ライフサイエンスコーパス: slack

1 found in certain neurons that do not express Slack.

2 he voltage-gated sodium channel Na(V)1.6 and Slack.

3 e sodium-activated potassium (K(Na)) channel Slack.

4 ave described previously the distribution of Slack, a Na+-activated K+ channel subunit.

5 When expressed in CHO cells, Slack-A channels activate rapidly upon depolarization an

6 Neuronal expression of Slack-A channels and of the previously described Slack i

7 hannels with alternate amino-termini such as Slack-A channels are present at these locations.

8 Two of these, termed Slack-A channels, contain an amino-terminus domain close

9 e approximately 6-fold longer than those for Slack-A channels.

10 Slack-A mRNAs were enriched in the brainstem and olfacto

11 in which outward currents are dominated by a Slack-A-like conductance adapt very rapidly to repeated

12 Our findings suggest that Slack activity provides a link between patterns of neuro

13 teraction provides a molecular mechanism for Slack activity-dependent regulation of translation and s

14 ductive behaviors, to examine the effects of Slack and FMRP on excitability.

15 prevention, however, Chilton and Fertig and Slack and Martin were certainly among the early caries c

16 ystem may result from an interaction between Slack and Slo channel subunits.

17 es cell shrinking, which results in membrane slack and the deepening of eisosomes.

18 uring diastole, when the mitral leaflets are slack and unstressed, the leaflets appear markedly thick

19 with unitary properties similar to those of Slack and/or Slick channels, which are gated by [Na+]i a

20 ctivated potassium channels K(Na)1.1 (SLO2.2/Slack) and K(Na)1.2 (SLO2.1/Slick) to the primary audito

21 Sarcomere shortening to lengths below slack (approximately 1.85 microns) also results in strai

22 Two genes encoding these channels, Slick and Slack, are expressed throughout the brain.

23 6 complex challenge the traditional view of 'Slack as an isolated target' for anti-epileptic drug dis

24 This cytoplasmic N-terminal domain of Slack-B also facilitates the localization of heteromeric

25 In contrast, Slack-B channels activate slowly over hundreds of millis

26 In contrast, Slack-B currents promote rhythmic firing during maintain

27 cytochemical studies indicate that Slick and Slack-B subunits are coexpressed in many central neurons

28 eviously described Slack isoform, now called Slack-B, are driven by independent promoters.

29 formation requires the N-terminal domain of Slack-B, one of the alternative splice variants of the S

30 ctivity is present at locations that have no Slack-B-specific staining, including olfactory bulb glom

31 Using the super-efficiency Slacks-Based Measure (SBM) analysis method, the main agr

32 eating a competitive peptide blocker of AP-2-Slack binding, we demonstrated that this interaction is

33 Our data suggest that Phactr1 regulates the Slack by linking PP1 to the channel.

34 a dileucine motif housed in the cytoplasmic Slack C terminus that binds AP-2.

35 NAD+ also potentiated recombinant Slack channel activity.

36 Sequence analysis indicated that the Slack channel contains a putative nicotinamide adenine d

37 or clathrin recruitment to the DRG membrane, Slack channel endocytosis, and DRG neuronal hyperexcitab

38 Slack channel expression at the DRG membrane is necessar

39 The highest Slack channel expression was detected in the olfactory b

40 ings uncover AP-2 and clathrin as players in Slack channel regulation.

41 The Slack channel showed primarily a diffuse immunostaining

42 eterologous expression studies suggests that Slack channel subunits can also combine with the Slo sub

43 ng inflammation is the result of PKA-induced Slack channel trafficking.

44 alters the single-channel properties of the Slack channel.

45 ne of the alternative splice variants of the Slack channel.

46 The sodium-activated potassium (Slack) channel was the first ion channel shown to direct

47 t this PKA-induced retrograde trafficking of Slack channels also occurs in intact spinal cord slices

48 16C modulated the single-channel activity of Slack channels and increased its sodium sensitivity.

49 ed in the extended cytoplasmic C-terminus of Slack channels and result in increased Slack current.

