Feedback inhibitor of fibroblast growth factor mediated Ras-MAPK signaling and ERK activation (PubMed:12958313, PubMed:12807873). Regulates the nuclear ERK signaling pathway by spatially blocking nuclear translocation of activated ERK without inhibiting cytoplasmic phosphorylation of ERK (PubMed:15239952). Mediates JNK activation and may be involved in apoptosis (By similarity). May inhibit FGF-induced FGFR1 tyrosine phosphorylation (By similarity). Might have a role in the early stages of fate specification of GnRH-secreting neurons (By similarity). Inhibits TGFB-induced epithelial-to-mesenchymal transition in lens epithelial cells (By similarity). Interacts with MAP3K7 (By similarity). Self-associates. Interacts with FGFR1, FGFR2 and phosphorylated MAP2K1 or MAP2K2. Associates with a MAP2K1/2-MAPK1/3 complex. Predominantly associated with the Golgi apparatus and is partially translocated to the plasma membrane upon stimulation. Expressed in umbilical vein endothelial cells and in several highly vascularized tissues such as kidney, colon, skeletal muscle, heart and small intestine. Highly expressed in ductal epithelial cells of salivary glands, seminal vesicles and the collecting tubules of the kidney. Isoform 1 is also highly expressed in both fetal and adult brain, pituitary, tonsils, spleen, adenoids, fetal kidney, liver, testes and ovary. Isoform 1 is also expressed at moderate levels in primary aortic endothelial cells and adrenal medulla, and at low levels in adrenal cortex. Isoform 4 is specifically and highly expressed in pituitary, fetal brain and umbilical vein endothelial cells. The disease is caused by variants affecting distinct genetic loci, including the gene represented in this entry. Some patients carrying mutations in IL17RD also have a heterozygous mutation in another HH-associated gene including FGFR1 and KISS1R (PubMed:23643382).