Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Processing by proprotein convertases is required for glypican-3 modulation of cell survival, Wnt signaling, and gastrulation movements.
The Simpson-Golabi-Behmel syndrome causative glypican-3, binds to and inhibits the dipeptidyl peptidase activity of CD26.
Glypican-3 binds to Frizzled and plays a direct role in the stimulation of canonical Wnt signaling.
EB1-binding-myomegalin protein complex promotes centrosomal microtubules functions.
A proteomic atlas of glypican-3 interacting partners: Identification of alpha-fetoprotein and other extracellular proteins as potential immunotherapy targets in liver cancer.
K-glypican: a novel GPI-anchored heparan sulfate proteoglycan that is highly expressed in developing brain and kidney.
Mutations in GPC3, a glypican gene, cause the Simpson-Golabi-Behmel overgrowth syndrome.
activated thrombin (factor IIa) + antithrombin III:heparan sulfate -> thrombin:antithrombin III:heparan sulfate
thrombin:antithrombin III:heparan sulfate -> thrombin:cleaved antithrombin III:heparan sulfate
thrombin:cleaved SERPINC1:HSPGs-> thrombin:cleaved SERPINC1 + HSPGs
Heparanase (HPSE) cleaves heparan sulfate from its proteoglycan (lysosome)
Heparanase 2 (HPSE2) binds heparan sulfate proteoglycans
XYLTs transfer Xyl to core protein
B3GAT dimers transfer GlcA to tetrasaccharide linker
B3GALT6 transfers Gal to the tetrasaccharide linker
B4GALT7 transfers Gal group to xylosyl-unit of the tetrasaccharide linker
EXT1:EXT2 transfers GlcNAc to the heparan chain
EXT1:EXT2 transfers GlcA to heparan
NDST1-4 can sulfate a glucosamine residue in heparan to form heparan sulfate (HS)
NDST1-4 N-deacetylates GlcNAc residues in heparan
HS-GAGs translocate to the lysosome for degradation
Some HSPGs are secreted to the plasma membrane
HS3ST1 sulfates GlcN at C3 in heparan sulfate
EXT1:EXT2 transfers GlcA to heparan
HS6STs sulfate GlcN at C6 in heparan sulfate/heparin
HS2ST1 trimer sulfates IdoA at C2 in heparan sulfate
HS3ST2-6 sulfate GlcN at C3 in heparan sulfate
LRPs transport extracellular CR:atREs:HSPG:apoE to cytosol
CR:atREs binds apoE and HSPG
NREH hydrolyses atREs (HSPG:apoE) to atROL and FAs
Defective B3GAT3 does not transfer GlcA to tetrasaccharide linker
Defective B4GALT7 does not transfer Gal to xylosyl-unit of the tetrasaccharide linker
Defective EXT2 (in EXT1:EXT2) does not transfer GlcNAc to the heparan chain
Defective EXT1 (in EXT1:EXT2) does not transfer GlcA to heparan
Defective EXT1 (in EXT1:EXT2) does not transfer GlcNAc to the heparan chain
Defective EXT2 (in EXT1:EXT2) does not transfer GlcA to heparan
Defective B3GALT6 does not transfer Gal to the tetrasaccharide linker
FAM20C phosphorylates FAM20C substrates
Defective EXT1 (in EXT1:EXT2) does not transfer GlcA to heparan
Defective EXT2 (in EXT1:EXT2) does not transfer GlcA to heparan
Spike glycoprotein of SARS-CoV-2 binds ACE2 on host cell
TMPRSS2 Mediated SARS-CoV-2 Spike Protein Cleavage and Endocytosis
Direct Host Cell Membrane Membrane Fusion and Release of SARS-CoV-2 Nucleocapsid
FURIN Mediated SARS-CoV-2 Spike Protein Cleavage and Endocytosis
SERPINC1 binds heparan sulfate
PXYLP1 dephosphorylates Xyl moiety
FAM20B phosphorylates Xyl moiety
EXTL3 dimer transfers GlcNAc to the GAG linker
Processing by convertases is not required for glypican-3-induced stimulation of hepatocellular carcinoma growth.
Glypican-3 promotes the growth of hepatocellular carcinoma by stimulating canonical Wnt signaling.
Glypican-3 inhibits Hedgehog signaling during development by competing with patched for Hedgehog binding.
Processing by convertases is required for glypican-3-induced inhibition of Hedgehog signaling.
Glypican-3: a novel serum and histochemical marker for hepatocellular carcinoma.
UniProtKB entry P51654 (GPC3_HUMAN)