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1 rt the intermolecular model for pH gating of inward rectifier K channels.
2 nd 3.1 are bacterial homologues of mammalian inward rectifier K channels.
3 els and heterotetrameric G-protein-regulated inward rectifier K channels.
4 RK2 to constitute a neuronal G protein-gated inward rectifier K+ channel.
5 gh-affinity ligands that directly target any inward-rectifier K+ channel.
6 itical in trafficking and conductance of the inward rectifier K+ channels.
7 age-dependent manner, characteristic of many inward rectifier K+ channels.
8 yotic pore into eukaryotic voltage-gated and inward-rectifier K+ channels.
9 very useful molecular probe for studying the inward-rectifier K+ channels.
10 , and synthesized a protein inhibitor of the inward-rectifier K+ channels.
11  all-or-none-like conductance changes of the inward-rectifier K(+) channel.
12 resembles the cytoplasmic pore structures of inward rectifier K(+) channels.
13  modulated N-type Ca(2+) and G-protein-gated inward rectifier K(+) channels.
14  and cerebral arteries through activation of inward rectifier K(+) channels.
15     We report that the IRK3 but not the IRK1 inward rectifier K+ channel activity is inhibited by m1
16               However, it is unknown whether inward-rectifier K+ channels and reentry are also import
17                                              Inward rectifier K(+) channels apparent lack of selectiv
18                          The hypothesis that inward rectifier K(+) channels are involved in the vasod
19                                              Inward-rectifier K+ channels are a group of highly speci
20 lls under resting conditions is dominated by inward-rectifier K(+) channels belonging to the Kir 2 fa
21 uine's effectiveness may be explained by its inward-rectifier K+ channel blockade profile and suggest
22 (Q)), a honey bee toxin derivative, inhibits inward-rectifier K(+) channels by binding to their exter
23                                  Blockade of inward-rectifier K+ channels by chloroquine terminates r
24                                              Inward rectifier K(+) channels commonly exhibit long ope
25                                              Inward rectifier K+ channels control the cell's membrane
26                                         ROMK inward-rectifier K+ channels control renal K+ secretion.
27                                              Inward-rectifier K+ channels differ from voltage-activat
28           Here we report that several cloned inward rectifier K+ channels directly bind PIP2, and tha
29          A cytoplasmic pore, conserved among inward rectifier K(+) channels, extends the ion pathway
30        Kir4.1 and Kir5.1, two members of the inward rectifier K+ channel family, are expressed in sev
31  receptor (SUR1) and Kir6.2, a member of the inward rectifier K+ channel family.
32 bitory agents specific to each member of the inward-rectifier K+ channel family.
33 opmental features caused by mutations in the inward rectifier K+ channel gene KCNJ2.
34 ive sequence homology with previously cloned inward rectifier K+ channel genes.
35 a mouse liver cDNA library to identify novel inward rectifier K+ channel genes.
36                            G protein-coupled inward rectifier K(+) channels (GIRK channels) are activ
37                          The G-protein gated inward rectifier K+ channel (GIRK) is activated in vivo
38 ular N- and C termini of the G protein-gated inward rectifier K(+) channel GIRK1 at 1.8 A resolution.
39 sion systems showed that the G protein-gated inward rectifier K+ channel (GIRK2) bearing the weaver p
40                                              Inward rectifier K(+) channels govern the resting membra
41             Each of the four subunits of the inward-rectifier K+ channels has only two instead of six
42 he effect of TGF-beta(1) on the 14-pS Kir2.3 inward rectifier K(+) channel in rat primary cultured re
43 nd extracellular K(+) on the distribution of inward rectifier K(+) channels in the glial endfoot and
44           The molecular nature of the strong inward rectifier K+ channel in vascular smooth muscle wa
45          We conclude that Kir2.1 encodes for inward rectifier K+ channels in arterial smooth muscle.
46 dependent lipid kinases is known to activate inward rectifier K+ channels in cardiac membrane patches
47                         Structural models of inward rectifier K+ channels incorporate four identical
48 ly, we have demonstrated that hIRK, a cloned inward rectifier K+ channel (IRK) isolated from human at
49  patches from Xenopus oocytes expressing the inward rectifier K+ channel IRK1.
