Target intelligence / Profile preview

Synapse defective Rho GTPase homolog 2 (SYDE2)

Target
SYDE2
Molecular classification
Enzyme (specifically, Rho GTPase-activating protein, or RhoGAP), Other (scaffold protein, synaptic signaling hub)
01

Overview

Synapse defective Rho GTPase homolog 2 (SYDE2) is an enzyme of the RhoGAP family found primarily in the cytosol and synaptic membrane, where it acts as a GTPase activator for Rho-type GTPases by converting them to an inactive GDP-bound state[3][5][8]. SYDE2 contains conserved C2 and RhoGAP domains, mediating its role as a regulator of actin cytoskeleton dynamics, neuronal differentiation, and signaling during embryonic brain development[1][6]. Predicted protein-protein interaction sites and phosphorylation motifs are conserved, supporting a dynamic regulatory role in synaptic scaffolding and neuronal signaling complexes[1]. Disease-associated mutations (e.g., truncations) in SYDE2 can affect brain development or neurodevelopmental outcomes[1][3]. No approved drugs specifically interact with SYDE2, and the lack of crystal structure information currently limits structure-based drug discovery opportunities[1][8].

Other names
Rho GTPase-activating protein SYDE2Synapse defective protein 1 homolog 2Protein syd-1 homolog 2FLJ13815Synapse defective protein 1 homolog 2, protein syd-1 homolog 2, synapse defective 1SYDE2
02

Biological functions

GTPase activation (converts Rho-type GTPases to inactive GDP-bound state)Regulation of signal transduction (Rho GTPase-dependent)Neuronal differentiation signalingSynaptic membrane signalingCell migrationEmbryonic brain development
03

Disease associations

Neurodevelopmental disorders (e.g., intellectual disability, due to truncating mutations)Chondrodysplasia, Blomstrand type (association)Spherocytosis, type 1 (association)Possible involvement in neurological diseases (based on function in neurodevelopment)
04

Safety considerations

Potential impact on neurodevelopment if targeted (due to role in neuronal differentiation and synaptic signaling)Limited functional redundancy with paralog SYDE1 suggests loss-of-function mutations may yield CNS-specific phenotypes

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