PMID- 10419540
OWN - NLM
STAT- MEDLINE
DCOM- 19990819
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 31
DP  - 1999 Jul 30
TI  - Mutational analysis of the Shab-encoded delayed rectifier K(+) channels in 
      Drosophila.
PG  - 22109-13
AB  - K(+) currents in Drosophila muscles have been resolved into two voltage-activated 
      currents (I(A) and I(K)) and two Ca(2+)-activated currents (I(CF) and I(CS)). 
      Mutations that affect I(A) (Shaker) and I(CF) (slowpoke) have helped greatly in 
      the analysis of these currents and their role in membrane excitability. Lack of 
      mutations that specifically affect channels for the delayed rectifier current 
      (I(K)) has made their genetic and functional identity difficult to elucidate. 
      With the help of mutations in the Shab K(+) channel gene, we show that this gene 
      encodes the delayed rectifier K(+) channels in Drosophila. Three mutant alleles 
      with a temperature-sensitive paralytic phenotype were analyzed. Analysis of the 
      ionic currents from mutant larval body wall muscles showed a specific effect on 
      delayed rectifier K(+) current (I(K)). Two of the mutant alleles contain missense 
      mutations, one in the amino-terminal region of the channel protein and the other 
      in the pore region of the channel. The third allele contains two deletions in the 
      amino-terminal region and is a null allele. These observations identity the 
      channels that carry the delayed rectifier current and provide an in vivo 
      physiological role for the Shab-encoded K(+) channels in Drosophila. The 
      availability of mutations that affect I(K) opens up possibilities for studying 
      I(K) and its role in larval muscle excitability.
FAU - Hegde, P
AU  - Hegde P
AD  - Department of Biochemical Pharmacology, State University of New York, Buffalo, 
      New York 14260, USA.
FAU - Gu, G G
AU  - Gu GG
FAU - Chen, D
AU  - Chen D
FAU - Free, S J
AU  - Free SJ
FAU - Singh, S
AU  - Singh S
LA  - eng
SI  - GENBANK/AF084525
GR  - GM-50779/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (DNA, Complementary)
RN  - 0 (Delayed Rectifier Potassium Channels)
RN  - 0 (Drosophila Proteins)
RN  - 0 (Potassium Channels)
RN  - 0 (Potassium Channels, Voltage-Gated)
RN  - 0 (Shab Potassium Channels)
RN  - 0 (Shab protein, Drosophila)
SB  - IM
MH  - Amino Acid Sequence
MH  - Amino Acid Substitution
MH  - Animals
MH  - Base Sequence
MH  - DNA Mutational Analysis
MH  - DNA, Complementary
MH  - Delayed Rectifier Potassium Channels
MH  - Drosophila/*genetics/physiology
MH  - Drosophila Proteins
MH  - Humans
MH  - Larva
MH  - Molecular Sequence Data
MH  - Muscles/physiology
MH  - Mutation, Missense
MH  - Potassium Channels/chemistry/*genetics/*physiology
MH  - *Potassium Channels, Voltage-Gated
MH  - Protein Structure, Secondary
MH  - Rats
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sequence Alignment
MH  - Sequence Homology, Amino Acid
MH  - Shab Potassium Channels
EDAT- 1999/07/27 00:00
MHDA- 1999/07/27 00:01
CRDT- 1999/07/27 00:00
PHST- 1999/07/27 00:00 [pubmed]
PHST- 1999/07/27 00:01 [medline]
PHST- 1999/07/27 00:00 [entrez]
AID - S0021-9258(19)72493-4 [pii]
AID - 10.1074/jbc.274.31.22109 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 Jul 30;274(31):22109-13. doi: 10.1074/jbc.274.31.22109.