aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability

The cell polarity regulator aPKC is associated with cell proliferation but the precise mechanism are unknown. Here, the authors find that aPKC lambda phosphorylates the FoxO1 transcription factor, a gatekeeper of endothelial growth, during both angiogenesis and angiosarcomas.

Bibliographic Details
Main Authors: Meghan Riddell, Akiko Nakayama, Takao Hikita, Fatemeh Mirzapourshafiyi, Takuji Kawamura, Ayesha Pasha, Mengnan Li, Mikio Masuzawa, Mario Looso, Tim Steinbacher, Klaus Ebnet, Michael Potente, Tomonori Hirose, Shigeo Ohno, Ingrid Fleming, Stefan Gattenlöhner, Phyu P. Aung, Thuy Phung, Osamu Yamasaki, Teruki Yanagi, Hiroshi Umemura, Masanori Nakayama
Format: Article
Language:English
Published: Nature Publishing Group 2018-12-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-07739-0
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spelling doaj-262aa7beda84463ca8dfda4862f93e832021-05-11T10:15:26ZengNature Publishing GroupNature Communications2041-17232018-12-019111310.1038/s41467-018-07739-0aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding abilityMeghan Riddell0Akiko Nakayama1Takao Hikita2Fatemeh Mirzapourshafiyi3Takuji Kawamura4Ayesha Pasha5Mengnan Li6Mikio Masuzawa7Mario Looso8Tim Steinbacher9Klaus Ebnet10Michael Potente11Tomonori Hirose12Shigeo Ohno13Ingrid Fleming14Stefan Gattenlöhner15Phyu P. Aung16Thuy Phung17Osamu Yamasaki18Teruki Yanagi19Hiroshi Umemura20Masanori Nakayama21Laboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung ResearchDepartment of Pharmacology, Max Planck Institute for Heart and Lung ResearchLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung ResearchLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung ResearchLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung ResearchLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung ResearchLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung ResearchDepartment of Molecular Diagnostics, School of Allied Health Sciences, Kitasato UniversityBioinformatics Service Group, Max Planck Institute for Heart and Lung ResearchInstitute-Associated Research Group: Cell Adhesion and Cell Polarity, Institute of Medical Biochemistry, ZMBE, University of MünsterInstitute-Associated Research Group: Cell Adhesion and Cell Polarity, Institute of Medical Biochemistry, ZMBE, University of MünsterAngiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung ResearchDepartment of Molecular Biology, Yokohama City University School of MedicineDepartment of Molecular Biology, Yokohama City University School of MedicineInstitute for Vascular Signaling, Centre for Molecular Medicine, Goethe UniversityInstitute of Pathology, University Hospital, Justus-Liebig-University GiessenDepartment of Pathology University of Texas, M.D. Anderson Cancer CenterDepartment of Pathology & Immunology, Baylor College of Medicine, Texas Children’s HospitalDepartment of Dermatology, Okayama University, School of MedicineDepartment of Dermatology, Hokkaido University Graduate School of MedicineDepartment of Dermatology, Okayama University, School of MedicineLaboratory for Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung ResearchThe cell polarity regulator aPKC is associated with cell proliferation but the precise mechanism are unknown. Here, the authors find that aPKC lambda phosphorylates the FoxO1 transcription factor, a gatekeeper of endothelial growth, during both angiogenesis and angiosarcomas.https://doi.org/10.1038/s41467-018-07739-0
collection DOAJ
language English
format Article
sources DOAJ
author Meghan Riddell
Akiko Nakayama
Takao Hikita
Fatemeh Mirzapourshafiyi
Takuji Kawamura
Ayesha Pasha
Mengnan Li
Mikio Masuzawa
Mario Looso
Tim Steinbacher
Klaus Ebnet
Michael Potente
Tomonori Hirose
Shigeo Ohno
Ingrid Fleming
Stefan Gattenlöhner
Phyu P. Aung
Thuy Phung
Osamu Yamasaki
Teruki Yanagi
Hiroshi Umemura
Masanori Nakayama
spellingShingle Meghan Riddell
Akiko Nakayama
Takao Hikita
Fatemeh Mirzapourshafiyi
Takuji Kawamura
Ayesha Pasha
Mengnan Li
Mikio Masuzawa
Mario Looso
Tim Steinbacher
Klaus Ebnet
Michael Potente
Tomonori Hirose
Shigeo Ohno
Ingrid Fleming
Stefan Gattenlöhner
Phyu P. Aung
Thuy Phung
Osamu Yamasaki
Teruki Yanagi
Hiroshi Umemura
Masanori Nakayama
aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability
Nature Communications
author_facet Meghan Riddell
Akiko Nakayama
Takao Hikita
Fatemeh Mirzapourshafiyi
Takuji Kawamura
Ayesha Pasha
Mengnan Li
Mikio Masuzawa
Mario Looso
Tim Steinbacher
Klaus Ebnet
Michael Potente
Tomonori Hirose
Shigeo Ohno
Ingrid Fleming
Stefan Gattenlöhner
Phyu P. Aung
Thuy Phung
Osamu Yamasaki
Teruki Yanagi
Hiroshi Umemura
Masanori Nakayama
author_sort Meghan Riddell
title aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability
title_short aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability
title_full aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability
title_fullStr aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability
title_full_unstemmed aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability
title_sort apkc controls endothelial growth by modulating c-myc via foxo1 dna-binding ability
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2018-12-01
description The cell polarity regulator aPKC is associated with cell proliferation but the precise mechanism are unknown. Here, the authors find that aPKC lambda phosphorylates the FoxO1 transcription factor, a gatekeeper of endothelial growth, during both angiogenesis and angiosarcomas.
url https://doi.org/10.1038/s41467-018-07739-0
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