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: MRC1
Gene Name: MRC1
Protein Full Name: Macrophage mannose receptor 1
Alias: CD206; CLEC13D; Mannose receptor, C type 1
Mass (Da): 166012
Number AA: 1456
UniProt ID: P22897
Locus ID: 4360
COSMIC ID: MRC1
Gene location on chromosome: 10p12.33
Cancer protein type: UNCLEAR
Effect of cancer mutation on protein: UNCLEAR
Effect of active protein on cancer: UNCLEAR
Number of cancer specimens: 7033
Percent of cancer specimens with mutations: 0.17
Normal role description: MRC1 is a type I membrane receptor responsible for mediating the endocytosis of glycoproteins by macrophages. It binds high-mannose structures on the surface of potentially pathogenic viruses, bacteria, and fungi, leading to the neutralization by phagocytic engulfment. It is also resonsible for rapidly clearing a subset of mannose-bearing serum glycoproteins that are elevated during inflammation; for internalizing collagen and gelatin in a carbohydrate-independent mechanism; and for regulating macrophage migration during different stages of pathogenesis. It has been implicated in Acute Lymphoblastic Leukemia with MLL rearrangements, where its expression is lower than in normal cells, possibly suggesting an involvement of MRC1 in MLL-mediated growth of leukemic cells; and in Acute Monocytic Leukemia, where binding of trimannose conjugate (TMC) to the receptor is thought to play a role in the activation of monocytic leukemia cells. In lymphatic endothelial cells, MRC1 is involved in leukocyte trafficking and contributes to the metastatic behavior of cancer cells, and the gene is over-expressed in vascular endothelial cells during early development, suggesting that it may function as a regulator of vasculature formation.


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