Tyrosine kinase substrate that inhibits growth-factor- mediated activation of MAP kinase. Negatively regulates hematopoiesis of bone marrow. Defects in SPRED1 are the cause of neurofibromatosis type 1-like syndrome (NFLS). It is a disorder characterized mainly by cafe au lait macules without neurofibromas or other tumor manifestations of neurofibromatosis type 1, axillary freckling, and macrocephaly. Additional clinical manifestations include Noonan-like facial dysmorphism, lipomas, learning disabilities and attention deficit-hyperactivity. Note: This description may include information from UniProtKB.
Molecular Function: phosphatase binding; protein binding; protein kinase binding; protein serine/threonine kinase inhibitor activity; stem cell factor receptor binding
Biological Process: fibroblast growth factor receptor signaling pathway; inactivation of MAPK activity; MAPKKK cascade; positive regulation of DNA damage response, signal transduction by p53 class mediator
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.