ライフサイエンスコーパス: mink

1 or the slow sigmoidal activation produced by minK.

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

3 the etiological agent of Aleutian disease of mink.

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

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

6 the etiological agent of Aleutian disease of mink.

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

8 endangered black-footed ferret and European mink.

9 virus, causes acute hemorrhagic enteritis in minks.

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

11 CE MEV causes fatal hemorrhagic enteritis in minks.

12 ilar to that induced during MEV infection in minks.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 t channel activation characteristics of both minK and KCNE3.

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

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

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

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

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

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

36 by coassembling with KCNE ancillary subunits MinK and MiRP2.

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

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

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

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

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

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

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

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

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

46 ived H10 viruses recovered from human, seal, mink, and various avian species in Asia, Europe, and Nor

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

48 MINK appears to antagonize Rap2 signal transduction by b

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

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

51 n species to mammals (i.e., human, seal, and mink) are well documented.

52 MinK assembles with KvLQT1 to produce the slow delayed r

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

54 tracking economically valuable fur traits in mink breeding programmes.

55 tracking economically valuable fur traits in mink breeding programs to contribute to global fur produ

56 the whole genome sequencing for two American mink breeds with Silverblue and Hedlund white coats.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 fect of lymphomagenic MLVs was restricted to mink cells.

96 d nonecotropic virus that was infectious for mink cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 lk chronic wasting disease and transmissible mink encephalopathy uncovered that incomplete PrP(Sc) gl

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

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

136 Mink enteritis virus (MEV), an autonomous parvovirus, ca

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

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

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

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

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

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

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

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

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

146 ed thymic lymphomas and chronically infected mink epithelial cells.

147 stine, mesenteric lymph nodes, and kidney in minks experimentally infected with strain MEVB.

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

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

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

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

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

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

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

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

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

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

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

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

160 MinK influences surface expression, voltage-dependence o

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

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

163 MINK is activated after Ras induction via a mechanism in

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

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

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

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

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

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

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

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

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

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

174 MinK-KCNQ1 channels generate the slowly activating, volt

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 Mink lung cells were more sensitive than the commonly us

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 5 may be complicated by differing effects of minK mutations on KvLQT1 and HERG.

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

242 1 mRNA and protein levels in human HepG2 and mink Mv1Lu cells.

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

244 The fur colour of American mink (Neovison vison) involves over 35 traits, but only

245 fur colours have been described in American mink (Neovison vison), only six of which have been previ

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

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

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

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

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

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

252 deer prions from diseased TgD infected with mink prions.

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

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

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

256 idase expression is controlled by endogenous minK regulatory elements.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

281 Additional MinK subunits do not enter channels of monomeric subunit

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

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

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

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

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

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

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

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

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

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

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

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

294 t genetic mutant of fur colour identified in minks, while the latter is a commercially valuable pheno

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

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

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

298 med whole genome sequencing for two American minks with Moyle (m/m) and Violet (a/a m/m /p/p) phenoty

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.