Protein Details: KCa1.1 (large conductance calcium-activated potassium channels)

Protein ID

ICDB_Pro_0815

Protein Name

KCa1.1 (large conductance calcium-activated potassium channels)

Gene Name

KCNMA1; KCNMA; SLO

Organism

Homo sapiens (Human)

Length

1236 amino acids

AlphaFoldDB

AF-Q12791-F1-model_v4.pdb

Function

Potassium channel activated by both membrane depolarization or increase in cytosolic Ca(2+) that mediates export of K(+). It is also activated by the concentration of cytosolic Mg(2+). Its activation dampens the excitatory events that elevate the cytosolic Ca(2+) concentration and/or depolarize the cell membrane. It therefore contributes to repolarization of the membrane potential. Plays a key role in controlling excitability in a number of systems;such as regulation of the contraction of smooth muscle;the tuning of hair cells in the cochlea;regulation of transmitter release;and innate immunity. In smooth muscles;its activation by high level of Ca(2+);caused by ryanodine receptors in the sarcoplasmic reticulum;regulates the membrane potential. In cochlea cells;its number and kinetic properties partly determine the characteristic frequency of each hair cell and thereby helps to establish a tonotopic map. Kinetics of KCNMA1 channels are determined by alternative splicing;phosphorylation status and its combination with modulating beta subunits. Highly sensitive to both iberiotoxin (IbTx) and charybdotoxin (CTX)

Sequence

MANGGGGGGGSSGGGGGGGGSSLRMSSNIHANHLSLDASSSSSSSSSSSSSSSSSSSSSSVHEPKMDALIIPVTMEVPCDSRGQRMWWAFLASSMVTFFGGLFIILLWRTLKYLWTVCCHCGGKTKEAQKINNGSSQADGTLKPVDEKEEAVAAEVGWMTSVKDWAGVMISAQTLTGRVLVVLVFALSIGALVIYFIDSSNPIESCQNFYKDFTLQIDMAFNVFFLLYFGLRFIAANDKLWFWLEVNSVVDFFTVPPVFVSVYLNRSWLGLRFLRALRLIQFSEILQFLNILKTSNSIKLVNLLSIFISTWLTAAGFIHLVENSGDPWENFQNNQALTYWECVYLLMVTMSTVGYGDVYAKTTLGRLFMVFFILGGLAMFASYVPEIIELIGNRKKYGGSYSAVSGRKHIVVCGHITLESVSNFLKDFLHKDRDDVNVEIVFLHNISPNLELEALFKRHFTQVEFYQGSVLNPHDLARVKIESADACLILANKYCADPDAEDASNIMRVISIKNYHPKIRIITQMLQYHNKAHLLNIPSWNWKEGDDAICLAELKLGFIAQSCLAQGLSTMLANLFSMRSFIKIEEDTWQKYYLEGVSNEMYTEYLSSAFVGLSFPTVCELCFVKLKLLMIAIEYKSANRESRILINPGNHLKIQEGTLGFFIASDAKEVKRAFFYCKACHDDITDPKRIKKCGCKRPKMSIYKRMRRACCFDCGRSERDCSCMSGRVRGNVDTLERAFPLSSVSVNDCSTSFRAFEDEQPSTLSPKKKQRNGGMRNSPNTSPKLMRHDPLLIPGNDQIDNMDSNVKKYDSTGMFHWCAPKEIEKVILTRSEAAMTVLSGHVVVCIFGDVSSALIGLRNLVMPLRASNFHYHELKHIVFVGSIEYLKREWETLHNFPKVSILPGTPLSRADLRAVNINLCDMCVILSANQNNIDDTSLQDKECILASLNIKSMQFDDSIGVLQANSQGFTPPGMDRSSPDNSPVHGMLRQPSITTGVNIPIITELVNDTNVQFLDQDDDDDPDTELYLTQPFACGTAFAVSVLDSLMSATYFNDNILTLIRTLVTGGATPELEALIAEENALRGGYSTPQTLANRDRCRVAQLALLDGPFADLGDGGCYGDLFCKALKTYNMLCFGIYRLRDAHLSTPSQCTKRYVITNPPYEFELVPTDLIFCLMQFDHNAGQSRASLSHSSHSSQSSSKKSSSVHSIPSTANRQNRPKSRESRDKQKYVQEERL

PDB Structures

Ligand Binding

1. DICL_CP

2. DICL_Pep

Binding Site

439;462;464;1012;1015;1018;1020

Disease

Paroxysmal Nonkinesigenic Dyskinesia;3;With Or Without Generalized Epilepsy and Liang-Wang Syndrome

Location

Widely expressed. Except in myocytes; it is almost ubiquitously expressed.

DOI ID

10.1016/0169-328x(94)90203-8; 10.1152/ajpheart.1995.269.3.h767; 10.1038/nature02462; 10.1101/gr.2596504; 10.1016/0896-6273(94)90418-9; 10.1093/hmg/3.8.1239; 10.1523/jneurosci.22-05-01840.2002; 10.1073/pnas.93.25.14922; 10.1073/pnas.94.25.14066; 10.1074/jbc.273.49.32430; 10.1073/pnas.96.7.4137; 10.1074/jbc.275.9.6453; 10.1016/s0896-6273(01)00444-5; 10.1523/jneurosci.22-05-01550.2002; 10.1038/nature02003; 10.1085/jgp.20028721; 10.1074/jbc.m110.153940; 10.1074/jbc.m111.335547; 10.1038/nature09162; 10.1124/jpet.110.166017; 10.1073/pnas.1205435109; 10.1126/science.1190414; 10.1038/ng1585; 10.1002/mds.26216; 10.1007/s00439-016-1726-y; 10.1038/s41431-017-0073-3; 10.1093/hmg/ddz117; 10.4274/balkanmedj.2017.0986

RefSeq

NP_001014797.1; NP_001154824.1 [Q12791-1]; NP_001154825.1 [Q12791-2]; NP_001258447.1; NP_001258451.1 [Q12791-6]; NP_002238.2 [Q12791-5]

Feature