Common and specific effects of TIE2 mutations causing venous malformations - Wikidata - thesis-toulmin - TriplyDB

Common and specific effects of TIE2 mutations causing venous malformations

Common and specific effects of TIE2 mutations causing venous malformations

http://www.wikidata.org/entity/Q30670028

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Angiopoietin-Tie signalling in the cardiovascular and lymphatic systems Somatic Activating PIK3CA Mutations Cause Venous Malformation Tie1 controls angiopoietin function in vascular remodeling and inflammation.Phosphoinositide 3-kinase: a new kid on the block in vascular anomalies.Somatic PIK3CA mutations as a driver of sporadic venous malformations.Therapeutic targeting of the angiopoietin-TIE pathway.Somatic activating mutations in Pik3ca cause sporadic venous malformations in mice and humans.Transgenic Expression of A Venous Malformation Related Mutation, TIE2-R849W, Significantly Induces Multiple Malformations of Zebrafish.Characterization of microparticles in patients with venous malformations of the head and neck.Changes in expression profiles of internal jugular vein wall and plasma protein levels in multiple sclerosis Angiopoietin-4-dependent venous maturation and fluid drainage in the peripheral retina

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Common and specific effects of TIE2 mutations causing venous malformations

http://www.wikidata.org/entity/Q30670028

description

2015 nî lūn-bûn

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2015 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2015 թվականի օգոստոսին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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Common and specific effects of TIE2 mutations causing venous malformations

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Common and specific effects of TIE2 mutations causing venous malformations

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Common and specific effects of TIE2 mutations causing venous malformations

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Common and specific effects of TIE2 mutations causing venous malformations

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Common and specific effects of TIE2 mutations causing venous malformations

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Human Molecular Genetics

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Common and specific effects of TIE2 mutations causing venous malformations

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Ilkka Miinalainen

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Julie Soblet

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Laurence M Boon

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Lauri Eklund

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Marjut Nätynki

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Nisha Limaye

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Raija Sormunen

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Riikka Pietilä

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Intracellular retention, degradation, and signaling of glycosylation-deficient FGFR2 and craniosynostosis syndrome-associated FGFR2C278F

Vascular dysmorphogenesis caused by an activating mutation in the receptor tyrosine kinase TIE2

Angiopoietins assemble distinct Tie2 signalling complexes in endothelial cell-cell and cell-matrix contacts

Differential function of Tie2 at cell-cell contacts and cell-substratum contacts regulated by angiopoietin-1

Angiopoietin-1 is essential in mouse vasculature during development and in response to injury.

Rapamycin improves TIE2-mutated venous malformation in murine model and human subjects

Structure of the Tie2 RTK domain: self-inhibition by the nucleotide binding loop, activation loop, and C-terminal tail

Identification of Tek/Tie2 binding partners. Binding to a multifunctional docking site mediates cell survival and migration

GRB2 and SH-PTP2: potentially important endothelial signaling molecules downstream of the TEK/TIE2 receptor tyrosine kinase

Requisite role of angiopoietin-1, a ligand for the TIE2 receptor, during embryonic angiogenesis

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10.1093/HMG/DDV349

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22

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24

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4614705

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