|Institutional Source||Beutler Lab|
|Gene Name||potassium voltage gated channel, Shab-related subfamily, member 2|
|Essential gene?||Non essential (E-score: 0.000)|
|Stock #||R0266 (G1)|
|Chromosomal Location||15287254-15723750 bp(+) (GRCm38)|
|Type of Mutation||unclassified|
|DNA Base Change (assembly)||G to A at 15712913 bp (GRCm38)|
|Amino Acid Change|
|Ref Sequence||ENSEMBL: ENSMUSP00000135382 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000170146] [ENSMUST00000175681]|
|Meta Mutation Damage Score||0.0898|
|Coding Region Coverage||
|Validation Efficiency||100% (79/79)|
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shab-related subfamily. This member is a delayed rectifier potassium channel. The gene is expressed in gastrointestinal smooth muscle cells. [provided by RefSeq, Jul 2008]
PHENOTYPE: Mice homozygous for a targeted mutation exhibit neurological abnormalities when compared with controls, including an abnormal sleep/wake cycle, decreased exploratory and locomotor activity, and a motor strength deficit. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Kcnb2||
(F):5'- AGTACACGGTGCAGGAAAATGTCC -3'
(R):5'- TTTTGCTGCCGCAAAACCTGAG -3'
(F):5'- ATGTCCTTGTAGACGTAAGTCC -3'
(R):5'- CTGAGCATTGCCAGGAAAC -3'