GPC2

Existing Annotations Review

GO Term	Evidence	Action	Reason
GO:0015026 coreceptor activity	NAS UniProtKB:Q8N158	NEW	Summary: GPC2 functions as a signaling co-receptor at the cell surface, modulating ligand-receptor interactions through its heparan sulfate chains. It binds growth factors such as PTN and MDK to regulate neurite outgrowth signaling. This is the core molecular function of GPC2. Reason: This annotation captures the core molecular function of GPC2 as described in UniProt and the deep research literature. As a GPI-anchored HSPG, GPC2 serves as a cell-surface co-receptor that modulates ligand-receptor interactions. Supporting Evidence: UniProtKB:Q8N158 Interacts (via heparan sulfate) with PTN; this interaction promotes neurite outgrowth through binding of PTN with chondroitin sulfate of proteoglycans file:human/GPC2/GPC2-deep-research-falcon.md As a GPI-anchored HSPG, GPC2 serves as a cell-surface co-receptor that modulates ligand-receptor interactions
GO:0016477 cell migration	IBA GO_REF:0000033	ACCEPT	Summary: GPC2 is annotated to cell migration based on phylogenetic inference (IBA). Glypicans are known to modulate cell motility through their effects on growth factor signaling. UniProt states GPC2 may fulfill a function related to the motile behaviors of developing neurons. While the annotation is phylogenetically supported and consistent with glypican family function, direct experimental evidence for human GPC2 in cell migration is limited. Reason: The IBA annotation is well-supported by the known role of glypicans in modulating cell motility and the phylogenetic evidence from orthologs. UniProt independently notes the potential role in neuronal motile behaviors. Supporting Evidence: UniProtKB:Q8N158 May fulfill a function related to the motile behaviors of developing neurons
GO:0031012 extracellular matrix	IBA GO_REF:0000033	KEEP AS NON CORE	Summary: GPC2 is annotated to extracellular matrix based on phylogenetic inference. As a GPI-anchored heparan sulfate proteoglycan, GPC2 is primarily localized to the cell surface, not as a structural component of the extracellular matrix. While glypicans can interact with ECM components and may transiently associate with the ECM, particularly after shedding, this annotation conflates the secreted form with typical ECM structural components. Reason: While GPC2 may interact with ECM components or be shed into the extracellular space, its primary localization is as a GPI-anchored cell surface protein. The ECM annotation is not incorrect but represents a secondary localization rather than the core function. Supporting Evidence: UniProtKB:Q8N158 Cell membrane {ECO:0000250}; Lipid-anchor, GPI- anchor {ECO:0000250}; Extracellular side {ECO:0000250}
GO:0009986 cell surface	IBA GO_REF:0000033	ACCEPT	Summary: GPC2 is annotated to cell surface based on phylogenetic inference. This is strongly supported by the known biology of glypicans as GPI-anchored proteins that localize to the external surface of the plasma membrane. UniProt confirms GPC2 has a GPI-anchor site and localizes to the cell membrane extracellular side. Recent cancer research confirms GPC2 as a cell-surface target for immunotherapy. Reason: The cell surface localization is a core feature of GPC2 function as a GPI-anchored signaling co-receptor. This is supported by UniProt, phylogenetic inference, and extensive cancer immunotherapy literature demonstrating cell surface expression. Supporting Evidence: UniProtKB:Q8N158 Cell membrane {ECO:0000250}; Lipid-anchor, GPI- anchor {ECO:0000250}; Extracellular side {ECO:0000250} file:human/GPC2/GPC2-deep-research-falcon.md GPC2 is cell-surface localized and GPI-anchored, consistent with glypican family features and its role as an extracellular signaling co-receptor
GO:0045202 synapse	IBA GO_REF:0000033	KEEP AS NON CORE	Summary: GPC2 is annotated to synapse localization based on phylogenetic inference from orthologs. The related glypican GPC4 is known to be involved in synapse formation and function. GPC2 is expressed in developing neurons and promotes neurite outgrowth, which could involve synaptic localization. However, direct evidence for human GPC2 synaptic localization is limited. Reason: While the IBA annotation is phylogenetically supported and consistent with GPC2's role in neuronal development, synaptic localization is not the primary/core localization for GPC2. The core localization is general cell surface. Supporting Evidence: UniProtKB:Q8N158 May fulfill a function related to the motile behaviors of developing neurons
GO:1905475 regulation of protein localization to membrane	IBA GO_REF:0000033	ACCEPT	Summary: GPC2 is annotated to regulation of protein localization to membrane based on phylogenetic inference. As a cell-surface proteoglycan co-receptor, glypicans can influence the localization and clustering of signaling receptors at the membrane. The UniProt entry notes that MDK interaction with GPC2 induces GPC2 clustering through heparan sulfate chain. Reason: The annotation is consistent with the known function of glypicans as signaling co-receptors that can modulate receptor localization and clustering at the cell surface. The MDK-induced GPC2 clustering provides mechanistic support. Supporting Evidence: UniProtKB:Q8N158 this interaction induces GPC2 clustering through heparan sulfate chain
