戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 nodine receptors type 1 and type 3 (RyR1 and RyR3).
2  ryanodine receptor/calcium release channel (RyR3).
3 LUSC (P = 0.036, RYR2) and KIRC (P = 0.0042, RYR3).
4 natal muscles contain two isoforms (RyR1 and RyR3).
5 erase (GST) fused to its amino terminus (GST-RyR3).
6 -shaped cytoplasmic region of homotetrameric RyR3.
7  reticulum Ca(2+) release channels, RyR1 and RyR3.
8 for RyR1 and does not express either RyR1 or RyR3.
9 n as diversity region 2) that is absent from RyR3.
10 ells independently expressing either RyR1 or RyR3.
11 L3873Q/Q3874K) imparted 4-CmC sensitivity to RyR3.
12        Reduced RyR1 was greater than that of RyR3.
13 ble to restore skeletal-type E-C coupling to RyR3.
14 382) that each imparted 4-CmC sensitivity to RyR3.
15 ender depolarization-induced Ca2+ release to RyR3.
16 fic isoform of the ryanodine Ca(2+) channel, RyR3.
17 taneous release events generated by RyR1 and RyR3.
18 nes expressed not only RYR1 or RYR2 but also RYR3.
19 overweight that of RYR1 (1439 mutations) and RYR3 (1573 mutations).
20          Under reducing conditions, RyR1 and RyR3 activities are inhibited with a similar affinity at
21        In muscles containing RyR1 as well as RyR3, additional feet are located in lateral parajunctio
22  airway smooth muscle increases, RyR1 and/or RyR3 also mediate the calcium response and thus bronchoc
23                  Surprisingly, we found that RyR3, although incapable of supporting EC coupling or te
24 a(2+)-induced Ca(2+) release (CICR) and that RyR3 amplifies RyR1-mediated CICR in neonatal skeletal m
25 bility to produce sparks, and they also lose RyR3, an isoform abundant in spark-producing skeletal mu
26 le, some muscles also express high levels of RyR3, an isoform with a wide tissue distribution.
27                       Biochemical content of RyR3 and content of parajunctional feet are highly corre
28 re inserted into the corresponding region of RyR3 and expressed in dyspedic 1B5 myotubes.
29       3D reconstructions of both recombinant RyR3 and GST-RyR3 appeared very similar to that of the n
30                         Purified recombinant RyR3 and GST-RyR3 proteins exhibited high-affinity [(3)H
31      Comparison of the 3D reconstructions of RyR3 and GST-RyR3 revealed that the GST domains and, hen
32 trations (<1 microM), CaM activates RyR1 and RyR3 and inhibits RyR2.
33 the specific Ca(2+) release channel subtypes RyR3 and IP(3)R2 in patches along OP processes.
34 examine the local Ca(2+) release behavior of RyR3 and RyR1 in a homologous cellular system.
35  in HEK293 cells, one encoding the wild-type RyR3 and the other encoding RyR3 containing glutathione
36 lly affect CaM binding and CaM regulation of RyR3 and those of the two other isoforms.
37  chromosome 15 included intronic variants of RYR3 and was within an African-specific genomic region a
38 nstructions of both recombinant RyR3 and GST-RyR3 appeared very similar to that of the native RyR3 pu
39  1 (RyR1) and type 2 (RyR2), but not type 3 (RyR3), are efficiently activated by 4-chloro-m-cresol (4
40 e of e-c coupling in muscle cells containing RyR3 but lacking RyR1 (see the accompanying report, ).
41 to cytoplasmic domain constructs of RyR1 and RyR3, but not of RyR2.
42 lts thus indicate that both the RYR1 and the RYR3, but not the RYR2, may be targets for dantrolene in
43 we report that the regulation of recombinant RyR3 by CaM is sensitive to redox regulation.
44                          Substitution of the RyR3 C terminus into RyR1 disrupted 4-CmC sensitivity in
45   Such functional interplay between RyR1 and RyR3 can serve important roles in Ca(2+) signaling of ce
46 r Cs(+) in bilayer lipid membranes, 74 of 88 RyR3 channels exhibited pronounced subconductance behavi
47 ting and conductance level of single RyR1 or RyR3 channels when studied in lipid bilayers.
48 ic enhancement of EC coupling restored by an RyR3 chimera containing amino acids 1,681-3,770 of RyR1.
49 in vivo, we have studied the ability of RyR1/RyR3 chimera to rescue skeletal EC coupling in dyspedic
50 f DHPR into tetrad arrays by expressing RyR1-RyR3 chimerae in dyspedic myotubes.
51 ating activation by 4-CmC, we expressed RyR1-RyR3 chimeric proteins in dyspedic 1B5 myotubes and then
52 s trigger Ca(2+), and a slave parajunctional RyR3 cohort.
