ライフサイエンスコーパス: mink

1 or the slow sigmoidal activation produced by minK.

2 the etiological agent of Aleutian disease of mink.

3 , including humans, pigs, horses, seals, and mink.

4 the etiological agent of Aleutian disease of mink.

5 ates in CrFK cells but does not replicate in mink.

6 nsmembrane segment of the non-P-loop protein minK.

7 n combination with both wild-type KvLQT1 and minK.

8 ubunits, the method is applied here to human MinK.

9 endangered black-footed ferret and European mink.

10 d wild strains of mice and from hamsters and minks.

11 he second proposes that Cd(2+) binds between MinK-55C and a cysteine in KCNQ1 that is posited to lie

12 ave supported a pore-associated location for MinK-55C because Cd(2+) block is sensitive to voltage, p

13 Second, MinK-55C channels are found to remain sensitive to Cd(2+

14 First, Cd(2+) block of MinK-55C channels formed with wild-type KCNQ1 is shown t

15 Conversely, MinK-55C channels with K318I, V319Y KCNQ1 are found to d

16 Two recent reports argue that MinK-55C is distant from the pore: one finds TEA does no

17 hen MinK position 55 is mutated to cysteine (MinK-55C), I(Ks) channels can be blocked by external cad

18 t Cd(2+) enters and leaves the pore to reach MinK-55C, placing that residue in or near the pore.

19 teine binds Cd(2+) and can serve to localize MinK-55C.

20 of the interactions, MiRP2-72/KCNQ1-338 and MinK-58/KCNQ1-340, are required for the contrasting gati

21 interaction of MiRP2-72 with KCNQ1-338; and MinK-59,58 with KCNQ1-339, 340.

22 ative regulator of thymocyte apoptosis while MINK, a MEKK kinase, is required for negative selection.

23 contain four pore-forming KCNQ1 subunits and MinK accessory subunits in a number that has been contro

24 compare the cellular phenotypes of wild-type minK and four LQT5 mutants co-expressed with KvLQT1 in X

25 -15 kidney cell line (PERV-PK) infected pig, mink and human kidney 293 cell lines and co-cultivation

26 ed with periodic paralysis; the analogs K69H-MinK and K75H-MiRP1 were also studied.

27 sing site-directed mutations that substitute minK and KCNE3 residues, we determined that a hydroxylat

28 t channel activation characteristics of both minK and KCNE3.

29 Human MinK and KCNQ1 subunits assemble to form I(Ks) channels.

30 sed by cells co-transfected with independent MinK and KvLQT1 cDNA.

31 Co expression of minK and KvLQT1 channel subunits induces a slow delayed

32 current, I(Ks), in heart is composed of the minK and KvLQT1 proteins.

33 ne-localized 'activation triplet' regions of MinK and MiRP2 to identify pairs of residues that intera

34 by MinK or MiRP2, dissimilar positioning of MinK and MiRP2 within the channel complex, or both.

35 by coassembling with KCNE ancillary subunits MinK and MiRP2.

36 quired for the contrasting gating effects of MinK and MiRP2.

37 Here we report that MINK and TNIK are postsynaptically enriched proteins who

38 Thus, although both MINK and TNIK bind GTP-bound Rap2, these kinases employ

39 Expression of MINK and TNIK in neurons is required for normal dendriti

40 central amino acid of the triplet (Thr-58 of minK and Val-72 of KCNE3) is essential for the specific

41 Ks (Nck-interacting kinases)-related kinase (MINK) and closely related TRAF2/Nck-interacting kinase (

42 The specificity of KCNE1 (minK) and KCNE3 control of activation of the potassium c

43 in 3 potassium channel genes, KVLQT1, KCNE1 (minK), and HERG, and the cardiac sodium channel gene SCN

44 NQ1 gating processes and their modulation by MinK, and present a unique system for further mechanisti

45 ut not to X-MLVs, whereas those from humans, minks, and several wild mice (Mus dunni, SC-1 cells, and

