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Guðrún Valdimarsdóttir - Dósent

Guðrún Valdimarsdóttir

–

Heilbrigðisvísindasvið

Guðrún Valdimarsdóttir

Dósent

Aðsetur
Sturlugata 8
Sími
5254797
Tölvupóstur
gudrunva [hjá] hi.is

Starfseining
Læknadeild, Líffærafræði
Vefsíða
http://www.lifvisindi.hi.is/page/lif_hop_gv

ORCID vefsíða
https://orcid.org/0000-0001-5560-9532
Rannsóknagátt – Guðrún Valdimarsdóttir

Útgefið efni

2020

The TGFβ Family in Human Placental Development at the Fetal-Maternal InterfaceBiomolecules

2019

EGFL7 Mediates BMP9-Induced Sprouting Angiogenesis of Endothelial Cells Derived from Human Embryonic Stem CellsStem Cell Reports

2016

BMP-SMAD signalingCytokine and Growth Factor Reviews

2015

Straumhvörf í rannsóknum á fjölhæfum stofnfrumum og notagildi þeirra í læknavísindumLæknablaðið
Straumhvörf í rannsóknum á fjölhæfum stofnfrumum og notagildi Theirra í læknavísindumLaeknabladid

2014

BMP4 promotes EMT and mesodermal commitment in human embryonic stem cells via SLUG and MSX2Stem Cells

2009

VEGF and inhibitors of TGFβ type-I receptor kinase synergistically promote blood-vessel formation by inducing α5-integrin expressionJournal of Cell Science

2006

Smad7 and protein phosphatase 1α are critical determinants in the duration of TGF-β/ALK1 signaling in endothelial cellsBMC Cell Biology

2005

Functions of the TGFβ superfamily in human embryonic stem cellsAPMIS

2004

Endoglin promotes endothelial cell proliferation and TGF-β/ALK1 signal transductionEMBO Journal
Synergy and antagonism between Notch and BMP receptor signaling pathways in endothelial cellsEMBO Journal

2003

Controlling the angiogenic switchTrends in Cardiovascular Medicine
Activin receptor-like kinase (ALK)1 is an antagonistic mediator of lateral TGFβ/ALK5 signalingMolecular Cell
Controlling cell fate by bone morphogenetic protein receptorsMolecular and Cellular Endocrinology

2002

Transient disruption of autocrine TGF-β signaling leads to enhanced survival and proliferation potential in single primitive human hemopoietic progenitor cellsJournal of Immunology
Stimulation of Id1 expression by bone morphogenetic protein is sufficient and necessary for bone morphogenetic protein-induced activation of endothelial cellsCirculation
Balancing the activation state of the endothelium via two distinct TGF-β type I receptorsEMBO Journal

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