53                                         RyR1-RyR3 constructs bearing RyR1 residues 1-1681 restored wi
54 ng the wild-type RyR3 and the other encoding RyR3 containing glutathione S-transferase (GST) fused to
55 (containing both RyR1 and RyR3 isoforms) and RyR3-/- (containing only RyR1) myotubes in the presence
56         Mutagenesis studies demonstrate that RyR3 contains a single conserved CaM binding site.
57 ) and Lys(4021)) that, when mutated to their RyR3 counterparts (Leu(3873) and Gln(3874)), abolished 4
58  and RyR2, but divergent in RyR3, with their RyR3 counterparts reduced 4-CmC sensitivity to the same
59 ranscript levels increased, whereas those of RyR3 decreased after T cell activation.
60 l muscles of adult mice expressing exogenous RyR3, demonstrated as immunoreactivity at triad junction
61                       The reconstructions of RyR3 determined under "open" and "closed" conditions wer
62                   Intact myotubes expressing RyR3 did not, however, respond to K(+) depolarization.
63 ype excitation-contraction coupling, whereas RyR3 did not.
64 ve of a link to RyRs, those transfected with RyR3 do not.
65                                      Because RyR3 does not contact voltage sensors, their opening was
66 hese functional differences between RyR1 and RyR3 expressed in a mammalian muscle context may reflect
67 e to caffeine and CMC but were never seen in RyR3-expressing 1B5 cells.
68 ricted "Ca(2+) spark"-like events, events in RyR3-expressing myotubes were larger in amplitude and du
69                                     Although RyR3-expressing myotubes were more sensitive to caffeine
70  spatially more extensive than those seen in RyR3-expressing myotubes; however, when analysis was lim
71                          This indicates that RyR3 fails to link to DHPRs in a specific manner.
72 2+) stores and are selective in their use of Ryr3 for amplification of intracellular Ca(2+) .
73 be, in part, the result of lower affinity of RyR3 for FKBP12.
74                                              RyR3 genetic knockdown by siRNA led to a significant dec
75 vel and we pinpointed four genes, ESR1, PHB, RYR3, GRIK2, that are associated with the phenotype thou
76       Recombinant type 3 ryanodine receptor (RyR3) has been purified in quantities sufficient for str
77                However, studies on mammalian RyR3 have been difficult because of low expression level
78 itution of the C-terminal third of RyR1 into RyR3 imparted 4-CmC sensitivity to the resulting chimera
79 amplicon system, we expressed either RyR1 or RyR3 in 1B5 RyR-deficient myotubes.
80              We studied the participation of RyR3 in calcium release in wild type (containing both Ry
81 ptors, but a >30-fold enriched expression of Ryr3 in EECs.
82                        Moreover, RyR1 and/or RyR3 in mouse airway smooth muscle also appear to mediat
83 e supports the hypothesis that activation of RyR3 in skeletal muscle cells must be indirect and provi
84      We have explored the structural role of RyR3 in the assembly of CRUs in 1B5 cells independently
85                                              RyR3 in the presence of reduced glutathione binds CaM wi
86 ween the Ca(2+) release behavior of RyR1 and RyR3 in this homologous expression system.
87             With the co-presence of RyR1 and RyR3 in wild-type cells, unmitigated radial CICR propaga
88 y inhibited by dantrolene, and the extent of RYR3 inhibition was similar to that displayed by the RYR
89 nd skeletal muscle (RyR1) receptor isoforms, RyR3 is a homotetrameric complex comprising two main com
90 t IpTxa can interact with both RyRs and that RyR3 is functional in myotubes and it can amplify the ca
91 he periphery near the cell membrane, whereas RyR3 is more centrally localized.
92  1B5 myotubes is activated by 4-CmC, whereas RyR3 is not.
93                   Because it applies whether RyR3 is present or not, it is this exclusion by voltage
94                     In contrast, the role of RyR3 is unknown.
95                           By comparison, the RYR3 isoform expressed in HEK-293 cells was significantl
96 operated sparks phenotype is specific to the RyR3 isoform.
97 yR3 KO myotubes concluded that both RyR1 and RyR3 isoforms participated in Ca2+-dependent Ca2+ releas
98 lease in wild type (containing both RyR1 and RyR3 isoforms) and RyR3-/- (containing only RyR1) myotub
99 ibed to the absence of ryanodine receptor 3 (RyR3) isoforms in adult mammalian muscle.
100 s of wild-type or ryanodine receptor type 3 (RyR3) knockout mice.
101                                           In RyR3-knockout myotubes (655 events, 83 cells) the amplit
102 on under voltage clamp of both wild-type and RyR3-knockout myotubes produced substantial Ca2+ release
103 events were detected in intact wild-type and RyR3-knockout myotubes.
