NCBI Accession #
NP_567651.1
NCBI GenBank Nucleotide #
NM_118342.3
NCBI Official Full Name
potassium transport 2/3
NCBI Official Symbol
KT2/3
NCBI Official Synonym Symbols
AKT2; AKT2/3; AKT3; potassium transport 2/3; T10I14.30; T10I14_30
NCBI Protein Information
potassium transport 2/3
NCBI Summary
Encodes AKT2, a photosynthate- and light-dependent inward rectifying potassium channel with unique gating properties that are regulated by phosphorylation. Expressed in guard cell protoplasts and in the phloem and xylem of aerial portions of the plant. The channel can coassemble with another K+ channel, KAT1, in vitro. In guard cells, AKT2/3 is responsible for the Ca2+ sensitivity of the K+ uptake channel. In the phloem, it regulates the sucrose/H+ symporters via the phloem potential. AKT2 belongs to the Shaker family K+ channels which include the following groups based on phylogenetic analysis (FEBS Letters (2007) 581: 2357): I (inward rectifying channel): AKT1 (AT2G26650), AKT5 (AT4G32500) and SPIK (also known as AKT6, AT2G25600); II (inward rectifying channel): KAT1 (AT5G46240) and KAT2 (AT4G18290); III (weakly inward rectifying channel): AKT2 (AT4G22200); IV (regulatory subunit involved in inwardly rectifying conductance formation): KAT3 (also known as AtKC1, AT4G32650); V (outward rectifying channel): SKOR (AT3G02850) and GORK (AT5G37500).
UniProt Synonym Gene Names
AKT3
UniProt Protein Name
Potassium channel AKT2/3
UniProt Primary Accession #
Q38898
UniProt Secondary Accession #
Q0WMS8; Q42408; Q9M0L6
UniProt Related Accession #
Q38898
UniProt Comments
Highly selective and weak inward-rectifying potassium channel. Plays a role in both loading and unloading potassium into/from the phloem sap. Seems to control sugar loading into phloem via a voltage-dependent process. Blocked by physiological concentrations of external calcium and by external acidification. May interact with the cytoskeleton or with regulatory proteins. Dephosphorylation by PP2CA not only leads to the inhibition of potassium currents but also to an increase of the voltage-dependence of the channel. Regulated by the CBL4/CIPK6 calcium sensor/protein kinase complex via a kinase interaction-dependent but phosphorylation-independent translocation of the channel to the plasma membrane.