Aliases for DUSP6 Gene
External Ids for DUSP6 Gene
Previous GeneCards Identifiers for DUSP6 Gene
The protein encoded by this gene is a member of the dual specificity protein phosphatase subfamily. These phosphatases inactivate their target kinases by dephosphorylating both the phosphoserine/threonine and phosphotyrosine residues. They negatively regulate members of the mitogen-activated protein (MAP) kinase superfamily (MAPK/ERK, SAPK/JNK, p38), which are associated with cellular proliferation and differentiation. Different members of the family of dual specificity phosphatases show distinct substrate specificities for various MAP kinases, different tissue distribution and subcellular localization, and different modes of inducibility of their expression by extracellular stimuli. This gene product inactivates ERK2, is expressed in a variety of tissues with the highest levels in heart and pancreas, and unlike most other members of this family, is localized in the cytoplasm. Mutations in this gene have been associated with congenital hypogonadotropic hypogonadism. Alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jan 2014]
GeneCards Summary for DUSP6 Gene
DUSP6 (Dual Specificity Phosphatase 6) is a Protein Coding gene. Diseases associated with DUSP6 include Hypogonadotropic Hypogonadism 19 With Or Without Anosmia and Normosmic Congenital Hypogonadotropic Hypogonadism. Among its related pathways are Interleukin-3, 5 and GM-CSF signaling and MAPK targets/ Nuclear events mediated by MAP kinases. GO annotations related to this gene include phosphatase activity and phosphoprotein phosphatase activity. An important paralog of this gene is DUSP7.
UniProtKB/Swiss-Prot for DUSP6 Gene
Inactivates MAP kinases. Has a specificity for the ERK family (PubMed:9858808). Plays an important role in alleviating chronic postoperative pain. Necessary for the normal dephosphorylation of the long-lasting phosphorylated forms of spinal MAPK1/3 and MAP kinase p38 induced by peripheral surgery, which drives the resolution of acute postoperative allodynia (By similarity).