46 I(Kr) in an atrial tumour line subjected to minK antisense suppression.

47 MINK appears to antagonize Rap2 signal transduction by b

48 Two adjacent residues in this segment of minK are exposed in the pore on either side of a short b

49 ier currents (IKr and IKs), and mutations in minK are now recognized as one cause of the congenital l

50 MinK assembles with KvLQT1 to produce the slow delayed r

51 hat PAstV3 has the closest relationship with mink AstV and the human AstV strains VA1, VA2, and SG, i

52 tward shift in the activation curve of KCNQ1+minK, but affected none of these parameters for KCNQ1 al

53 Also, XE991 block of KCNQ1+minK, but not of KCNQ1, was time- and voltage-dependent.

54 nes is entirely abrogated by coexpression of MINK, but not TNIK.

55 a histidine allowed replication of ADV-G in mink, but the ability to replicate was not sufficient to

56 odegenerative disorders occurring in humans, mink, cats, and ruminant herbivores.

57 The two parvoviruses of mink cause very different diseases.

58 solate ADV-Utah replicates to high levels in mink, causing severe Aleutian disease that results in de

59 H534D also replicated in mink, causing transient viremia at 30 days postinfection

60 The human and cat minK cDNA have been cloned, but their regulation by prot

61 ermed Rh-MLV) that is derived from the ampho-mink cell focus-forming (AMP/MCF) retrovirus in the seru

62 ion of apoptosis in mink epithelial cells by mink cell focus-forming (MCF) MLV infection results in t

63 Mink cell focus-forming (MCF) murine leukemia viruses (M

64 To examine the possible role of mink cell focus-forming (MCF) recombinant virus in raisi

65 e for the classic toxicity of the polytropic mink cell focus-forming (MCF) retrovirus in mink cells.

66 ro resistance to infection by the polytropic mink cell focus-forming (MCF) virus subgroup of murine l

67 Given the sequence similarity of XMRV to mink cell focus-forming (MCF) viruses and the enhanced l

68 y the emergence of recombinant polytropic or mink cell focus-forming (MCF) viruses.

69 that infection of thymic lymphocytes by the mink cell focus-forming murine leukemia virus (MCF MLV)

70 Upon inoculation into AKR mice, mink cell focus-forming murine leukemia virus (MCF MLV)

71 Infection of thymic lymphocytes by a mink cell focus-forming murine leukemia virus induces ap

72 cer (DEN) of the long terminal repeat of the mink cell focus-forming murine leukemia virus is importa

73 xpressed ecotropic MuLVs, and most expressed mink cell focus-inducing (MCF) MuLVs.

74 Mink cell focus-inducing (MCF) proviral DNA was readily

75 is resistant to infection by the polytropic mink cell focus-inducing (MCF) subgroup of murine leukem

76 urine leukemia virus MCF 247, a leukemogenic mink cell focus-inducing (MCF) virus, the U3 enhancer se

77 Mink cell focus-inducing (MCF) viruses induce T-cell lym

78 The ability of mink cell focus-inducing (MCF) viruses to induce thymoma

79 The murine mink cell focus-inducing (MCF) viruses with this propert

80 appearance of env gene recombinants known as mink cell focus-inducing (MCF) viruses.

81 mbinants were able to generate and replicate mink cell focus-inducing viruses.

82 eptors and expressed these constructs in the mink cell line Mv-1-lu.

83 m of unintegrated viral DNA, particularly in mink cells after MCF13 MLV infection.

84 MCF13 MLV infection of mink cells also resulted in a significant upregulation o

85 d MCF-like cytopathic activities in cultured mink cells but found none.

86 GRP78/BiP, which was not observed for either mink cells infected with NZB-9 MLV or M. dunni fibroblas

87 MCF13 MLV infection of mink cells produced low cell surface expression of envel

88 We previously demonstrated that mink cells undergo apoptosis after MCF13 murine leukemia

89 In contrast, infection of mink cells with the 4070A amphotropic MLV did not produc

90 Infection of mink cells with the noncytopathic NZB-9 MLV did not resu

91 ated mice were plated on Mus dunni cells and mink cells, since these cells do not support the replica

92 mink cell focus-forming (MCF) retrovirus in mink cells.