GO:0007224 smoothened signaling pathway	IBA GO_REF:0000033	ACCEPT	Summary: GPC2 is annotated to smoothened signaling pathway based on phylogenetic inference. Glypicans are well-established modulators of Hedgehog/smoothened signaling, with the Drosophila glypican Dally-like being essential for Hedgehog signaling. Mammalian glypicans including GPC2 are believed to function similarly in modulating Hedgehog pathway components. Reason: The role of glypicans in smoothened/Hedgehog signaling is well-established across species and the IBA inference from phylogenetic data is appropriate for this conserved function. Supporting Evidence: GO_REF:0000033 Phylogenetic inference from glypican orthologs known to modulate Hedgehog signaling
GO:0005576 extracellular region	IEA GO_REF:0000044	ACCEPT	Summary: GPC2 is annotated to extracellular region based on UniProt subcellular location mapping. The annotation is appropriate as GPC2 exists as a GPI-anchored protein on the extracellular face of the membrane, and can also be shed as Secreted glypican-2 into the extracellular space. Reason: The annotation is correct for both the GPI-anchored form (exposed to extracellular space) and the secreted/shed form. UniProt confirms both localizations. Supporting Evidence: UniProtKB:Q8N158 RecName: Full=Secreted glypican-2
GO:0005886 plasma membrane	IEA GO_REF:0000120	ACCEPT	Summary: GPC2 is annotated to plasma membrane based on automated annotation methods. This is correct for the mature GPI-anchored form of the protein, which is attached to the external leaflet of the plasma membrane. Reason: GPC2 is a GPI-anchored protein that localizes to the plasma membrane. UniProt confirms this localization. Supporting Evidence: UniProtKB:Q8N158 Cell membrane {ECO:0000250}; Lipid-anchor, GPI- anchor {ECO:0000250}; Extracellular side {ECO:0000250}
GO:0009966 regulation of signal transduction	IEA GO_REF:0000002	ACCEPT	Summary: GPC2 is annotated to regulation of signal transduction based on InterPro glypican domain mapping. This is appropriate as glypicans are established signaling co-receptors that modulate ligand-receptor interactions. GPC2 specifically interacts with PTN and MDK to regulate signaling pathways affecting neurite outgrowth. Reason: The annotation correctly captures the signaling co-receptor function of GPC2. This is a core function of all glypicans and is supported by specific interaction data for GPC2 with growth factors PTN and MDK. Supporting Evidence: UniProtKB:Q8N158 Interacts (via heparan sulfate) with PTN; this interaction promotes neurite outgrowth file:human/GPC2/GPC2-deep-research-falcon.md As a GPI-anchored HSPG, GPC2 serves as a cell-surface co-receptor that modulates ligand-receptor interactions
GO:0031012 extracellular matrix	IEA GO_REF:0000002	KEEP AS NON CORE	Summary: Duplicate annotation of extracellular matrix via InterPro mapping. Same assessment as the IBA annotation - GPC2 is primarily a cell-surface protein, though it may interact with ECM components. Reason: Same rationale as IBA annotation - ECM is a secondary/non-core localization for this GPI-anchored cell surface proteoglycan. Supporting Evidence: UniProtKB:Q8N158 Cell membrane {ECO:0000250}; Lipid-anchor, GPI- anchor {ECO:0000250}; Extracellular side {ECO:0000250}
GO:0043202 lysosomal lumen	IEA GO_REF:0000117	KEEP AS NON CORE	Summary: GPC2 is annotated to lysosomal lumen based on ARBA machine learning. This likely reflects the degradation pathway for heparan sulfate proteoglycans, where they are internalized and degraded in lysosomes. This is part of the normal turnover of the protein rather than a functional localization. Reason: Lysosomal localization represents the degradation pathway for GPC2, not its functional site. The primary function occurs at the cell surface. Supporting Evidence: GO_REF:0000117 ARBA machine learning prediction for lysosomal localization based on proteoglycan turnover patterns
GO:0098552 side of membrane	IEA GO_REF:0000043	MODIFY	Summary: GPC2 is annotated to side of membrane based on UniProt keyword mapping. This is a very general term; the more specific annotation should be external side of plasma membrane given the GPI-anchor localization. Reason: While not incorrect, this annotation is too general. The protein is specifically on the external side of the plasma membrane via GPI anchor. Proposed replacements: external side of plasma membrane Supporting Evidence: UniProtKB:Q8N158 Extracellular side {ECO:0000250}
GO:0007224 smoothened signaling pathway	IEA GO_REF:0000107	ACCEPT	Summary: Duplicate annotation of smoothened signaling pathway via Ensembl Compara ortholog transfer from rat GPC2 (P51653). Same assessment as IBA annotation. Reason: Consistent with IBA annotation and supported by known glypican biology in Hedgehog/smoothened signaling modulation. Supporting Evidence: GO_REF:0000107 Automatic transfer from rat ortholog P51653 based on Ensembl Compara