50 In neurons, Slick and Slack channels are involved in the generation of slow af

51 Our studies indicate that, in BC neurons, Slack channels are required for prolonged changes in neu

52 e an animal model for EIMFS and suggest that Slack channels are required for the development of proce

53 xperiments have shown that the C-terminus of Slack channels binds a number of cytoplasmic signaling p

54 we examined the modulation of native KNa and Slack channels by NAD+.

55 but arises from the internal trafficking of Slack channels from DRG membranes.

56 of the inflammatory milieu, PKA internalizes Slack channels from the DRG membrane, reduces IKNa, and

57 on and subcellular localization of Slick and Slack channels in the mouse brain have not yet been esta

58 the expression and distribution of Slick and Slack channels in these species.

59 s the current amplitude but has no effect on Slack channels in which a conserved PKC phosphorylation

60 inside-out patches containing native Aplysia Slack channels increased channel opening and, in current

61 rs, our findings suggest that suppression of Slack channels may be an early step in the progression o

62 Slack channels rectify outwardly with a unitary conducta

63 that co-expression of Phactr1 with wild-type Slack channels reduces the current amplitude but has no

64 fferent transcripts for Slack, which produce Slack channels that differ in their predicted cytoplasmi

65 tes of hippocampal neurones, suggesting that Slack channels with alternate amino-termini such as Slac

66 f native neuronal AP-2 adaptor proteins with Slack channels, facilitated by a dileucine motif housed

67 Human mutations alter the function of Slack channels, resulting in epilepsy and intellectual d

68 y exposure to a pharmacological activator of Slack channels, significantly enhance the accuracy of ti

69 disorders associated with the malfunction of Slack channels.

70 e compliant cell pairs grown on circles have slack contacts, while stiffer triangular cell pairs favo

71 stration that a KCNT1 mutation increases the Slack current in neurons.

72 us of Slack channels and result in increased Slack current.

73 We now find that Slack currents are rapidly suppressed by oligomers of mu

74 of PP1 but not that of actin fails to alter Slack currents.

75 The subcellular and regional distribution of Slack differs from that previously reported for the Slo

76 Two known genes, Slick and Slack, encode K(Na) channels.

77 Suppression of Slack expression did not alter the ability of BC neurons

78 RG from TMEM16C knockout rats had diminished Slack expression, broadened action potentials and increa

79 In their 1983 paper in JEEM, Smith and Slack extended these classical experiments in newts to t

80 rvable, trust and enable reinvention, create slack for change, and lead by example.

81 ified antibody against the N-terminal of rat Slack, for biochemical and immunohistochemical studies.

82 on of Slack's C-terminus can protect against Slack(G269S)-induced seizures in mice.

83 ta suggest that alternative promoters of the Slack gene differentially modulate the properties of neu

84 The Slack gene encodes a voltage-dependent K(+) channel that

85 ne class of K(Na) channels is encoded by the Slack gene.

86 Using a modified Slack-Hall operational model, we quantified the constitu

87 Using a modified Slack-Hall operational model, we quantified the constitu

88 ognizes all amino-termini isoforms of Slack, Slack immunoreactivity is present at locations that have

89 Most prominent Slack immunoreactivity occurs in the brainstem, in parti

90 The only cortical region in which Slack immunoreactivity was detected was the frontal cort

91 Strong Slack immunoreactivity was present in the olfactory bulb

92 FMRP and Slack immunoreactivity were colocalized at the periphery

93 ated K+ channel is Slick, which differs from Slack in its rapid activation and its sensitivity to int

94 Given the significant role of Slack in nociceptive neuronal excitability, the AP-2 cla

95 The localization of Slack in rat brain slices was then determined using the

96 Previous studies identified Slack in sensory neurons, but its contribution to acute

97 Nonetheless, the function of Slack in the brain remains to be identified.

98 little delay, implying that there is little slack in the system.

99 est that Slick may function independently of Slack in these regions.

