Asporin

Asporin is a protein that in humans is encoded by the ASPN gene.^[4]

ASPN
Identifiers
Aliases	ASPN, OS3, PLAP-1, PLAP1, SLRR1C, asporin, Asporin
External IDs	OMIM: 608135; MGI: 1913945; HomoloGene: 32357; GeneCards: ASPN; OMA:ASPN - orthologs
Gene location (Mouse) Chr. Chromosome 13 (mouse)[1] Band 13|13 A5 Start 49,697,919 bp[1] End 49,721,041 bp[1]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in synovial joint periodontal fiber Achilles tendon saphenous vein visceral pleura right coronary artery ascending aorta vena cava gallbladder left coronary artery Top expressed in body of femur calvaria dermis intercostal muscle umbilical cord skin of external ear efferent ductule soleus muscle lumbar spinal ganglion ankle More reference expression data BioGPS More reference expression data
Gene ontology Molecular function calcium ion binding protein kinase inhibitor activity collagen binding extracellular matrix structural constituent conferring compression resistance Cellular component cytoplasm extracellular matrix extracellular region collagen-containing extracellular matrix Biological process bone mineralization biomineral tissue development negative regulation of transforming growth factor beta receptor signaling pathway negative regulation of tooth mineralization negative regulation of protein kinase activity cytokine-mediated signaling pathway negative regulation of receptor signaling pathway via JAK-STAT Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 54829 66695 Ensembl n/a ENSMUSG00000021388 UniProt Q9BXN1 Q99MQ4 RefSeq (mRNA) NM_017680 NM_001193335 NM_001172481 NM_025711 RefSeq (protein) NP_001180264 NP_060150 NP_001165952 NP_079987 Location (UCSC) n/a Chr 13: 49.7 – 49.72 Mb PubMed search [2] [3]
Wikidata
View/Edit Human View/Edit Mouse

Function

ASPN belongs to a family of leucine-rich repeat (LRR) proteins associated with the cartilage matrix. The name asporin reflects the unique aspartate-rich N terminus and the overall similarity to decorin (MIM 125255) (Lorenzo et al., 2001).^[4]