Silencing of adaptor protein SH 3 BP 2 reduces KIT / PDGFRA receptors expression and impairs gastrointestinal stromal tumors growth-Reference-Cited by-同舟云学术

Silencing of adaptor protein SH 3 BP 2 reduces KIT / PDGFRA receptors expression and impairs gastrointestinal stromal tumors growth

Published:2018-06-30 Issue:8 Volume:12 Page:1383-1397
ISSN:1574-7891
Container-title:Molecular Oncology
language:en
Short-container-title:Mol Oncol

Author:

Serrano‐Candelas Eva¹²,Ainsua‐Enrich Erola¹²,Navinés‐Ferrer Arnau¹²,Rodrigues Paulo³,García‐Valverde Alfonso⁴,Bazzocco Sarah³,Macaya Irati³,Arribas Joaquín⁴⁵⁶⁷,Serrano César⁴⁸,Sayós Joan⁹,Arango Diego³,Martin Margarita¹²

Affiliation:

1. Biochemistry Unit, Biomedicine Department Faculty of Medicine University of Barcelona Spain

2. Laboratory of Clinic and Experimental Immunoallergy IDIBAPS Barcelona Spain

3. Group of Biomedical Research in Digestive Tract Tumors CIBBIM‐Nanomedicine Vall d'Hebron University Hospital Research Institute (VHIR) Autonomous University of Barcelona Spain

4. Preclinical Research Program Vall d'Hebron Institute of Oncology (VHIO) Barcelona Spain

5. The Catalan Institute of Research and Advanced Studies (ICREA) Barcelona Spain

6. CIBERONC Barcelona Spain

7. Department of Biochemistry and Molecular Biology Universitat Autónoma de Barcelona Bellaterra Spain

8. Vall d'Hebron University Hospital Barcelona Spain

9. Immune Regulation and Immunotherapy Group CIBBIM‐Nanomedicine Vall d'Hebron University Hospital Research Institute (VHIR) Autonomous University of Barcelona Spain

Funder

Instituto de Salud Carlos III

Secretaría de Estado de Investigación, Desarrollo e Innovación

Publisher

Wiley

Subject

Cancer Research,Genetics,Molecular Medicine,General Medicine,Oncology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/1878-0261.12332

Reference52 articles.

1. The Adaptor 3BP2 Is Required for Early and Late Events in FcεRI Signaling in Human Mast Cells

2. The Adaptor 3BP2 Is Required for KIT Receptor Expression and Human Mast Cell Survival