Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A high-sensitivity TIE2-GRB2 BRET platform for functional and pharmacologic profiling of pathogenic variants associated with venous malformations.

Angiogenesis - 13 Aug 2026

Matsutani Hitomi, Oishi Atsuro, Izumi-Tamura Takuya, Hayashi Yumiko, Kurita Masakazu, Muto Tomoya, Yoshimi Akihide, Ueno Hitoshi, Shiraishi Tomohiro, Harii Kiyonori, Takushima Akihiko, Kidoya Hiroyasu, Ozaki Mine

Abstract excerpt

TIE2 is an endothelial receptor tyrosine kinase (RTK) essential for vascular integrity, and constitutively active TIE2 mutants are involved in venous malformations (VMs). VMs are currently treated by surgery or sclerotherapy, but effective pharmacologic options remain limited, especially for surgically challenging Blue Rubber Bleb Nevus Syndrome (BRBNS). TIE2 activation has typically been assessed by...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Biosensing Techniques
Share to HEK293 Cells

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Human Umbilical Vein Endothelial Cells

Share to Mutation

Share to Receptor, TIE-2

Share to Signal Transduction

Share to Vascular Malformations

Source

Identifiers

PMID: 42593687
DOI: 10.1007/s10456-026-10071-7

Genes

GRB2
ANG

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A high-sensitivity TIE2-GRB2 BRET platform for functional and pharmacologic profiling of pathogenic variants associated with venous malformations.PMID 42593687Read ↗

Hereditary cutaneomucosal venous malformations are caused by TIE2 mutations with widely variable hyper-phosphorylating effects.Semantic proximity Read ↗

Blue Rubber Bleb Nevus (BRBN) Syndrome Is Caused by Somatic TEK (TIE2) Mutations.Semantic proximity Read ↗

Somatic RIT1 delins in arteriovenous malformations hyperactivate RAS-MAPK signaling amenable to MEK inhibitionSemantic proximity Read ↗

Loss of PTPRB function remodels VEGFR1 activation in tumors overexpressing the receptor tyrosine kinaseSemantic proximity Read ↗

Tie2-R849W mutant in venous malformations chronically activates a functional STAT1 to modulate gene expression.Semantic proximity Read ↗

Venous malformation-causative TIE2 mutations mediate an AKT-dependent decrease in PDGFBSemantic proximity Read ↗

EGFR signaling and pharmacology in oncology revealed with innovative BRET-based biosensorsSemantic proximity Read ↗

Repurposing alpelisib, an anti-cancer drug, for the treatment of severe TIE2-mutated venous malformations: preliminary pharmacokinetics and pharmacodynamic dataSemantic proximity Read ↗

Somatic RIT1 indels identified in arteriovenous malformations hyperactivate RAS-MAPK signaling and are amenable to MEK inhibitionSemantic proximity Read ↗

Nitazoxanide activates BMP9-ALK1-SMAD signaling cascade and improves HHT vascular pathologySemantic proximity Read ↗

Common and specific effects of TIE2 mutations causing venous malformations.Semantic proximity Read ↗

AKT-mTOR/P53 PathwayDriven RapamycinAlpelisib Efficacy in Animal Models of TIE2Mutant Venous Malformations.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.