An N-terminal splice variant of human Stat5a that interacts with different transcription factors is the dominant form expressed in invasive ductal carcinoma
Authors:
Open Access
- 30 December 2013
- journal article
- Published by Elsevier in Cancer Letters
- Vol. 346 (1) , 148-157
Abstract
No abstract availableKeywords
This publication has 39 references indexed in Scilit:
- Pharmacological modulation of beta‐catenin and its applications in cancer therapyJournal of Cellular and Molecular Medicine, 2013
- Vitamin D and the mammary gland: a review on its role in normal development and breast cancerBreast Cancer Research, 2012
- Signal transducer and activator of transcription 5 as a key signaling pathway in normal mammary gland developmental biology and breast cancerBreast Cancer Research, 2011
- IL-8 Signaling Plays a Critical Role in the Epithelial–Mesenchymal Transition of Human Carcinoma CellsCancer Research, 2011
- The two faces of Janus kinases and their respective STATs in mammary gland development and cancerJournal of Carcinogenesis, 2011
- Prolactin Inhibits BCL6 Expression in Breast Cancer through a Stat5a-Dependent MechanismCancer Research, 2010
- Direct glucocorticoid receptor–Stat5 interaction in hepatocytes controls body size and maturation-related gene expressionGenes & Development, 2007
- Stat5 activation inhibits prolactin-induced AP-1 activity: distinct prolactin-initiated signals in tumorigenesis dependent on cell contextOncogene, 2007
- Structure of a β-TrCP1-Skp1-β-Catenin ComplexMolecular Cell, 2003
- Identification of a Novel Retrovirus Long Terminal Repeat (LTR) That Is Targeted by p51A (TAp63γ) and Selective Dominant-Negative Activity of p73L (ΔNp63α) toward p53-Responsive Promoter ActivitiesBiochemical and Biophysical Research Communications, 2001