Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
Home | Login
About PhosphoSiteUsing PhosphoSiteprivacy & cookiesCuration ProcessContact
logos LINCs Logo Mt Sinai Logo NIH Logo NCI Logo
Search / Browse Functions
Protein Page:

Kv7.2 Probably important in the regulation of neuronal excitability. Associates with KCNQ3 to form a potassium channel with essentially identical properties to the channel underlying the native M-current, a slowly activating and deactivating potassium conductance which plays a critical role in determining the subthreshold electrical excitability of neurons as well as the responsiveness to synaptic inputs. KCNQ2/KCNQ3 current is blocked by linopirdine and XE991, and activated by the anticonvulsant retigabine. Muscarinic agonist oxotremorine-M strongly suppress KCNQ2/KCNQ3 current in cells in which cloned KCNQ2/KCNQ3 channels were coexpressed with M1 muscarinic receptors. Defects in KCNQ2 are the cause of benign familial neonatal seizures type 1 (BFNS1). A disorder characterized by clusters of seizures occurring in the first days of life. Most patients have spontaneous remission by 12 months of age and show normal psychomotor development. Some rare cases manifest an atypical severe phenotype associated with epileptic encephalopathy and psychomotor retardation. The disorder is distinguished from benign familial infantile seizures by an earlier age at onset. In some patients, neonatal convulsions are followed later in life by myokymia, a benign condition characterized by spontaneous involuntary contractions of skeletal muscles fiber groups that can be observed as vermiform movement of the overlying skin. Electromyography typically shows continuous motor unit activity with spontaneous oligo- and multiplet- discharges of high intraburst frequency (myokymic discharges). Some patients may have isolated myokymia. Defects in KCNQ2 are the cause of epileptic encephalopathy early infantile type 7 (EIEE7). EIEE7 is an autosomal dominant seizure disorder characterized by infantile onset of refractory seizures with resultant delayed neurologic development and persistent neurologic abnormalities. Belongs to the potassium channel family. KQT (TC 1.A.1.15) subfamily. Kv7.2/KCNQ2 sub-subfamily. 6 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Channel, potassium; Membrane protein, integral; Membrane protein, multi-pass
Chromosomal Location of Human Ortholog: 20q13.33
Cellular Component: integral component of membrane; integral component of plasma membrane; plasma membrane; voltage-gated potassium channel complex
Molecular Function: ankyrin binding; calmodulin binding; voltage-gated potassium channel activity
Biological Process: nervous system development; synaptic transmission
Disease: Epileptic Encephalopathy, Early Infantile, 7; Seizures, Benign Familial Neonatal, 1
Reference #:  O43526 (UniProtKB)
Alt. Names/Synonyms: BFNC; EBN; EBN1; ENB1; HNSPC; KCNA11; KCNQ2; KQT-like 2; KV7.2; KVEBN1; neuroblastoma-specific potassium channel protein; Neuroblastoma-specific potassium channel subunit alpha KvLQT2; Potassium voltage-gated channel subfamily KQT member 2; potassium voltage-gated channel, KQT-like subfamily, member 2; Voltage-gated potassium channel subunit Kv7.2
Gene Symbols: KCNQ2
Molecular weight: 95,848 Da
Basal Isoelectric point: 9.35  Predict pI for various phosphorylation states
Protein-Specific Antibodies or siRNAs from Cell Signaling Technology® Total Proteins
Select Structure to View Below


Protein Structure Not Found.
Download PyMol Script
Download ChimeraX Script

STRING  |  cBioPortal  |  Wikipedia  |  Reactome  |  neXtProt  |  Protein Atlas  |  BioGPS  |  Scansite  |  Pfam  |  RCSB PDB  |  Phospho.ELM  |  NetworKIN  |  GeneCards  |  UniProtKB  |  Entrez-Gene  |  GenPept  |  Ensembl Gene  |  Ensembl Protein