GO:0010976 positive regulation of neuron projection development	IEA GO_REF:0000107	ACCEPT	Summary: GPC2 is annotated to positive regulation of neuron projection development based on ortholog transfer from rat. This is strongly supported by UniProt which describes GPC2 interactions with PTN and MDK that promote neurite outgrowth. Reason: The annotation is well-supported by the mechanistic data on GPC2-PTN and GPC2-MDK interactions promoting neurite outgrowth. UniProt explicitly states this function. Supporting Evidence: UniProtKB:Q8N158 this interaction promotes neurite outgrowth through binding of PTN with chondroitin sulfate of proteoglycans UniProtKB:Q8N158 this interaction induces neuronal cell adhesion and neurite outgrowth
GO:0030182 neuron differentiation	IEA GO_REF:0000107	KEEP AS NON CORE	Summary: GPC2 is annotated to neuron differentiation based on Ensembl ortholog transfer. Given GPC2's role in neurite outgrowth and its expression in developing neurons, this annotation is reasonable though somewhat general. Reason: While GPC2 promotes neurite outgrowth which is part of neuron differentiation, the more specific annotation (positive regulation of neuron projection development) better captures its function. This broader term is kept as non-core. Supporting Evidence: UniProtKB:Q8N158 May fulfill a function related to the motile behaviors of developing neurons
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-9940993	KEEP AS NON CORE	Summary: GPC2 is annotated to Golgi lumen based on Reactome pathway annotations for heparan sulfate proteoglycan biosynthesis. As a proteoglycan, GPC2 transits through the Golgi where its heparan sulfate chains are synthesized and modified. This represents biosynthetic trafficking rather than the functional site. Reason: Golgi localization reflects the biosynthetic pathway for HS-GAG addition, not the functional localization of mature GPC2 at the cell surface. Supporting Evidence: Reactome:R-HSA-9940993 PXYLP1 dephosphorylates Xyl moiety
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-9941039	KEEP AS NON CORE	Summary: Duplicate Golgi lumen annotation from Reactome FAM20B phosphorylation pathway. Same assessment as above. Reason: Biosynthetic localization, not functional site. Supporting Evidence: Reactome:R-HSA-9941039 FAM20B phosphorylates Xyl moiety
GO:0010976 positive regulation of neuron projection development	ISS GO_REF:0000024	ACCEPT	Summary: GPC2 is annotated to positive regulation of neuron projection development by sequence similarity (ISS) transfer. This is consistent with the IEA annotation and supported by mechanistic data on PTN and MDK interactions. Reason: Core function annotation consistent with known GPC2 biology. The ISS annotation provides additional support to the IEA annotation. Supporting Evidence: UniProtKB:Q8N158 this interaction induces neuronal cell adhesion and neurite outgrowth
GO:0005515 protein binding	IPI PMID:29162697 EB1-binding-myomegalin protein complex promotes centrosomal ...	REMOVE	Summary: GPC2 is annotated to protein binding based on high-throughput interactome analysis. The cited paper (PMID:29162697) is about EB1-binding-myomegalin complex and centrosomal microtubules - it does not appear to directly study GPC2 function. This appears to be from a large-scale protein-protein interaction screen. The annotation is too general to be informative. Reason: Per curation guidelines, protein binding does not provide informative functional annotation. The cited paper does not directly study GPC2, and the interactions detected in high-throughput screens lack specificity for GO annotation purposes. Supporting Evidence: PMID:29162697 EB1-binding-myomegalin protein complex promotes centrosomal microtubules functions
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-1878002	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome xylosyltransferase pathway for GAG linker biosynthesis. Non-core biosynthetic localization. Reason: Biosynthetic trafficking pathway, not functional localization. Supporting Evidence: Reactome:R-HSA-1878002 XYLTs transfer Xyl to core protein
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-1889955	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome B3GAT pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-1889955 B3GAT dimers transfer GlcA to tetrasaccharide linker
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-1889978	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome B3GALT6 pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-1889978 B3GALT6 transfers Gal to the tetrasaccharide linker
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2022851	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome EXT1:EXT2 heparan chain extension pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2022851 EXT1:EXT2 transfers GlcNAc to the heparan chain
