Gene Information
Gene Symbol
Entrez Gene ID
Gene Name
Wnt family member 5A
Chromosomal Location
The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene encodes a member of the WNT family that signals through both the canonical and non-canonical WNT pathways. This protein is a ligand for the seven transmembrane receptor frizzled-5 and the tyrosine kinase orphan receptor 2. This protein plays an essential role in regulating developmental pathways during embryogenesis. This protein may also play a role in oncogenesis. Mutations in this gene are the cause of autosomal dominant Robinow syndrome. Alternate splicing results in multiple transcript variants. [provided by RefSeq, Jan 2012]
RefSeq DNA
RefSeq mRNA

Gene Ontology (GO)

GO ID Ontology Function Evidence Reference
GO:0000187 Biological process Activation of MAPK activity IDA 20034610
GO:0001837 Biological process Epithelial to mesenchymal transition IEP 12841867
GO:0001938 Biological process Positive regulation of endothelial cell proliferation IMP 17986384
GO:0002088 Biological process Lens development in camera-type eye ISS 16258938
GO:0002741 Biological process Positive regulation of cytokine secretion involved in immune response IMP 18174455
Protein Information
Protein Name
Protein Wnt-5a, WNT-5A protein, epididymis secretory sperm binding protein, wingless-type MMTV integration site family, member 5A
Ligand for members of the frizzled family of seven transmembrane receptors. Can activate or inhibit canonical Wnt signaling, depending on receptor context. In the presence of FZD4, activates beta-catenin signaling. In the presence of ROR2, inhibits the canonical Wnt pathway by promoting beta-catenin degradation through a GSK3-independent pathway which involves down-regulation of beta-catenin-induced reporter gene expression (By similarity). Suppression of the canonical pathway allows chondrogenesis to occur and inhibits tumor formation. Stimulates cell migration. Decreases proliferation, migration, invasiveness and clonogenicity of carcinoma cells and may act as a tumor suppressor (PubMed:15735754). Mediates motility of melanoma cells (PubMed:17426020). Required during embryogenesis for extension of the primary anterior-posterior axis and for outgrowth of limbs and the genital tubercle. Inhibits type II collagen expression in chondrocytes (By similarity).
Refseq Proteins
Pfam Accession Pfam ID
PF00110 wnt

mTOR signaling pathway
Wnt signaling pathway
Axon guidance
Hippo signaling pathway
Signaling pathways regulating pluripotency of stem cells
Cushing syndrome
Human papillomavirus infection
Pathways in cancer
Proteoglycans in cancer
Basal cell carcinoma
Breast cancer
Hepatocellular carcinoma
Gastric cancer


TCF dependent signaling in response to WNT
WNT ligand biogenesis and trafficking
Ca2+ pathway
PCP/CE pathway
Asymmetric localization of PCP proteins
WNT5A-dependent internalization of FZD4
WNT5A-dependent internalization of FZD2, FZD5 and ROR2
Cargo recognition for clathrin-mediated endocytosis
Clathrin-mediated endocytosis
WNT5:FZD7-mediated leishmania damping

ENSP00000416293 P11166 P11166
    View interactions

Associated Diseases

Disease groupDisease NameReferences
Endocrine System Diseases
Robinow Syndrome
Endometrial Cancer
Cervical Cancer
Lung Cancer
PubMed ID Associated gene/s Associated condition Genetic Mutation Diagnostic Criteria Association with PCOS Ethnicity Conclusion
ROR2, TNFA , SFRP5, PI3K, IL-1?, IL-6, IL-8, CCL2,, AKT, JNK, ERK1/2 CRP,  
PCOS, Hyperandrogenism, anovulation, metabolic aberrations, inflammation 
2003 Rotterdam Criteria 
35 PCOS patients and 87 control women 
WNT5a acts as a proinflammatory factor in human ovarian GCs. The up-regulated expression of WNT5a in PCOS increases inflammation and oxidative stress predominantly via the phosphatidylinositol 3-kinase/AKT/NF-?B signaling pathway. The proinflammatory cytokines induced might further enhance WNT5a expression via NF-?B-dependent regulation, indicating a novel regulatory system for chronic inflammation in PCOS. 

| © 2019, Biomedical Informatics Centre, NIRRH |
National Institute for Research in Reproductive Health, Jehangir Merwanji Street, Parel, Mumbai-400 012
Tel: 91-22-24192104, Fax No: 91-22-24139412