93 d nonecotropic virus that was infectious for mink cells.

94 icated that MCF13 MLV is able to superinfect mink cells.

95 fect of lymphomagenic MLVs was restricted to mink cells.

96 Strikingly, ferret (but not mink) cells engineered to express human HIV-1 entry rece

97 In cardiac myocytes, the KCNQ1-KCNE1 (IsK or minK) channel is thought to underlie the I(Ks) current,

98 HERG and KvLQT1+minK channels were heterologously expressed in human emb

99 that cocaine suppresses HERG, but not KvLQT1+minK, channels by preferentially blocking activated chan

100 ting and reduced amplitudes compared with WT-minK, co-expression with L51H produced KvLQT1 current ra

101 erial lacZ gene has been substituted for the minK coding region such that beta-galactosidase expressi

102 f a 500-ms step, XE991 blockade of the KCNQ1+minK current had a K(D) value of 11.1 +/- 1.8 microM, ap

103 Cocaine had no effect on KvLQT1+minK current in concentrations up to 200 microM.

104 ore originates from the observation that two minK cysteine mutants (G55C and F54C) render I(Ks) Cd2+-

105 We have generated minK-deficient mice in which the bacterial lacZ gene has

106 Aleutian mink disease parvovirus (ADV) causes a persistent infect

107 Aleutian mink disease parvovirus (ADV) is the etiological agent o

108 However, Aleutian mink disease parvovirus (ADV) is the first example of a

109 Other parvoviruses, including Aleutian mink disease parvovirus (ADV), canine parvovirus (CPV),

110 ion of the transcription profile of Aleutian mink disease parvovirus (AMDV)-infected CRFK cells at ei

111 by the single left-end promoter of Aleutian mink disease parvovirus is tricistronic; it not only exp

112 Aleutian mink disease virus (AMDV) is currently the only known me

113 ed structural similarity to that of Aleutian mink disease virus and human parvovirus B19, autonomous

114 fication (PMCA)-generated hypertransmissible mink encephalopathy (HY TME) PrP(Sc) is highly infectiou

115 ng of the hyper (HY) strain of transmissible mink encephalopathy (TME) (hamster) prions to a silty cl

116 ith the long-incubation-period transmissible mink encephalopathy (TME) agent DY TME prior to superinf

117 oculated with the HY strain of transmissible mink encephalopathy (TME) agent had an incubation period

118 the drowsy (DY) strain of the transmissible mink encephalopathy (TME) agent prior to superinfection

119 and drowsy (DY) strains of the transmissible mink encephalopathy (TME) agent was investigated using t

120 h the HY and DY strains of the transmissible mink encephalopathy (TME) agent.

121 ) or drowsy (DY) strain of the transmissible mink encephalopathy (TME) agent.

122 lation of the HY strain of the transmissible mink encephalopathy (TME) agent.

123 h the HY and DY strains of the transmissible mink encephalopathy (TME) agent.

124 passaged a biological clone of transmissible mink encephalopathy (TME) into Syrian golden hamsters an

125 eport that the transmission of transmissible mink encephalopathy (TME) is 100,000-fold more efficient

126 transport of the HY strain of transmissible mink encephalopathy (TME), a prion disease of mink, in t

127 on-period hyper (HY) strain of transmissible mink encephalopathy (TME).

128 lation of the HY strain of the transmissible mink encephalopathy agent.

129 using the HY and DY strains of transmissible mink encephalopathy resulted in minor differences in pri

130 on diseases (scrapie of sheep, transmissible mink encephalopathy, chronic wasting disease of cervids,

131 n of a noise-variance strategy suggests that MinK enhances blockade by increasing the dwell time of T

132 Mink enteritis virus (MEV) is associated with rapid, hig

133 ction of apoptosis was observed for cultured mink epithelial cells after MCF13 MLV infection.