50 tigated on wild-type and mutant forms of the inward rectifier K+ channel, IRK1 (Kir2.1).
51 s of metabolic inhibitors on the activity of inward rectifier K(+) channels K(ir)2.1, K(ir)2.2, and K
52  from the endothelium, and (b) activation of inward rectifier K(+) channels (K(ir)) and Na(+)-K(+) pu
53              Expression cloning of the first inward rectifier K channel (Kir) genes provided the nece
54 of the nucleus basalis (NB) by inhibiting an inward rectifier K(+) channel (Kir).
55                         The ROMK subtypes of inward rectifier K+ channels (Kir 1.1, KCNJ1) mediate po
56  localize the pH-sensitive gate in the renal inward-rectifier K(+) channel Kir1.1a (ROMK1).
57 sed by mutations in KCNJ2, which encodes the inward rectifier K(+) channel Kir2.1.
58                                          The inward rectifier K+ channel Kir2.3 is inhibited by hyper
59 e COOH-terminal region of an ATP-insensitive inward rectifier K(+) channel (Kir2.1).
60  pore-forming H5 (or P) region of the strong inward rectifier K+ channel, Kir2.1, based initially on
61  containing the ABC transporter SUR1 and the inward-rectifier K(+) channel Kir6.2, in the presence of
62 e, these results support the hypothesis that inward rectifier K(+) channels may be involved in metabo
63                The Kir1.1 (ROMK) subtypes of inward rectifier K+ channels mediate potassium secretion
64                         The ROMK subtypes of inward-rectifier K(+) channels mediate potassium secreti
65 in SUR1 (Sulfonylurea receptor 1) or KIR6.2 (Inward rectifier K(+) channel member 6.2), which encode
66  a blocker explains the signature feature of inward rectifier K+ channels, namely, that at a given co
67 ct on a cloned voltage-gated Na+ channel, an inward rectifier K+ channel, or on lymphocyte Ca2+ and C
68 ) in KCNJ2, the gene that encodes the strong inward rectifier K(+) channel protein (Kir2.1), in an 11
69  which results in the phosphorylation of the inward rectifier K+ channel protein.
70                        GIRK (G protein-gated inward rectifier K(+) channel) proteins play critical fu
71 lactotrophs and the subsequent activation of inward rectifier K(+) channels provide an effective and
72   We have purified a protein inhibitor of an inward-rectifier K+ channel, ROMK1, from the venom of th
73                                              Inward rectifier K(+) channel subfamily 2 (Kir2) channel
74                                    ABSTRACT: Inward rectifier K(+) channel subfamily 2 (Kir2) channel
75           In the present study, we show that inward rectifier K(+) channel subfamily 2 isoform 1 (Kir
76  ATP-binding cassette protein family, and an inward rectifier K(+) channel subunit (Kir6.x).
77 ATP channel is a complex of two proteins: an inward-rectifier K+ channel subunit, Kir6.2, and the sul
78                              G protein-gated inward rectifier K+ channel subunits 1-4 (GIRK1-4) have
79                      IKAChis composed of two inward rectifier K+ channel subunits, GIRK1 and GIRK4.
80 g characteristics of two ion channels in the inward-rectifier K+ channel superfamily were compared at
81  for two representative genes, i.e. the weak inward rectifier K(+) channel (TWIK-1), and phosphate an
82                                Inhibition of inward rectifier K(+) channels under ischemic conditions
83  cells were also transfected with the Kir2.3 inward rectifier K(+) channel, which allows for changing
84                                              Inward rectifier K+ channels, which modulate electrical
85        TPN(Q) inhibits the ROMK1 and GIRK1/4 inward-rectifier K(+) channels with affinities very simi

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