Canopy FGF signaling regulator 3 (CNPY3)

Canopy FGF signaling regulator 3 (CNPY3) is an endoplasmic reticulum-resident co-chaperone protein that is essential for the proper folding, assembly, and subcellular trafficking of multiple Toll-like receptors (TLRs), which are key molecules in the innate immune system[1][4]. CNPY3 ensures the export of TLRs from the ER to their sites of action and plays a regulatory role in inflammasome activation, impacting interleukin-1β and interleukin-18 secretion[1]. In the nervous system, CNPY3 is required for neural development, as biallelic loss-of-function variants cause early-onset epileptic encephalopathy (West syndrome)[1][4]. In cancer, CNPY3 is highly expressed in aggressive forms of glioma, enhances migration and invasion of tumor cells, and is associated with increased infiltration by pro-tumor M2 macrophages. High CNPY3 expression serves as a poor prognostic biomarker in glioma and is linked to drug sensitivity in some tumors[2][3].

Other names

Protein canopy homolog 3CTG4AERDA5PRAT4ATNRC5HSPC084UNQ1934/PRO4409CAG4ACTG repeat protein 4aExpanded repeat-domain protein CAG/CTG 5Protein associated with TLR4Trinucleotide repeat-containing gene 5 proteinDEE60EIEE60

Drugs listed are cytotoxic agents used in cancer; their activity may be increased in CNPY3-high tumors, but there is no evidence of direct molecular targeting of CNPY3[2]