134 We showed that the induction of apoptosis in mink epithelial cells by mink cell focus-forming (MCF) M

135 Immunoblot analysis for MCF13 MLV-infected mink epithelial cells did not show a significant change

136 this study, we observed that virus-infected mink epithelial cells had significantly larger amounts o

137 Moreover, a time course analysis for mink epithelial cells infected with MCF13 MLV did not re

138 Western blot analysis of mink epithelial cells infected with MCF13 MLV showed an

139 MCF13 MLV infection of mink epithelial cells resulted in the production of cyto

140 preleukemic thymic lymphocytes and cultured mink epithelial cells, results in the accumulation of th

141 ed thymic lymphomas and chronically infected mink epithelial cells.

142 culum stress, which may mediate apoptosis in mink epithelial cells.

143 o the conducting system, thereby implicating minK expression as an early event in conduction system d

144 More generally, the restricted nature of minK expression in the mouse heart suggests species-spec

145 ve method of Minimally Invasive Karyotyping (MINK) for the diagnosis of the fetal genetic disease.

146 Here we show that HERG and minK form a stable complex, and that this heteromultimer

147 The minK gene encodes a 129-amino acid peptide the expressio

148 Mutations in the minK gene KCNE1 have been linked to the LQT5 variant of

149 Mutations that map to the KvLQT1 and minK genes account for more than 50% of an inherited car

150 beta-Galactosidase staining in postnatal minK (-/-) hearts is highly restricted, to the sinus-nod

151 s across the single transmembrane segment of MinK identifies positions that alter TEA blockade of I(K

152 ed; these results further support a role for minK in modulating both IKs and IKr.

153 way suggested that the essential function of MINK in the elimination of self-reactive thymocytes may

154 We conclude that the presence of minK in the I(Ks) channel complex gives rise to differen

155 shable from native cardiac I(Kr), a role for minK in this current is suggested by the diminished I(Kr

156 Expression of minK in Xenopus oocytes results in a current similar to

157 ink encephalopathy (TME), a prion disease of mink, in the central nervous system following unilateral

158 MinK influences surface expression, voltage-dependence o

159 We suggest that MINK interaction with Rap2 plays a critical role in main

160 We conclude that minK is a co-factor in the expression of both IKs and IK

161 MINK is activated after Ras induction via a mechanism in

162 tic amino acid substituted at position 58 of minK is capable of reproducing KCNE3-like kinetics and v

163 These findings indicate that MinK is intimately associated with an oocyte protein who

164 artate to asparagine (D --> N) to yield D76N-MinK is linked to cardiac arrhythmia and deafness; the a

165 MinK is seen to determine the pharmacology of I(Ks) chan

166 MINK is thus a distal target of Ras signaling in the ind

167 Misshapen/NIKs-related kinase (MINK) is a member of the germinal center family of kinas

168 KCNE1, also known as minK, is a member of the KCNE family of membrane protein

169 pression with the KCNQ1 beta subunit, KCNE1 (minK, IsK).

170 In contrast to HERG, the KvLQT1/minK K+ channel was not a target for block by the fluoro

171 d potassium channel that when complexed with minK (KCNE1) produces the slowly activating delayed rect

172 Here, we demonstrate that MinK-KCNQ1 (I(Ks)) channels with an S6-domain mutation,

173 MinK-KCNQ1 channels generate the slowly activating, volt

174 nnels of monomers and those with a fixed 2:4 MinK:KCNQ1 valence.

175 channels (I(Na)-hH1), and K channels (I(Ks)-minK+KvLQT1) expressed in XENOPUS: oocytes.

176 ited T-type I(Ba) but not I(Na)-hH1 or I(Ks)-minK+KvLQT1.

177 ffect, however, on either I(Na)-hH1 or I(Ks)-minK+KvLQT1.

