Double layer of lipid molecules that encloses all cells, and, in eukaryotes, many organelles; may be a single or double lipid bilayer; also includes associated proteins.
external side of plasma membrane
The side of the plasma membrane that is opposite to the side that faces the cytoplasm.
integral to membrane
Penetrating at least one phospholipid bilayer of a membrane. May also refer to the state of being buried in the bilayer with no exposure outside the bilayer. When used to describe a protein, indicates that all or part of the peptide sequence is embedded in the membrane.
Invagination of the plasma membrane of a muscle cell that extends inward from the cell surface around each myofibril. The ends of T-tubules make contact with the sarcoplasmic reticulum membrane.
Co-expression of Kir2.1 with Kir3.4 in Xenopus oocytes and HEK293T cells did not
yield currents with distinguishable features. However, co-expression of a dominant-negative Kir2.1 with
the wild-type Kir3.4 decreased the Kir3.4 current amplitude in Xenopus oocytes. The results indicate that Kir2.1 is capable of forming heteromultimeric channels with Kir3.4. (Ishihara
Stimulation of the M2 receptor by ACh causes
dissociation of the coupled G-protein and the Gbc-subunits activate the Kir3.1/3.4 channel by direct binding
(PIP2) is a requirement for
Kir channels activity and a decrease in bound PIP2
strongly decreases the open probability of the Kir3.1/
3.4 channels (Huang , Sui ).
GIRK1/4 channel current can be blocked by BaCl(2) and enhanced by increasing the driving force for K(+) across the cell membrane. (Walsh )
Kir3.1 is expressed in the heart and brain (Kubo ), and is known to assemble with Kir3.4 in SAN and atrial myocytes in the heart and with Kir3.2 in the brain to form functional channels
(Krapivinsky , Velimirovic ).
Kir3.4, expressed mainly in SAN and atrial myocytes in the heart,
form heterotetrameric channels, which are coupled to m2 muscarinic receptor via G-protein bc subunits and carry the ACh-activated K+ current (IK,ACh) regulating the heart rate (Krapivinsky , Corey ).
Mice deficient of Kir3.1 or 3.4 exhibit mild resting
tachycardia (Bettahi ) and impaired beat-to-beat control (Wickman ).
Kir3.4 deficient mice were resistant to
atrial fibrillation caused by vagal stimulation (Kovoor ). Kir3.4 could be predisposing to or even protecting against atrial fibrillation (Calloe ).