about
In vivo notch signaling blockade induces abnormal spermatogenesis in the mouseOverexpression of delta-like 4 induces arterialization and attenuates vessel formation in developing mouse embryosDosage-sensitive requirement for mouse Dll4 in artery developmentLoss of Notch signalling induced by Dll4 causes arterial calibre reduction by increasing endothelial cell response to angiogenic stimuli.Combination of Dll4/Notch and Ephrin-B2/EphB4 targeted therapy is highly effective in disrupting tumor angiogenesis.miR-21 ablation and obeticholic acid ameliorate nonalcoholic steatohepatitis in miceDll4-Notch signaling determines the formation of native arterial collateral networks and arterial function in mouse ischemia models.Bone marrow-derived endothelial progenitors expressing Delta-like 4 (Dll4) regulate tumor angiogenesis.Low-dosage inhibition of Dll4 signaling promotes wound healing by inducing functional neo-angiogenesisDynamics of Notch pathway expression during mouse testis post-natal development and along the spermatogenic cycleNotch1 is pan-endothelial at the onset of flow and regulated by flow.Incomplete Dll4/Notch signaling inhibition promotes functional angiogenesis supporting the growth of skin papillomasDelta-like 4/Notch signaling promotes Apc Min/+ tumor initiation through angiogenic and non-angiogenic related mechanismsEndothelial Dll4 overexpression reduces vascular response and inhibits tumor growth and metastasization in vivoEndothelial Jagged1 promotes solid tumor growth through both pro-angiogenic and angiocrine functions.Erratum to: Delta-like 4/Notch signaling promotes Apc Min/+ tumor initiation through angiogenic and non-angiogenic related mechanisms.Notch signaling dynamics in the adult healthy prostate and in prostatic tumor development.Inhibition of Notch signaling by Dll4-Fc promotes reperfusion of acutely ischemic tissues.Notch signaling in the epididymal epithelium regulates sperm motility and is transferred at a distance within epididymosomes.Endothelial Jagged1 antagonizes Dll4 regulation of endothelial branching and promotes vascular maturation downstream of Dll4/Notch1.Differential expression of Notch component and effector genes during ovarian follicle and corpus luteum development during the oestrous cycle.Dynamics of Notch signalling in the mouse oviduct and uterus during the oestrous cycleMethods to Study Angiogenesis in a Mouse Model of Prostate CancerMetastasis is impaired by endothelial-specific Dll4 loss-of-function through inhibition of epithelial-to-mesenchymal transition and reduction of cancer stem cells and circulating tumor cells
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description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Alexandre Trindade
@ast
Alexandre Trindade
@en
Alexandre Trindade
@es
Alexandre Trindade
@nl
type
label
Alexandre Trindade
@ast
Alexandre Trindade
@en
Alexandre Trindade
@es
Alexandre Trindade
@nl
prefLabel
Alexandre Trindade
@ast
Alexandre Trindade
@en
Alexandre Trindade
@es
Alexandre Trindade
@nl
P106
P1153
56432456900
P21
P31
P496
0000-0002-3104-9259