Cancer Protein Description
This report provides a detailed description of a selected cancer protein with information collected from various sources, including UniProt, the Wellcome Trust Sanger Institute’s Catalogue of Somatic Mutations in Cancer (COSMIC), and the Atlas of Genetics and Cytogenetics in Oncology and Haematology.
Protein Name: | DDR1 |
Gene Name: | DDR1 |
Protein Full Name: | Epithelial discoidin domain-containing receptor 1 |
Alias: | CAK; CD167; CD167a; CD167a antigen; Cell adhesion kinase; Discoidin domain receptor tyrosine kinase 1; Discoidin receptor tyrosine kinase; EC 2.7.1.112; EC 2.7.10.1; EDDR1; Epithelial discoidin domain receptor 1 precursor; HGK2; NEP; NTRK4; Protein-tyrosine kinase RTK 6; PTK3A; RTK 6; RTK6; TRK E; TRKE; Tyrosine kinase DDR; Tyrosine- protein kinase CAK |
Mass (Da): | 101128 |
Number AA: | 913 |
UniProt ID: | Q08345 |
Locus ID: | 780 |
COSMIC ID: | DDR1 |
Gene location on chromosome: | 6p21.33 |
Cancer protein type: | OP |
Effect of cancer mutation on protein: | UNCLEAR |
Effect of active protein on cancer: | PROMOTES |
Number of cancer specimens: | 20660 |
Percent of cancer specimens with mutations: | 0.63 |
Mutations observed as inherited: | NA |
Found in amplified chromosomal regions in human cancers: | NA |
Deregulated in translocations: | NA |
Deregulated by viral insertion: | NA |
Transduced into viral genome: | NA |
Gene undergoes hypermethylation: | NA |
Normal role description: | DDR1 is an adhesion protein and a receptor tyrosine kinase part of the insulin receptor subfamily that may be involved in cell-cell interactions and recognition. In addition, it has been shown to promote the proliferation of neoplastic cells. It is mainly expressed by epithelial cells in the kidneys, lungs, gastrointestinal tract, and brain, and may be activated by various types of collagen including types I, II, III, and V. It has been shown to be overexpressed in several tumors. DDR1 can interact with Notch1 and produce a prosurvival effect. It can also enhance cancer cell migration. |