100 The antibody recognized Slack in transiently transfected CHO cells both by immun

101 is realignment, including incorporating more slack into schedules and establishing realistic work exp

102 However, when Slack is co-expressed with Slo, channels with pharmacolo

103 2, these heads will detach from actin before slack is taken up into a backwardly displaced high stiff

104 ium-activated potassium (KNa) channel Kcnt1 (Slack) is abundantly expressed in nociceptor (pain-sensi

105 k-A channels and of the previously described Slack isoform, now called Slack-B, are driven by indepen

106 Our modelling informs that slack junctions arise from failure of circular cell pair

107 r findings indicate that gain-of-function in Slack K(Na) channels causes hyperexcitability in both is

108 Magi-1 scaffolds Na(V)1.8 and Slack K(Na) channels in dorsal root ganglion neurons reg

109 nction mutations in KCNT1, the gene encoding Slack (K(Na)1.1) channels, result in epilepsy of infancy

110 Mutations in the KCNT1 (Slack, K(Na)1.1) sodium-activated potassium channel prod

111 shown the sodium-activated potassium channel SLACK (KCNT1) can contribute to neuronal excitability, t

112 The Slack (KCNT1) gene encodes sodium-activated potassium ch

113 Mutations that alter levels of Slack (KCNT1) Na(+)-activated K(+) current produce devas

114 rupted by mutations in the potassium channel Slack (KCNT1, Slo2.2).

115 own limitation of alkaline fuel cells is the slack kinetics of the cathodic half-cell reaction, the o

116 istry, we found ubiquitous expression of the Slack KNa channel subunit in small-, medium-, and large-

117 TMEM16C knockout rats, as well as rats with Slack knockdown by intrathecal injection of short interf

118 Global ablation of Slack led to increased hypersensitivity in models of neu

119 staircase protocol and rapid stretches from slack length to increasing strains.

120 in the absence of added phosphate, plots of slack length versus duration of unloaded shortening were

121 Colonic elongation (140% of its empty slack length) applied oral to the recording site abolish

122 titin domains by approximately 15% of their slack length, and is therefore likely to be an important

123 n titin in conjunction with shortening below slack length.

124 ac myocytes quickly relengthen back to their slack length.

125 that tends to bring sarcomeres back to their slack length.

126 e found evidence that in sarcomeres that are slack (length, approximately 1.85 microns) the elastic t

127 tening velocities (declining with increasing slack lengths).

128 or the Slo channel subunit and suggests that Slack may also have an autonomous role in regulating the

129 mbrane channel expression leading to reduced Slack-mediated IKNa expression underlies DRG neuronal se

130 emented asynchronous communication using the Slack messaging platform and an asynchronous journal clu

131 l leaflets is due to anterior malposition of slack mitral leaflet portions into the LVOT.

132 generated global and sensory neuron-specific Slack mutant mice and analyzed their behavior in various

133 of this channel and a constitutively active Slack mutation stimulate mRNA translation of a reporter

134 were all increased in neurons with the P924L Slack mutation.

135 translation and suggests that the effects of Slack mutations on this process may explain the severe i

136 s indicate that FMRP interacts directly with Slack Na(+)-activated K(+) channels (K(Na)), producing a

137 ) channels in neurons.SIGNIFICANCE STATEMENT Slack Na(+)-activated K(+) channels (KCNT1, KNa1.1) regu

138 These insights about a Slack-Na(V)1.6 complex challenge the traditional view of

139 Moreover, disrupting the Slack-Na(V)1.6 interaction by viral expression of Slack'

140 Notably, the Slack opener loxapine ameliorated persisting neuropathic

141 hannel conductances that do not match either Slack or Slo are formed.

142 a(2+)and other divalent cations, while SLO2 (Slack or SLO2.2 from rat) is activated by Na(+) Curiousl

143 asticity originates from pulling the thermal slack out of the network, and this is consistent with th

144 Moreover, human Slo2.2/Slack P(o) is doubled by SCYL1 in a heterologous express

145 Targeting Slack-Phactr1 interactions may therefore be helpful in d

146 s of this current matched that of the native Slack potassium current, which was identified using an s

147 ctivated potassium channel sodium-activated (Slack) potassium channels, demonstrating macrocomplexing

148 derlying quinidine's blockade against KCNT1 (Slack) remains elusive.