178 independent PKC phosphorylation sites in the minK-KvLQT1 channel.

179 ur data raise the possibility 1) of multiple MinK/KvLQT1 stoichiometries and 2) indicate that uniquel

180 acing of the hydroxyl group was required for minK-like activation.

181 modimer of KvLQT1); and MKK44 (C terminus of MinK linked to N terminus of KK40).

182 e tested are as follows: MK24 (C terminus of MinK linked to N terminus of KvLQT1); KK40 (a tandem hom

183 tophagy-dependent, LPHA-positive vesicles in mink lung alveolar cells, suggesting that the coarse ves

184 The performance of a mixture of mink lung and A549 cell lines in shell vials (MSVs) for

185 ned by enzyme-linked immunosorbent assay and mink lung cell culture bioassay.

186 These MuLVs comprised ecotropic and mink lung cell focus-forming (MCF) virus classes and are

187 We also isolated a mink lung cell line that was transformed with SINrep/Lac

188 TGF-beta pretreatment of mink lung cells expressing wild-type TbetaR1 caused a ma

189 particles did not permeabilize canine A72 or mink lung cells to alpha-sarcin, but canine adenovirus t

190 Mink lung cells were more sensitive than the commonly us

191 HCMV carries out an abortive infection in mink lung cells, but it was able to induce the SINrep/La

192 In mink lung cells, homo-oligomerization of a myristoylated

193 sion active in HEp-2 cells, MRC-5 cells, and mink lung cells.

194 e PAI-A promoter and inhibited the growth of mink lung cells.

195 Transient cotransfection assays in mink lung epithelial (CCL64) cells, using a human c-Fos

196 the Man-6-P/IGF-II receptor and in wild-type mink lung epithelial (Mv1Lu cells) metabolically labeled

197 d by sRIII-expressing cells on the growth of mink lung epithelial CCL64 cells in comparison with the

198 Then, using a TGF-beta-sensitive mink lung epithelial cell (luciferase) reporter system,

199 onditioned medium (CM) was measured with the mink lung epithelial cell bioassay.

200 have demonstrated for the first time that a mink lung epithelial cell line (Mv1Lu) supports the repl

201 still was able to inhibit DNA synthesis in a mink lung epithelial cell line in which inhibition by wi

202 ells, and Smad2-dependent transcription in a mink lung epithelial cell line, L17, was enhanced by co-

203 Using mink lung epithelial cell lines devoid of TbetaR-I, we e

204 athway, infection levels were studied in the mink lung epithelial cell lines JD1, JM2, and JM3.

205 porcine kidney epithelial line [PK(15)], and mink lung epithelial cells (Mv 1 Lu).

206 ) antagonize growth inhibition by IGFBP-3 in mink lung epithelial cells (Mv1Lu cells) stimulated by s

207 tions of high affinity IGFBPs with TbetaR-V, mink lung epithelial cells (Mv1Lu cells) were incubated

208 inding to cell-surface TGF-beta receptors in mink lung epithelial cells (Mv1Lu cells).

209 Mink lung epithelial cells (Mv1Lu) and R-Mix, a mixed mo

210 ta1 is the principal mechanism that protects mink lung epithelial cells (Mv1Lu) from etoposide-induce

211 Using mink lung epithelial cells (MvlLu), we found that TGF-be

212 r MDM2 to confer TGF-beta resistance in both mink lung epithelial cells and human mammary epithelial

213 nist activity and inhibited DNA synthesis of mink lung epithelial cells and rat thyroid cells.

214 gonize TGF-beta-induced growth inhibition of mink lung epithelial cells and the fusion between gag an

215 Here we report that UV irradiation of mink lung epithelial cells causes near complete inhibiti

216 olonged, constitutive expression of MDM-2 in mink lung epithelial cells could overcome the antiprolif

217 sphorylated CREB and ATF-1, respectively, in mink lung epithelial cells treated with TGF-beta1.

