Zeb1 potentiates genome‐wide gene transcription with Lef1 to promote glioblastoma cell invasion-Reference-Cited by-同舟云学术

Zeb1 potentiates genome‐wide gene transcription with Lef1 to promote glioblastoma cell invasion

Published:2018-06-14 Issue:15 Volume:37 Page:
ISSN:0261-4189
Container-title:The EMBO Journal
language:en
Short-container-title:EMBO J

Author:

Rosmaninho Pedro¹^ORCID,Mükusch Susanne²³,Piscopo Valerio⁴,Teixeira Vera¹,Raposo Alexandre ASF¹^ORCID,Warta Rolf⁵,Bennewitz Romina²³,Tang Yeman⁴,Herold‐Mende Christel⁵,Stifani Stefano⁴,Momma Stefan²³^ORCID,Castro Diogo S¹^ORCID

Affiliation:

1. Molecular Neurobiology Laboratory Instituto Gulbenkian de Ciência Oeiras Portugal

2. Institute of Neurology (Edinger Institute) Frankfurt University Medical School Frankfurt Germany

3. German Cancer Consortium (DKTK) German Cancer Research Center (DKFZ) Heidelberg Germany

4. Department of Neurology and Neurosurgery Montreal Neurological Institute McGill University Montreal QC Canada

5. Division of Experimental Neurosurgery Department of Neurosurgery University Hospital of Heidelberg Heidelberg Germany

Funder

Deutsche Forschungsgemeinschaft

Canadian Institutes of Health Research

Cryptobranchid Interest Group

Publisher

EMBO

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology,General Neuroscience

Link

https://onlinelibrary.wiley.com/doi/pdf/10.15252/embj.201797115

Reference81 articles.

1. The transcription factor ZEB1 (δEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity

2. Activated type I phosphatidylinositol kinase is associated with the epidermal growth factor (EGF) receptor following EGF stimulation.

3. GlioVis data portal for visualization and analysis of brain tumor expression datasets

4. The ZEB/miR‐200 feedback loop—a motor of cellular plasticity in development and cancer?

5. A Double-Negative Feedback Loop between ZEB1-SIP1 and the microRNA-200 Family Regulates Epithelial-Mesenchymal Transition

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