENT KINASE; CYCLINE; DIMETHYL SULFOXIDE; PROTEIN P21; ANTIINFLAMMATORY AGENT; CCND2 PROTEIN, MOUSE; CDK2 PROTEIN, MOUSE; CDK4 PROTEIN, MOUSE; CDKN1A PROTEIN, MOUSE; CDKN1B PROTEIN, MOUSE; CELL CYCLE PROTEIN; CYCLIN A; CYCLIN DEPENDENT KINASE 2; CYCLIN DEPENDENT KINASE 4; CYCLIN DEPENDENT KINASE INHIBITOR 1A; CYCLIN DEPENDENT KINASE INHIBITOR 1B; CYCLIN E; MICROTUBULE ASSOCIATED PROTEIN; ONCOPROTEIN; PROTEIN SERINE THREONINE KINASE; RETINOBLASTOMA PROTEIN; TUMOR SUPPRESSOR PROTEIN;

ANIMAL CELL; ARTICLE; B LYMPHOCYTE; CELL CYCLE G1 PHASE; CELL PROLIFERATION; CONTROLLED STUDY; GENE INDUCTION; GROWTH DISORDER; HYBRIDOMA; MOUSE; NONHUMAN; PRIORITY JOURNAL; TUMOR SUPPRESSOR GENE; ANIMAL; CELL DIVISION; CYTOLOGY; DRUG ANTAGONISM; DRUG EFFECT; GENE EXPRESSION; GENE EXPRESSION REGULATION; GENETICS; METABOLISM; PHOSPHORYLATION; PHYSIOLOGY; TOPICAL DRUG ADMINISTRATION;

ANIMALIA;

ADMINISTRATION, TOPICAL; ANIMALS; ANTI-INFLAMMATORY AGENTS; B-LYMPHOCYTES; CDC2-CDC28 KINASES; CELL CYCLE PROTEINS; CELL DIVISION; CYCLIN A; CYCLIN E; CYCLIN-DEPENDENT KINASE 2; CYCLIN-DEPENDENT KINASE 4; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLIN-DEPENDENT KINASE INHIBITOR P27; CYCLIN-DEPENDENT KINASES; CYCLINS; DIMETHYL SULFOXIDE; G1 PHASE; GENE EXPRESSION; GENE EXPRESSION REGULATION; HYBRIDOMAS; MICE; MICROTUBULE-ASSOCIATED PROTEINS; PHOSPHORYLATION; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; RETINOBLASTOMA PROTEIN; TUMOR SUPPRESSOR PROTEINS;

EID: 0032480047     PISSN: 09509232     EISSN: None     Source Type: Journal    
DOI: 10.1038/sj.onc.1202040     Document Type: Article

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