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2022856	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome heparan sulfate biosynthesis. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2022856 EXT1:EXT2 transfers GlcA to heparan
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2022860	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome NDST sulfation pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2022860 NDST1-4 can sulfate a glucosamine residue in heparan
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2022887	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome NDST deacetylation pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2022887 NDST1-4 N-deacetylates GlcNAc residues in heparan
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2024108	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome HSPG secretion pathway. Reason: Biosynthetic/secretory pathway localization. Supporting Evidence: Reactome:R-HSA-2024108 Some HSPGs are secreted to the plasma membrane
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2076383	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome HS3ST1 sulfation pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2076383 HS3ST1 sulfates GlcN at C3 in heparan sulfate
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2076392	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome heparan biosynthesis. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2076392 EXT1:EXT2 transfers GlcA to heparan
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2076419	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome HS6ST sulfation pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2076419 HS6STs sulfate GlcN at C6 in heparan sulfate/heparin
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2076508	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome HS2ST1 sulfation pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2076508 HS2ST1 trimer sulfates IdoA at C2 in heparan sulfate
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-2076611	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome HS3ST2-6 sulfation pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-2076611 HS3ST2-6 sulfate GlcN at C3 in heparan sulfate
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-3560802	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective B3GAT3 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-3560802 Defective B3GAT3 does not transfer GlcA to tetrasaccharide linker
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-3656254	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective EXT2 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-3656254 Defective EXT2 (in EXT1:EXT2) does not transfer GlcNAc to the heparan chain
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-3656257	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective EXT1 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-3656257 Defective EXT1 (in EXT1:EXT2) does not transfer GlcA to heparan
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-3656261	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective EXT1 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-3656261 Defective EXT1 (in EXT1:EXT2) does not transfer GlcNAc to the heparan chain
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-3656267	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective EXT2 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-3656267 Defective EXT2 (in EXT1:EXT2) does not transfer GlcA to heparan
GO:0005886 plasma membrane	TAS Reactome:R-HSA-1678694	ACCEPT	Summary: Plasma membrane annotation from Reactome HPSE2 binding pathway. Reason: Plasma membrane is the core functional localization of GPC2 as a GPI-anchored signaling co-receptor. Supporting Evidence: Reactome:R-HSA-1678694 Heparanase 2 (HPSE2) binds heparan sulfate proteoglycans
GO:0005886 plasma membrane	TAS Reactome:R-HSA-2024084	ACCEPT	Summary: Plasma membrane annotation from Reactome HS-GAG degradation pathway. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-2024084 HS-GAGs translocate to the lysosome for degradation
GO:0005886 plasma membrane	TAS Reactome:R-HSA-2024108	ACCEPT	Summary: Plasma membrane annotation from Reactome HSPG secretion pathway. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-2024108 Some HSPGs are secreted to the plasma membrane
GO:0005886 plasma membrane	TAS Reactome:R-HSA-2404131	ACCEPT	Summary: Plasma membrane annotation from Reactome retinoid transport pathway. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-2404131 LRPs transport extracellular CR:atREs:HSPG:apoE to cytosol
GO:0005886 plasma membrane	TAS Reactome:R-HSA-2423785	ACCEPT	Summary: Plasma membrane annotation from Reactome retinoid metabolism pathway. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-2423785 CR:atREs binds apoE and HSPG
GO:0005886 plasma membrane	TAS Reactome:R-HSA-2429643	ACCEPT	Summary: Plasma membrane annotation from Reactome retinoid metabolism pathway. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-2429643 NREH hydrolyses atREs (HSPG:apoE) to atROL and FAs
