Kidins220/ARMS mediates the integration of the neurotrophin and VEGF pathways in the vascular and nervous systems View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-11-03

AUTHORS

F Cesca, A Yabe, B Spencer-Dene, J Scholz-Starke, L Medrihan, C H Maden, H Gerhardt, I R Orriss, P Baldelli, M Al-Qatari, M Koltzenburg, R H Adams, F Benfenati, G Schiavo

ABSTRACT

Signaling downstream of receptor tyrosine kinases controls cell differentiation and survival. How signals from different receptors are integrated is, however, still poorly understood. In this work, we have identified Kidins220 (Kinase D interacting substrate of 220 kDa)/ARMS (Ankyrin repeat-rich membrane spanning) as a main player in the modulation of neurotrophin and vascular endothelial growth factor (VEGF) signaling in vivo, and a primary determinant for neuronal and cardiovascular development. Kidins220−/− embryos die at late stages of gestation, and show extensive cell death in the central and peripheral nervous systems. Primary neurons from Kidins220−/− mice exhibit reduced responsiveness to brain-derived neurotrophic factor, in terms of activation of mitogen-activated protein kinase signaling, neurite outgrowth and potentiation of excitatory postsynaptic currents. In addition, mice lacking Kidins220 display striking cardiovascular abnormalities, possibly due to impaired VEGF signaling. In support of this hypothesis, we demonstrate that Kidins220 constitutively interacts with VEGFR2. These findings, together with the data presented in the accompanying paper, indicate that Kidins220 mediates the integration of several growth factor receptor pathways during development, and mediates the activation of distinct downstream cascades according to the location and timing of stimulation. More... »

PAGES

194-208

Journal

TITLE

Cell Death & Differentiation

ISSUE

2

VOLUME

19

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cdd.2011.141

DOI

http://dx.doi.org/10.1038/cdd.2011.141

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009631659

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22048155


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29 schema:description Signaling downstream of receptor tyrosine kinases controls cell differentiation and survival. How signals from different receptors are integrated is, however, still poorly understood. In this work, we have identified Kidins220 (Kinase D interacting substrate of 220 kDa)/ARMS (Ankyrin repeat-rich membrane spanning) as a main player in the modulation of neurotrophin and vascular endothelial growth factor (VEGF) signaling in vivo, and a primary determinant for neuronal and cardiovascular development. Kidins220−/− embryos die at late stages of gestation, and show extensive cell death in the central and peripheral nervous systems. Primary neurons from Kidins220−/− mice exhibit reduced responsiveness to brain-derived neurotrophic factor, in terms of activation of mitogen-activated protein kinase signaling, neurite outgrowth and potentiation of excitatory postsynaptic currents. In addition, mice lacking Kidins220 display striking cardiovascular abnormalities, possibly due to impaired VEGF signaling. In support of this hypothesis, we demonstrate that Kidins220 constitutively interacts with VEGFR2. These findings, together with the data presented in the accompanying paper, indicate that Kidins220 mediates the integration of several growth factor receptor pathways during development, and mediates the activation of distinct downstream cascades according to the location and timing of stimulation.
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36 Impaired vascular endothelial growth factor
37 Kidins220
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39 VEGF pathway
40 VEGFR2
41 abnormalities
42 activation
43 addition
44 brain-derived neurotrophic factor
45 cardiovascular abnormalities
46 cardiovascular development
47 cell death
48 cell differentiation
49 controls cell differentiation
50 current
51 data
52 death
53 determinants
54 development
55 different receptors
56 differentiation
57 distinct downstream
58 downstream
59 embryos
60 endothelial growth factor
61 excitatory postsynaptic currents
62 exhibit
63 extensive cell death
64 factors
65 findings
66 gestation
67 growth factor
68 growth factor receptor pathway
69 hypothesis
70 integration
71 kinase
72 later stages
73 location
74 main players
75 mice
76 mice exhibit
77 mitogen-activated protein kinase
78 modulation
79 modulation of neurotrophins
80 nervous system
81 neurite outgrowth
82 neurons
83 neurotrophic factor
84 neurotrophins
85 outgrowth
86 paper
87 pathway
88 peripheral nervous system
89 players
90 postsynaptic currents
91 potentiation
92 primary determinant
93 primary neurons
94 protein kinase
95 receptor pathway
96 receptors
97 responsiveness
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