V
Vanesa Muncan
Researcher at University of Amsterdam
Publications - 57
Citations - 3321
Vanesa Muncan is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Intestinal epithelium & Wnt signaling pathway. The author has an hindex of 22, co-authored 52 publications receiving 2881 citations. Previous affiliations of Vanesa Muncan include Royal Netherlands Academy of Arts and Sciences & Academic Medical Center.
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Journal ArticleDOI
Specific inhibition of gene expression using a stably integrated, inducible small-interfering-RNA vector.
Marc van de Wetering,Irma Oving,Vanesa Muncan,Menno Tjon Pon Fong,Helen Brantjes,Dik van Leenen,Frank C. P. Holstege,Thijn R. Brummelkamp,Reuven Agami,Hans Clevers +9 more
TL;DR: A doxycycline‐regulated form of the H1 promoter of RNA polymerase III that allows the inducible knockdown of gene expression by small interfering RNAs (siRNAs) is designed and targeted β‐catenin in colorectal cancer cells as a proof‐of‐principle.
Journal ArticleDOI
Myc deletion rescues Apc deficiency in the small intestine
Owen J. Sansom,Valerie Meniel,Vanesa Muncan,Toby J. Phesse,Julie A. Wilkins,Karen Ruth Reed,Keith Vass,Dimitris Athineos,Hans Clevers,Alan Richard Clarke +9 more
TL;DR: Loss of Myc rescued the phenotypes of perturbed differentiation, migration, proliferation and apoptosis, which occur on deletion of Apc, and Array analysis revealed that Myc is required for the majority of Wnt target gene activation following Apc loss.
Journal ArticleDOI
Rapid Loss of Intestinal Crypts upon Conditional Deletion of the Wnt/Tcf-4 Target Gene c-Myc
Vanesa Muncan,Owen J. Sansom,Leon Tertoolen,Toby J. Phesse,Harry Begthel,Elena Sancho,Alicia M. Cole,Alex Gregorieff,Ignacio Moreno de Alborán,Hans Clevers,Alan Richard Clarke +10 more
TL;DR: In this article, the role of the proto-oncogene c-Myc in colorectal cancer cell lines was assessed by conditional gene deletion, and it was shown that c-myc−/− crypt cells are on average much smaller than wild-type cells, cycle slower, and divide at a smaller cell size.
Journal ArticleDOI
ER Stress Causes Rapid Loss of Intestinal Epithelial Stemness through Activation of the Unfolded Protein Response
Jarom Heijmans,Jooske F. van Lidth de Jeude,Bon-Kyoung Koo,Sanne L. Rosekrans,Mattheus C. B. Wielenga,Marc van de Wetering,Marc Ferrante,Amy S. Lee,Jos J. M. Onderwater,James C. Paton,Adrienne W. Paton,A. Mieke Mommaas,Liudmila L. Kodach,James C. H. Hardwick,Daniel W. Hommes,Daniel W. Hommes,Hans Clevers,Vanesa Muncan,Gijs R. van den Brink +18 more
TL;DR: It is shown that in normal intestinal epithelium, endoplasmic reticulum stress and activity of the unfolded protein response (UPR) are induced at the transition from stem cell to transit-amplifying cell transition.
Journal ArticleDOI
Focal Adhesion Kinase Is Required for Intestinal Regeneration and Tumorigenesis Downstream of Wnt/c-Myc Signaling
Gabrielle H. Ashton,Jennifer P. Morton,Kevin Myant,Toby J. Phesse,Rachel A. Ridgway,Victoria Marsh,Julie A. Wilkins,Dimitris Athineos,Vanesa Muncan,Richard Kemp,Kristi L. Neufeld,Hans Clevers,Valerie G. Brunton,Douglas J. Winton,Xiaoyan Wang,Rosalie C. Sears,Alan R. Clarke,Margaret C. Frame,Owen J. Sansom +18 more
TL;DR: It is shown that the integrin effector protein Focal Adhesion Kinase (FAK) is dispensable for normal intestinal homeostasis and DNA damage signaling, but is essential for intestinal regeneration following DNA damage, and suggests that FAK inhibitors may suppress tumorigenesis in patients at high risk of developing colorectal cancer.