149 deprive reviewers and readers the cognitive slack required to fully recognize and understand novel i

150 ect on the rate of force redevelopment after slack/restretch.

151 nt of Na(V)1.6's N- and C-termini binding to Slack's C-terminus and is enhanced by transient sodium i

152 -Na(V)1.6 interaction by viral expression of Slack's C-terminus can protect against Slack(G269S)-indu

153 ilizing substitutions strongly decreased the slack sarcomere length (SL) at submaximal activating [Ca

154 After a complete extraction, the slack sarcomere length was reduced to approximately 1.7

155 relengthen until they reached their original slack sarcomere length.

156 In slack sarcomeres (approximately 2.0 micron) the tandem I

157 When slack sarcomeres of bovine atrium were stretched, the PE

158 In conclusion, Slack selectively controls the sensory input in neuropat

159 iors were also exaggerated after ablation of Slack selectively in sensory neurons.

160 The Slack (sequence like a calcium-activated K channel) and

161 hat recognizes all amino-termini isoforms of Slack, Slack immunoreactivity is present at locations th

162 As has also been shown for Slack, Slick is expressed in the olfactory bulb, red nuc

163 The Slack/Slo channels have intermediate conductances of abo

164 Slick (Slo2.1) and Slack (Slo2.2) are two novel members of the mammalian Sl

165 Slack (Slo2.2) is a sodium-activated potassium channel t

166 potassium channels Slick (Slo2.1, KCNT2) and Slack (Slo2.2, KCNT1) are high-conductance potassium cha

167 previously shown the abundant expression of Slack sodium-activated potassium (K(Na)) channels in noc

168 und that FMRP binds to the C terminus of the Slack sodium-activated potassium channel to activate the

169 Furthermore, we found that knocking down the Slack subunit by RNA interference causes a loss of firin

170 We have now found that Slick and Slack subunits coassemble to form heteromeric channels t

171 Although it is not yet known if Slick and Slack subunits heteromultimerize, the existence of two g

172 he perceptual and biomechanical impacts of a SLACK suit (non-assistive) controller versus three contr

173 Slack test measurements at 15 degrees C yielded unloaded

174 itional experiments showed that the slope of slack test plots produced by systematically increasing t

175 V(o) was measured with the slack-test method.

176 mically skinned fibres was determined by the slack-test method.

177 n the presence of 5 mM added MgADP, biphasic slack-test plots were apparent even during maximal Ca2+

178 in the presence of added phosphate, biphasic slack-test plots were no longer apparent.

179 Slack-test recordings of single, skinned human masseter

180 ded shortening velocity as determined by the slack-test technique.

181 he rate of force redevelopment following (1) slack tests in which force recovery followed a period of

182 n (EFS)-induced force, (iii) pCa-force, (iv) slack-tests and (v) passive length-tension curves.

183 dues with a high level of disorder providing slack that allows the dramatic shift, and the two confor

184 ave isolated a potassium channel gene called Slack that is abundantly expressed in the nervous system

185 a) is encoded by the rSlo2 gene (also called Slack), the mammalian ortholog of slo-2 in C. elegans.

186 Our findings suggest that slack titin molecules drive muscle disease, potentially

187 Na(V)1.6 binds to and highly sensitizes Slack to quinidine blockade.

188 oiled optic nerve that is likely to provide "slack" to reduce tension on the optic nerve during the e

189 associated with risk of fracture, including slack/tortuosity measures, pulse generator and superior

190 of cell rheology governs the transition of a slack, undulated cell-cell contact (weak adhesion) to a

191 Maximal diastolic width of the slack, unloaded anterior leaflet was significantly great

192 bath solution, or by knocking down levels of Slack using siRNA.

193 h- cells progressively protrudes into a more slack, wavy plasma membrane of h+ cells.

194 As for Slack, we find that Slick is widely distributed in the b

195 e to at least five different transcripts for Slack, which produce Slack channels that differ in their