ライフサイエンスコーパス: sup

1 sup-12 mutations strongly suppress muscle defects in unc

2 sup-39 mutations cause early embryonic lethality, but es

3 sup-6 also encodes a U1 snRNA and the mutant contains a

4 sup-6(st19) is an allele-specific suppressor of unc-13(e

5 quency on gnomAD version 4.1.0 of <1.25 x 10:sup>-6).

6 ir-35 family in this process, suppressor-26 (sup-26) and NHL (NCL-1, HT2A, and LIN-41 repeat) domain-

7 Similar to sup-35, sup-37 loss-of-function mutations can suppress both LOF

8 A sup-1 null mutant has no obvious deficits in cholinergic

9 hat converts an endogenous mouse tRNA into a sup-tRNA extensively rescued disease pathology in a mode

10 In the presence of a sup-39 mutation, these same three splice donors are used

11 We establish the significance of a sup-optimal paternal low protein diet for offspring vasc

12 techniques and by the analysis of additional sup-pf-2 alleles.

13 lly wild type in appearance, while hsf-1 and sup-45 mutants have egg-laying defects.

14 utants and virtually eliminated in hsf-1 and sup-45 mutants, as compared to wild-type expression.

15 cyl-1 and sup-45, but not hsf-1, mutations suppressed a defect cau

16 thermore, concomitant reduction of adm-4 and sup-17 activity causes the production of two anchor cell

17 We cloned sup-9 and sup-10 and found that they encode a two-pore K+ channel

18 c-93 and many fewer are alleles of sup-9 and sup-10.

19 Genetic studies of sup-9, unc-93, and sup-10 strongly suggest that these genes encode componen

20 Syrian hamster embryo cell lines (sup+I and sup-II) and a human colorectal carcinoma cell line (RKO)

21 utation activates a cryptic splice site, and sup-6(st19) restores splicing to the mutant splice donor

22 CTNP/B.b-sup exhibited a suitable morphology with a particle size

23 CTNP/B.b-sup induced the most significant reduction in TGF-alpha

24 It can be concluded that CTNP/B.b-sup is a suitable drug delivery system with anticancer p

25 investigation into the toxicity of CTNP/B.b-sup on Caco-2 cells by MTT assay, the expression of gene

26 The effects of CTNP/B.b-sup on the expression levels of various oncogenes reveal

27 e viability of Caco-2 cells against CTNP/B.b-sup was 90.3%.

28 In the present study, the CTNP/B.b-sup was demonstrated to possess the capability of modula

29 n and entrapment efficiency (EE) of CTNP/B.b-sup were assessed using a BCA protein assay.

30 rnatant of Bifidobacterium bifidum (CTNP/B.b-sup) on genes associated with CRC signaling pathways.

31 Concomitant reduction of both sup-17 and adm-4 activity in hermaphrodites results in h

32 mal gonads have a single row of oocytes, but sup-39 gonads often have two rows of oocytes.

33 and SUPERMAN (SUP) genes, as caf clv and caf sup double mutants show dramatically enhanced floral mer

34 wed that early, stage I preneoplastic cells (sup+ I) are highly susceptible to apoptosis, whereas the

35 Early preneoplastic cells (sup+) exhibit increased susceptibility to apoptosis, whi

36 eas the later, stage II preneoplastic cells (sup- II) are relatively resistant.

37 h is lost in late stage preneoplastic cells (sup-).

38 stic variant of Syrian hamster embryo cells, sup(+), exhibits decreased endoplasmic reticulum calcium

39 We cloned sup-9 and sup-10 and found that they encode a two-pore K

40 under growth factor deprivation conditions; sup+I cells were highly susceptible to apoptosis, wherea

41 In contrast sup- cells, which are resistant to apoptosis in low seru

42 tion, here we describe a rationally designed sup-tRNA (tRNAGluV13) with greatly improved ability to s

43 , offers a favorable scaffold for developing sup-tRNAs that restore protein synthesis from PTC-contai

44 lways successful at producing more efficient sup-tRNAs.

45 Mutations in the Caenorhabditis elegans sup-39 gene cause allele-specific suppression of the unc

46 rime editing agents to install an engineered sup-tRNA at a single genomic locus without overexpressio

47 n sites for nonsense mutations, yet existing sup-tRNAs are ineffective at suppressing Glu-to-Stop mut

48 domain of LIN-12 appears to be necessary for sup-17 to facilitate lin-12 signalling and that sup-17 d

49 ture-shift studies for two suppressor genes, sup-17 and lag-2, suggest that both genes act at approxi

50 These suppressors defined seven genes: sup-17, lag-2, sel-4, sel-5, sel-6, sel-7 and sel-8.

51 the [Ca2+]i level in logarithmically growing sup+ I cells (approximately 100 nM) was considerably low

52 methylation, also contains a hypermethylated sup allele.

