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SPRED1 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.
Protein type: Inhibitor
Chromosomal Location of Human Ortholog: 15q14
Cellular Component: cytosol; nucleus; plasma membrane
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
Disease: Legius Syndrome
Reference #:  Q7Z699 (UniProtKB)
Alt. Names/Synonyms: EVH1/Sprouty domain containing protein; FLJ33903; hSpred1; NFLS; SPRE1; Spred-1; SPRED1; sprouty-related, EVH1 domain containing 1; Sprouty-related, EVH1 domain-containing protein 1; suppressor of Ras/MAPK activation
Gene Symbols: SPRED1
Molecular weight: 50,477 Da
Basal Isoelectric point: 6.12  Predict pI for various phosphorylation states
CST Pathways:  Growth And Differentiation Control by MAPKs  |  Microtubule Dynamics
Protein-Specific Antibodies or siRNAs from Cell Signaling Technology® Total Proteins
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