GO:0005886 plasma membrane	TAS Reactome:R-HSA-9694579	ACCEPT	Summary: Plasma membrane annotation from Reactome SARS-CoV-2 entry pathway. HSPGs including glypicans can serve as attachment factors for viral entry. Reason: The localization is correct and represents the core plasma membrane localization, even though this particular pathway involves viral exploitation. Supporting Evidence: Reactome:R-HSA-9694579 Spike glycoprotein of SARS-CoV-2 binds ACE2 on host cell
GO:0005886 plasma membrane	TAS Reactome:R-HSA-9694661	ACCEPT	Summary: Plasma membrane annotation from Reactome SARS-CoV-2 entry pathway. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-9694661 TMPRSS2 Mediated SARS-CoV-2 Spike Protein Cleavage and Endocytosis
GO:0005886 plasma membrane	TAS Reactome:R-HSA-9698988	ACCEPT	Summary: Plasma membrane annotation from Reactome SARS-CoV-2 entry pathway. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-9698988 Direct Host Cell Membrane Membrane Fusion and Release of SARS-CoV-2 Nucleocapsid
GO:0005886 plasma membrane	TAS Reactome:R-HSA-9699007	ACCEPT	Summary: Plasma membrane annotation from Reactome SARS-CoV-2 entry pathway. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-9699007 FURIN Mediated SARS-CoV-2 Spike Protein Cleavage and Endocytosis
GO:0005886 plasma membrane	TAS Reactome:R-HSA-9836899	ACCEPT	Summary: Plasma membrane annotation from Reactome RSV attachment pathway. sG binds to HSPGs. Reason: Core localization annotation. Supporting Evidence: Reactome:R-HSA-9836899 The secreted soluble isoform of hRSV G protein (sG) binds to proteoglycans on the surface of host cells
GO:0043202 lysosomal lumen	TAS Reactome:R-HSA-1667005	KEEP AS NON CORE	Summary: Lysosomal lumen annotation from Reactome heparanase cleavage pathway. Reason: Degradation pathway localization, not functional site. Supporting Evidence: Reactome:R-HSA-1667005 Heparanase (HPSE) cleaves heparan sulfate from its proteoglycan
GO:0043202 lysosomal lumen	TAS Reactome:R-HSA-2024084	KEEP AS NON CORE	Summary: Lysosomal lumen annotation from Reactome HS-GAG degradation pathway. Reason: Degradation pathway localization. Supporting Evidence: Reactome:R-HSA-2024084 HS-GAGs translocate to the lysosome for degradation
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-1889981	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome B4GALT7 pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-1889981 B4GALT7 transfers Gal group to xylosyl-unit of the tetrasaccharide linker
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-3560804	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective B4GALT7 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-3560804 Defective B4GALT7 does not transfer Gal to xylosyl-unit of the tetrasaccharide linker
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-9036285	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective EXT1 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-9036285 Defective EXT1 (in EXT1:EXT2) does not transfer GlcA to heparan
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-9036289	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective EXT2 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-9036289 Defective EXT2 (in EXT1:EXT2) does not transfer GlcA to heparan
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-9953259	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome EXTL3 pathway. Reason: Biosynthetic pathway localization. Supporting Evidence: Reactome:R-HSA-9953259 EXTL3 dimer transfers GlcNAc to the GAG linker
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-1667005	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome heparanase pathway. Reason: This relates to the processing pathway for HSPGs. Supporting Evidence: Reactome:R-HSA-1667005 Heparanase (HPSE) cleaves heparan sulfate from its proteoglycan
GO:0005796 Golgi lumen	TAS Reactome:R-HSA-4420365	KEEP AS NON CORE	Summary: Golgi lumen annotation from Reactome defective B3GALT6 pathway. Reason: Biosynthetic pathway localization (disease context). Supporting Evidence: Reactome:R-HSA-4420365 Defective B3GALT6 does not transfer Gal to the tetrasaccharide linker
GO:0005783 endoplasmic reticulum	IDA GO_REF:0000054	KEEP AS NON CORE	Summary: GPC2 is annotated to endoplasmic reticulum based on LIFEdb fusion protein localization data. As a secreted/membrane protein, GPC2 would transit through the ER during biosynthesis. This represents a biosynthetic localization. Reason: ER localization represents the biosynthetic pathway for GPC2. The functional localization is at the plasma membrane. Supporting Evidence: GO_REF:0000054 Gene Ontology annotation based on curation of intracellular localizations of expressed fusion proteins in living cells

Gene Description

Existing Annotations Review

Core Functions

GPC2 functions as a signaling co-receptor at the cell surface, modulating ligand-receptor interactions through its heparan sulfate chains. It binds growth factors such as PTN and MDK to regulate neurite outgrowth signaling.

References

Deep Research

Falcon

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