53 We identified sup-45 as one of the two hitherto unknown C. elegans ort

54 In sup- cells in low serum, addition of BAPTA-AM also resul

55 In sup-12 mutants, expression of UNC-60B is decreased, wher

56 Raising extracellular Ca(2+) in sup+ cells resulted in a slight activation of I kappa B

57 ole for Ca(2+), lowering cytosolic Ca(2+) in sup- cells by addition of the cell-permeable Ca(2+) chel

58 ese data suggest that the elevated Ca(2+) in sup- cells causes a modest activation of IKK, which like

59 the onset of low-serum-induced apoptosis in sup+I cells and enhanced survival in sup-II cells.

60 tivated c-FosER protein induces apoptosis in sup-II preneoplastic cells in serum-free medium, indicat

61 ned that the basal activity of NF-kappa B in sup- cells is largely proteasome-independent, but sensit

62 sidered that the activation of NF-kappa B in sup- cells might be secondary to an increase in cytosoli

63 e enhanced basal activation of NF-kappa B in sup- cells; however, the predominant effect of Ca(2+) ap

64 directly whether Ca2+ entry was decreased in sup+ I cells in 0.2% serum, Mn2+ uptake was used to moni

65 e rate of thapsigargin-induced Mn2+ entry in sup+ I cells was approximately 50% lower than that of su

66 urther, coexpression of Bcl-2 and c-FosER in sup+I or sup-II cells protected the cells from c-FosER-i

67 calcium levels were exogenously increased in sup+ I cells by raising extracellular Ca2+ to 3 mM; ER c

68 imately 82 nM), whereas the [Ca2+]i level in sup- II cells did not change.

69 e previously demonstrated that a mutation in sup-39, a U1 snRNA gene, suppresses e936 by increasing s

70 The suppressor mutations in sup-17 and lag-2 were shown to be rare non-null alleles,

71 is a U1 snRNA gene; suppressor mutations in sup-39 are compensatory substitutions in the 5' end, whi

72 itutive activation of NF-kappa B observed in sup- cells is not due to loss of I kappa B alpha.

73 was considerably lower than that observed in sup- II cells (approximately 260 nM).

74 argin-releasable Ca2+ was greatly reduced in sup+ I cells (45 nM) as compared to sup- II cells (190 n

75 rating that capacitative entry is reduced in sup+ I cells.

76 t the flagellar beat frequency is reduced in sup-pf-2, but little else was known about the sup-pf-2 p

77 osis in sup+I cells and enhanced survival in sup-II cells.

78 ytosolic Ca(2+) level that is double that in sup+ cells.

79 id-borne motB(am) genes were introduced into sup(o), supE, and supF strains to see what motility defe

80 (rho;beta) = lim(M,N --> infinity)inf(lambda)sup(rank(X) </= rho . M)MSE(X,X(lambda)), where M/N -->

81 ned in two Syrian hamster embryo cell lines (sup+I and sup-II) and a human colorectal carcinoma cell

82 LNP-sup-tRNA formulations caused no discernible readthrough

83 -wide significant loci (P < 5 x 10-8) including 7 distinct signals asso

84 mented short-chain fatty acid metabolites1,2, although the immunoregulatory ro

85 SO(3), and the high energy of CH(3)-S(O)(2)O.

86 with ALK- ALCL who are phosphorylated STAT3.

87 ain fatty acid metabolites1,2, although the immunoregulatory roles of most fib

88 ant loci (P < 5 x 10-8) including 7 distinct signals associated with EC

89 Analysis of new sup-pf-2 mutations indicates that the severity of the ou

90 these conditions; however, developing novel sup-tRNAs with high efficiency and specificity often req

91 l lipid nanoparticle (LNP) administration of sup-tRNA in mice restored the production of functional p

92 Two independent suppressor alleles of sup-1 are associated with a glycine-to-glutamic acid sub

93 in, and we found three additional alleles of sup-45, a previously molecularly uncharacterized genetic

94 eles of unc-93 and many fewer are alleles of sup-9 and sup-10.

95 Biochemical analysis of sup-pf-2-1 axonemes indicates that both axonemal ATPase

96 ctively, these results unveil a new class of sup-tRNAs with encouraging potential for tRNA-based ther

97 Gonads of sup-39 mutant animals show a novel defect: normal gonads

98 tions should greatly expand the potential of sup-tRNA-based therapeutics.