218 addition, SmSmad2 localized in the nuclei of mink lung epithelial cells upon treatment with TGF-beta(

219 inding to cell-surface TGF-beta receptors in mink lung epithelial cells with an IC50 of approximately

220 a receptor was stimulated after treatment of mink lung epithelial cells with TGF-beta.

221 In contrast to atrial myocytes, in mink lung epithelial cells, in which TGFbeta signaling t

222 In mink lung epithelial cells, the type V TGF-beta receptor

223 ii significantly impaired growth of cultured mink lung epithelial cells, with effects observed after

224 and TGF-beta(1)-induced growth inhibition in mink lung epithelial cells.

225 DNAs that abrogated TGF-beta sensitivity in mink lung epithelial cells.

226 -beta-induced inhibition of DNA synthesis in mink lung epithelial cells.

227 -cdk2 and cyclin A-cdk2 complexes from Mv1Lu mink lung epithelial cells.

228 wth factor-beta (TGF-beta)/Smad signaling in mink lung epithelial cells.

229 nse in fibroblasts, FBLN-5 overexpression in mink lung Mv1Lu epithelial cells resulted in an antiprol

230 or beta (TGF-beta1) suppresses the growth of mink lung Mv1Lu epithelial cells, whereas testicular hya

231 layer of human lung-derived cells (A549) and mink lung-derived cells (Mv1Lu), are used by diagnostic

232 Coexpression with minK markedly decreased the sensitivity of KCNQ1 to bloc

233 eads to reduced dendritic branching and this MINK-mediated effect on neuronal morphology is dependent

234 el pore-forming (alpha) and accessory (beta, minK, MiRP) subunits have been cloned from or shown to b

235 Furthermore, MinK, MiRP1, and MiRP2 each form channels with Kv3.1-Kv3

236 ster ovary cells, we show that modulation by MinK, MiRP1, and MiRP2 is a general mechanism for slowin

237 To investigate whether MinK, MiRP1, and MiRP2 operate similarly with their know

238 as R/K --> H changes altered the activity of MinK, MiRP1, and MiRP2 with all three alpha subunits.

239 assembly of two channel proteins KvLQT1 and MinK, modulates the repolarization of cardiac action pot

240 carrying the genomic sequences of KvLQT1 and minK (molecular correlates of I(Ks)) and 41 littermate c

241 resent multiple datasets from phage-cholera, mink-muskrat, and gyrfalcon-rock ptarmigan systems that

242 Overexpression of a truncated MINK mutant unable to interact with Rap2 leads to reduce

243 5 may be complicated by differing effects of minK mutations on KvLQT1 and HERG.

244 Ep-2, and NCI-H292), monkey (Vero, LLC-MK2), mink (Mv1 Lu), and canine (MDCK).

245 1 mRNA and protein levels in human HepG2 and mink Mv1Lu cells.

246 In minK (-/-) myocytes, IKs is absent and IKr is significan

247 ol experiments (no DNA, control DNA, or only MinK), no time-dependent K+ current was observed.

248 xpected for other K(+) channels that contain MinK or MinK-related peptides (MiRPs).

249 either with perturbation of the S6 domain by MinK or MiRP2, dissimilar positioning of MinK and MiRP2

250 ubunits, respectively, showing 1.97 +/- 0.07 MinK per I(Ks) channel.

251 When MinK position 55 is mutated to cysteine (MinK-55C), I(Ks

252 ting that coassembly of mutant subunits with minK prevented normal channel gating.

253 deer prions from diseased TgD infected with mink prions.

254 In heart, KCNQ1 associates with KCNE1 (MinK), producing a slowly activating voltage-dependent c

255 Expression of the minK protein in Xenopus oocytes results in I(Ks)-like cu

256 nt on cells of some other species, including mink, rat, mouse, and dog, suggesting that such species

257 idase expression is controlled by endogenous minK regulatory elements.

258 complexes with transmembrane beta subunits, MinK-related peptide (MiRP) 1 (KCNE2) or MiRP2 (KCNE3).

