Zeitschriftenaufsatz | 2012 Open Access

STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia.

Autor:in

Warsch, Wolfgang; Grundschober, Eva; Berger, Angelika; Gille, Lars; Cerny-Reiterer, Sabine; Tigan, Anca-Sarmiza; Hoelbl-Kovacic, Andrea; Valent, Peter; Moriggl, Richard; Sexl, Veronika;

Publikationen als Autor:in / Herausgeber:in der Vetmeduni

Gille, Lars; Sexl, Veronika

Journal

OncoTarget

Schlagwörter

Animals; DNA Breaks, Double-Stranded; Disease Progression; Feedback, Physiological; Fusion Proteins, bcr-abl/genetics*; Gene Expression Regulation, Neoplastic; Humans; Janus Kinase 2/metabolism; K562 Cells; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism*; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology; Mice; Mice, Inbred NOD; Mice, SCID; Mutation*; Oxidative Stress*; Protein-Tyrosine Kinases/genetics*; RNA Interference; RNA, Messenger/metabolism; Reactive Oxygen Species/metabolism*; STAT5 Transcription Factor/genetics; STAT5 Transcription Factor/metabolism*; Signal Transduction; Transcription, Genetic; Transfection; Tumor Suppressor Proteins/genetics; Tumor Suppressor Proteins/metabolism*;

Dokumententyp

Originalarbeit

ISSN/eISSN

1949-2553 -

DOI

10.18632/oncotarget.806

WoS ID

WOS:000315801200025

PubMed ID

23458731