PMID- 10457052
OWN - NLM
STAT- MEDLINE
DCOM- 19991122
LR  - 20191210
IS  - 0022-3751 (Print)
IS  - 0022-3751 (Linking)
VI  - 519 Pt 2
DP  - 1999 Sep 1
TI  - Cloning and functional expression of a novel degenerin-like Na+ channel gene in
      mammals.
PG  - 323-33
AB  - 1. A degenerate polymerase chain reaction (PCR) homology screening procedure was 
      applied to rat brain cDNA in order to identify novel genes belonging to the
      amiloride-sensitive Na+ channel and degenerin (NaC/DEG) family of ion channels. A
      single gene was identified that encodes a protein related to but clearly
      different from the already cloned members of the family (18-30 % amino acid
      sequence identity). Phylogenetic analysis linked this protein to the group of
      ligand-gated channels that includes the mammalian acid-sensing ion channels and
      the Phe-Met-Arg-Phe-amide (FMRFamide)-activated Na+ channel. 2. Expression of
      gain-of-function mutants after cRNA injection into Xenopus laevis oocytes or
      transient transfection of COS cells induced large constitutive currents. The
      activated channel was amiloride sensitive (IC50, 1.31 microM) and displayed a low
      conductance (9-10 pS) and a high selectivity for Na+ over K+ (ratio of the
      respective permeabilities, PNa+/PK+ >= 10), all of which are characteristic of
      NaC/DEG channel behaviour. 3. Northern blot and reverse transcriptase-polymerase 
      chain reaction (RT-PCR) analysis revealed a predominant expression of its mRNA in
      the small intestine, the liver (including hepatocytes) and the brain. This
      channel has been called the brain-liver-intestine amiloride-sensitive Na+ channel
      (BLINaC). 4. Corresponding gain-of-function mutations in Caenorhabditis elegans
      degenerins are responsible for inherited neurodegeneration in the nematode.
      Besides the BLINaC physiological function that remains to be established,
      mutations in this novel mammalian degenerin-like channel might be of
      pathophysiological importance in inherited neurodegeneration and liver or
      intestinal pathologies.
FAU - Sakai, H
AU  - Sakai H
AD  - Institut de Pharmacologie Moleculaire et Cellulaire, CNRS-UPR 411, 660 route des 
      Lucioles, Sophia Antipolis, 06560 Valbonne, France.
FAU - Lingueglia, E
AU  - Lingueglia E
FAU - Champigny, G
AU  - Champigny G
FAU - Mattei, M G
AU  - Mattei MG
FAU - Lazdunski, M
AU  - Lazdunski M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Acid Sensing Ion Channels)
RN  - 0 (Asic2 protein, rat)
RN  - 0 (Degenerin Sodium Channels)
RN  - 0 (Epithelial Sodium Channels)
RN  - 0 (Ion Channels)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sodium Channels)
SB  - IM
MH  - Acid Sensing Ion Channels
MH  - Amino Acid Sequence
MH  - Animals
MH  - Biophysical Phenomena
MH  - Biophysics
MH  - Blotting, Northern
MH  - COS Cells
MH  - Chromosome Mapping
MH  - Cloning, Molecular
MH  - Degenerin Sodium Channels
MH  - Epithelial Sodium Channels
MH  - In Situ Hybridization, Fluorescence
MH  - Ion Channels/*biosynthesis/genetics
MH  - Liver/cytology/drug effects/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Molecular Sequence Data
MH  - Nerve Tissue Proteins/*biosynthesis/genetics
MH  - Oocytes/metabolism
MH  - RNA, Messenger/biosynthesis/isolation & purification
MH  - Rats
MH  - Rats, Wistar
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sodium Channels/*biosynthesis/*genetics
MH  - Tissue Distribution
MH  - Xenopus
PMC - PMC2269506
EDAT- 1999/08/24 00:00
MHDA- 1999/08/24 00:01
CRDT- 1999/08/24 00:00
PHST- 1999/08/24 00:00 [pubmed]
PHST- 1999/08/24 00:01 [medline]
PHST- 1999/08/24 00:00 [entrez]
AID - PHY_9480 [pii]
AID - 10.1111/j.1469-7793.1999.0323m.x [doi]
PST - ppublish
SO  - J Physiol. 1999 Sep 1;519 Pt 2:323-33. doi: 10.1111/j.1469-7793.1999.0323m.x.