259 ac subunit HERG and a polymorphic variant of MinK-related peptide 1 (MiRP1) exhibit increased suscept

260 Inherited mutations and a polymorphism in minK-related peptide 1 (MiRP1) have been linked to conge

261 In the present study, we demonstrate that minK-related peptide 1 (MiRP1) is a beta subunit for the

262 The gene encodes MinK-related peptide 1 (MiRP1), a small integral membran

263 KCNE2 encodes MinK-related peptide 1 (MiRP1), a subunit of the cardiac

264 MinK-related peptide 2 (MiRP2) and Kv3.4 subunits assemb

265 annel of skeletal muscle is shown to contain MinK-related peptide 2 (MiRP2) and the pore-forming subu

266 wer activating channels by coassembling with MinK-related peptide 2 (MiRP2), a single transmembrane d

267 d a family of Xenopus KCNE genes that encode MinK-related peptide K(+) channel beta subunits (xMiRPs)

268 MinK-related peptides (MiRPs) are single transmembrane p

269 Here, we investigated a neuronal role for MinK-related peptides (MiRPs), membrane-spanning modulat

270 de single transmembrane-domain subunits, the MinK-related peptides (MiRPs), which assemble with pore-

271 for other K(+) channels that contain MinK or MinK-related peptides (MiRPs).

272 MinK-related protein (MiRP1 or KCNE2) interacts with the

273 Mutations in KCNE2, which encodes the minK-related protein 1 (MiRP1), are associated with an i

274 This observation indicates that minK resides in close proximity to S6 in the I(Ks) chann

275 ral axis of the KvLQT1 pore and suggest that minK resides outside of the permeation pathway.

276 Evidence indicating that minK residues line the I(Ks) pore originates from the ob

277 e we report that the serine-threonine kinase MINK selectively connects the T cell receptor to a signa

278 Expression of MK24 plus additional MinK significantly slows current kinetics.

279 In this study, we examined the role of the minK subunit in determining the response of KCNQ1 channe

280 sembly of the KCNQ1 (KvLQT1) subunit and the minK subunit underlie slowly activating cardiac delayed

281 We conclude that two MinK subunits are necessary, sufficient, and the norm in

282 Additional MinK subunits do not enter channels of monomeric subunit

283 Thus, minK subunits eliminate, or greatly slow, the gating ass

284 y are used to directly quantify channels and MinK subunits, respectively, showing 1.97 +/- 0.07 MinK

285 -forming KvLQT1 subunits and pore-associated MinK subunits.

286 ore-forming KCNQ1 subunits and two accessory MinK subunits.

287 ting of pore-forming (KvLQT1) and accessory (minK) subunits belonging to the KCNQ and KCNE gene famil

288 coassembly of KvLQT1 and minimal K+ channel (minK) subunits did not inactivate.

289 e on the human K(+) channels HERG and KvLQT1+minK that encode native rapidly (I(Kr)) and slowly (I(Ks

290 the K(+) channel accessory proteins MiRP1 or minK, the stimulatory effects of cAMP are favored.

291 es during channel gating and which acts with MinK to establish ion conduction pore function.

292 The structure and location of the MinK transmembrane domain (TMD) remains a matter of scru

293 n with cysteine residues engineered into the minK transmembrane domain.

294 1), plus the MAP kinase kinase kinase kinase MINK, which had not previously been implicated in Ras si

295 HERG current but to a lesser extent than WT-minK, while L51H and W87R had no effect and D76N suppres

296 se findings indicate that the association of minK with KvLQT1 interferes with the binding of R-L3 or

297 Coexpression of minK with R243C or W248R KvLQT1 subunits suppressed curr

298 minary model illustrating the orientation of minK with S6 was validated by successful prediction of a

299 lts indicate the location and orientation of minK within the I(Ks) channel complex and further sugges

300 pression of KvLQT1 and the accessory protein minK yields an IKs-like current.