104 e receptor type 3 (RyR3) KO, and double RyR1/RyR3 KO mice under voltage clamp with simultaneous monit
105 ression in RyR3 KO, RyR1 KO, and double RyR1/RyR3 KO myotubes concluded that both RyR1 and RyR3 isofo
106     A comparison of beta2a overexpression in RyR3 KO, RyR1 KO, and double RyR1/RyR3 KO myotubes concl
107 type 1 (RyR1) KO, ryanodine receptor type 3 (RyR3) KO, and double RyR1/RyR3 KO mice under voltage cla
108 e 1 and type 3 ryanodine receptors (RyR1 and RyR3) located in the sarcoplasmic reticulum membrane.
109 ces in gating behavior exhibited by RyR1 and RyR3 may be, in part, the result of lower affinity of Ry
110                                              RyR3 moderately colocalized at junctions with JPH4, wher
111                                     RyR2 and RyR3 mRNAs were upregulated, RyR2 was S-glutathionylated
112                                              RYR3, MYOM2, ERGIC1, SPTBN4, and ABCA7 represent genes,
113     In addition, our data indicate that when RyR3-/- myotubes are voltage-clamped, the effect of IpTx
114 rom atrial muscle to the SAN center: RYR2 to RYR3, Na(v)1.5 to Na(v)1.1, Ca(v)1.2 to Ca(v)1.3 and K(v
115 es expressed twice the RyR2 but only 65% the RyR3 of arterioles and neither vessel expressed RyR1.
116            Purified recombinant RyR3 and GST-RyR3 proteins exhibited high-affinity [(3)H]ryanodine bi
117                                              RyR3 provides a preferable background than RyR2 for defi
118  appeared very similar to that of the native RyR3 purified from bovine diaphragm.
119 lify mechanically induced Ca(2+) entry, with RyR3 receptors selectively expressed in EECs and involve
120 well developed transverse tubule system, the RyR3 reinforcement of CICR seems to ensure a robust, uni
121 R, and the role of the transiently expressed RyR3 remains elusive.
122 , a significant difference between RyR1- and RyR3-rescued junctions is revealed by freeze fracture.
123 selective markers of neuronal vulnerability (Ryr3), resilience (Oxr1), and mitochondrial dynamics (Op
124  muscle and brain isoforms of RyRs (RyR1 and RyR3, respectively).
125                                Expression of RyR3 restored caffeine-sensitive, global Ca(2+) release
126 on of the 3D reconstructions of RyR3 and GST-RyR3 revealed that the GST domains and, hence, the amino
127 II; however, alphaKAP, beta2 CaMK-II and the RyR3 ryanodine receptor were also necessary for full CaM
128  addition, substitution of the corresponding RyR3 sequence into positions 4007-4180 of RyR1 disrupted
129                        By contrast, RyR1 and RyR3 strongly colocalized with JPH3, and RyR2 moderately
130 d a complementary set of chimeras containing RyR3 substitutions in RyR1.
131 ed that isolated ICC expressed both RyR2 and RyR3 subtypes.
132 domains and, hence, the amino termini of the RyR3 subunits are located in the "clamp" structures that
133 (2+) release after the induction of RYR2 and RYR3 that occurred after treatment with stromal cell-der
134 lf failed to restore skeletal EC coupling to RyR3, the addition of the D2 region resulted in a dramat
135                          In myotubes lacking RyR3, the peripheral VICR component is unaffected, and R
136 nds RyR3 with reduced affinity but activates RyR3 to a greater extent.
137 nd (iii) a form of retrograde signaling from RyR3 to the DHPR occurs in the absence of direct protein
138 n, mutation of the corresponding residues in RyR3 to their RyR1 counterparts (L3873Q/Q3874K) imparted
139                              RyR1, RyR2, and RyR3 transcripts were detected in human T cells.
140 Western blot analysis revealed that RyR1- or RyR3-transduced cells expressed the appropriate RyR isof
141                          Purification of GST-RyR3 was achieved by affinity chromatography by using gl
142                                              RyR3 was purified from detergent-solubilized transfected
143           [(3)H]ryanodine binding to RyR1 or RyR3 was significantly increased in the presence of IpTx
144                                  Type 3 RYR (RYR3) was not detected in PBMCs.
145 ression of the intracellular Ca(2+) receptor Ryr3, which contributed to the mechanically evoked incre
146                                              RyR3, which disappears in adult muscle, is not involved
147        In contrast, inhibiting only RyR1 and RyR3 with 25 microM dantrolene attenuated these response
148 reducing and oxidizing conditions, CaM binds RyR3 with reduced affinity but activates RyR3 to a great
149 ity of the isoforms, detailed comparisons of RyR3 with RyR1 showed one region of highly significant d
150 rved between RyR1 and RyR2, but divergent in RyR3, with their RyR3 counterparts reduced 4-CmC sensiti

 
Page Top