The t(12;21) translocation converts AML-1B from an activator to a repressor of transcription.

Hiebert, S W; Sun, W; Davis, J N; Golub, T; Shurtleff, S; Buijs, A; Downing, J R; Grosveld, G; Roussell, M F; Gilliland, D G; Lenny, N; Meyers, S

Hiebert, S W; Sun, W; Davis, J N; Golub, T; Shurtleff, S; Buijs, A; Downing, J R; Grosveld, G; Roussell, M F; Gilliland, D G; Lenny, N; Meyers, S.

Affiliation

Hiebert SW; Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.

Mol Cell Biol ; 16(4): 1349-55, 1996 Apr.

Article in En | MEDLINE | ID: mdl-8657108

Subject(s)

Chromosomes, Human, Pair 12; Chromosomes, Human, Pair 21; DNA-Binding Proteins/genetics; Leukemia/genetics; Repressor Proteins; Transcription Factors/genetics; Transcription, Genetic; Translocation, Genetic; Base Sequence; Enhancer Elements, Genetic/genetics; Helix-Loop-Helix Motifs; Humans; Molecular Sequence Data; Proto-Oncogene Proteins c-ets; Recombinant Fusion Proteins/genetics; Sequence Deletion; ETS Translocation Variant 6 Protein

Fulltext

XML

PubMed Links

Search on Google

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Repressor Proteins / Transcription Factors / Transcription, Genetic / Translocation, Genetic / Chromosomes, Human, Pair 12 / Chromosomes, Human, Pair 21 / Leukemia / DNA-Binding Proteins Limits: Humans Language: En Journal: Mol Cell Biol Year: 1996 Type: Article Affiliation country: United States

Fulltext

XML

PubMed Links

Search on Google