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Volumn 20, Issue 17, 2001, Pages 2186-2189
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Evidence of a possible epigenetic inactivation mechanism operating on a region of mouse chromosome 19 in γ-radiation-induced thymic lymphomas
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Author keywords
irradiation; Cd95; Chromosome 19; Epigenetic inactivation; Jak2; Mouse thymic lymphomas; Pten
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Indexed keywords
ONCOPROTEIN;
ONCOPROTEIN CD95;
ONCOPROTEIN JAK2;
PHOSPHATIDYLINOSITOL 3,4,5 TRISPHOSPHATE 3 PHOSPHATASE;
UNCLASSIFIED DRUG;
ANIMAL EXPERIMENT;
ANIMAL MODEL;
ANIMAL TISSUE;
ARTICLE;
CHROMOSOME 19;
CONTROLLED STUDY;
GAMMA RADIATION;
GENE INACTIVATION;
HETEROZYGOSITY LOSS;
MOUSE;
NONHUMAN;
NUCLEOTIDE SEQUENCE;
PRIORITY JOURNAL;
THYMUS LYMPHOMA;
ANIMALS;
ANTIGENS, CD95;
CHROMOSOMES;
CROSSES, GENETIC;
GAMMA RAYS;
GENE EXPRESSION REGULATION, NEOPLASTIC;
GENE SILENCING;
JANUS KINASE 2;
LOSS OF HETEROZYGOSITY;
LYMPHOMA;
MICE;
MICE, INBRED BALB C;
MICE, INBRED C57BL;
NEOPLASMS, RADIATION-INDUCED;
PHOSPHORIC MONOESTER HYDROLASES;
PROTEIN-TYROSINE KINASES;
PROTO-ONCOGENE PROTEINS;
PTEN PHOSPHOHYDROLASE;
THYMUS NEOPLASMS;
TUMOR SUPPRESSOR PROTEINS;
ANIMALIA;
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EID: 0035912104
PISSN: 09509232
EISSN: None
Source Type: Journal
DOI: 10.1038/sj.onc.1204297 Document Type: Article |
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Times cited : (28)
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References (24)
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