Promoter region of CDH13 is CpG rich and often hypermethylated in various malignant tumors, i.e. breast, lung, colorectal, skin, ovary, chronic myeloid leukemia, and more.

3828 bp mRNA; 2145 bp open reading frame.

Not yet reported.

713 amino acids.
Unlike classical cadherin molecules, CDH13 lacks a transmembrane domain or cytoplasmic region, and is anchored to surface membrane via glycosylphosphatidylinositol anchor. The extracellular domain of CDH13 shows significant homology with other cadherins; however, CDH13 EC1 lacks many amino acids crucial for the adhesive functions.
CDH13 lacks intracellular domain, which is believed to be critical for homophilic adhesion of other classical cadherins.

Heart, skeletal muscle, brain, bone (osteoblast), epidermal basal cell, endothelial cell (tumor vessel, active remodeling vascule).
Controversial experiments and arguments exist for the expression in the liver, hepatocyte.

Cell surface membrane, lipid raft (cytoplasmic and nuclear localization are also reported).

CDH13 is believed to have diverse functions.
1. Adiponectin receptor. CDH13 binds to the hexameric and larger adiponectin, an insulin-sensitizing hormone, which is secreted by adipocytes.
2. Homophilic adhesion. Unlike other classical cadherins, which have the strong homophilic adhesion function, EC1 domain of CDH13 lacks many amino acids crucial for the adhesive functions. Instead CDH13 is thought to form dimers through the non-swapped interface near the EC1-EC2 calcium binding site.
3. Tumor suppressor function. Especially against cancer invasion; however, the exact molecular mechanism which is responsible for inhibiting cancer progression still remains unclear.
4. Angiogenesis. CDH13 facilitates tumor neovascularization. In tumor microenvironment, CDH13 may recruit adiponectin to sequester various growth factors to assist the tumor associated angiogenesis.

CDH1 (approximately 38%).

Silencing of CDH13 expression is often found in various malignant tumors. Hypermethylation of the promoter region is the major molecular mechanism for loss of CDH13 expression.
Genomic mutation is little reported.