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Related Experiment Video

Updated: Jan 25, 2026

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development

Published on: June 15, 2017

GIPC proteins negatively modulate Plexind1 signaling during vascular development.

Jorge Carretero-Ortega¹, Zinal Chhangawala¹, Shane Hunt¹

¹Department of Cell Biology, Skirball Institute of Biomolecular Medicine, New York University Langone Medical Center, New York, United States.

|May 4, 2019

Summary

GIPC proteins negatively regulate Semaphorin-Plexin-D1 (SEMA-PLXND1) signaling, impacting blood vessel development. Modulating this interaction offers new therapeutic strategies for angiogenesis-related conditions.

Keywords:

GIPC PlexinD1 Zebrafish angiogenesis cell signaling developmental biology zebrafish

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Last Updated: Jan 25, 2026

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Area of Science:

Cellular Biology
Developmental Biology
Molecular Biology

Background:

Semaphorins (SEMAs) and Plexin (PLXN) receptors are crucial for cellular communication and development.
SEMA-PLXND1 signaling influences cardiovascular, nervous, and immune system development, as well as cancer biology.
The molecular mechanisms modulating SEMA-PLXND1 signaling are not fully understood.

Purpose of the Study:

To investigate the role of GIPC family endocytic adaptors in SEMA-PLXND1 signaling.
To determine the molecular determinants governing the association between PLXND1 and GIPC.
To elucidate the function of PLXND1 in vascular development.

Main Methods:

Utilized zebrafish models with genetically modified Plxnd1 receptors and GIPC mutations.
Assessed angiogenesis deficits and responses to antiangiogenic drugs in zebrafish.
Investigated SEMA-PLXND1 signaling in cultured endothelial cells following GIPC depletion.

Main Results:

Zebrafish with impaired GIPC binding to Plxnd1 showed angiogenesis deficits and hypersensitivity to antiangiogenic drugs.
GIPC mutations led to angiogenic impairments that were rescued by reducing Plxnd1 signaling.
GIPC depletion enhanced SEMA-PLXND1 signaling in endothelial cells.

Conclusions:

GIPCs act as negative modulators of antiangiogenic PLXND1 signaling, expanding their known vascular roles.
PLXND1 trafficking is a key factor shaping vascular development.
Findings suggest GIPCs are important regulators of angiogenesis beyond the VEGF pathway.