99 estigated potential functional redundancy of sup-17 and the C. elegans ortholog of TACE, adm-4, by ex

100 Genetic studies of sup-9, unc-93, and sup-10 strongly suggest that these ge

101 enotype arises from a loss of suppression of sup-35 toxicity.

102 lls was approximately 50% lower than that of sup- II cells, demonstrating that capacitative entry is

103 orhabditis elegans The element is made up of sup-35, a maternal-effect toxin that kills developing em

104 ispensable endogenous tRNA into an optimized sup-tRNA.

105 oexpression of Bcl-2 and c-FosER in sup+I or sup-II cells protected the cells from c-FosER-induced ap

106 egative bacterium Pseudomonas aeruginosa (PA sup)].

107 PMA, PA sup, and LPS increased MUC5AC gene expression and mucin

108 Knockdown of TACE inhibited PMA-, PA sup-, and LPS-induced TGF-alpha shedding, EGFR phosphory

109 ated peripheral blood mononuclear cells (PHA-sup) expressed high levels of CCR6 mRNA.

110 F)-alpha was largely responsible for the PHA-sup-induced CCR6 mRNA expression.

111 A seven amino acid yeast prion sup-35 fragment (GNNQQNY) forms amyloid fibrils.

112 rAAV.sup-tRNA had a limited effect on global readthrough at n

113 hat rAAV delivery of a suppressor tRNA (rAAV.sup-tRNA) safely and efficiently rescued a genetic disea

114 nd that reduced adm-4 activity, like reduced sup-17 activity, suppresses an allele of glp-1 that enco

115 We have reexamined sup-pf-2 using improved biochemical and structural techn

116 We thus renamed sup-45 as affl-2 (AF4/FMR2-Like).

117 use of engineered suppressor transfer RNAs (sup-tRNAs) that facilitate translational stop codon read

118 Suppressor transfer RNAs (sup-tRNAs) with the capacity to translate PTCs represent

119 While several sup-tRNAs have shown promising results in preclinical mo

120 ry to an increase in cytosolic Ca(2+), since sup- cells have a cytosolic Ca(2+) level that is double

121 an tRNAs identified tRNAs with the strongest sup-tRNA potential.

122 e mutants inner no outer (ino) and superman (sup), which lead to absent or symmetrical growth of the

123 t growth is eliminated, whereas in superman (sup) mutants integument growth on the adaxial side is ne

124 fy two genes disrupted in acd6-1 suppressor (sup) mutants: one encodes a known SA biosynthetic compon

125 revertants, extragenic dominant suppressors (sup-39), and a single apparently intragenic mutation tha

126 -17 to facilitate lin-12 signalling and that sup-17 does not act downstream of lin-12.

127 y, we show by cell ablation experiments that sup-17 can act cell autonomously to facilitate lin-12 ac

128 We demonstrate here that sup-39 is a U1 snRNA gene; suppressor mutations in sup-3

129 lts are consistent with the possibility that sup-17 and adm-4 are functionally redundant for at least

130 Here, we show that sup-17 encodes a member of the ADAM family of metallopro

131 Previous work suggested that sup-17 facilitates lin-12 signalling in Caenorhabditis e

132 scues this fertility defect, suggesting that sup-17 and adm-4 may mediate ectodomain shedding of LIN-

133 The sup-1 gene encodes a single-pass transmembrane protein t

134 The sup-pf-2 mutation is a member of a group of dynein regul

135 The sup-pf-2 mutations therefore appear to alter the activit

136 up-pf-2, but little else was known about the sup-pf-2 phenotype.

137 brane conductance regulator gene (CFTR), the sup-tRNAs re-established expression and function in cell

138 al resulted in a reduction of [Ca2+]i in the sup+ I cells (approximately 82 nM), whereas the [Ca2+]i

139 ific suppressors, including mutations in the sup-1 locus.

140 the sequence upstream of PTCs modulates the sup-tRNA readthrough efficacy.

141 Here we report the characterization of the sup-26 gene, which regulates sex determination in the so

142 Inactive copies of the sup-35/pha-1 element show high sequence divergence from

143 We previously showed that mutation of the sup-39 gene promotes splicing at the mutant splice donor

144 utation responsible for the phenotype of the sup-pf-4 strain, and biochemical comparison with a radia

145 n tests and linkage analysis reveal that the sup-pf-2 mutations are alleles of the PF28/ODA2 locus, w

146 We have found that the sup-pf-2 mutations are associated with defects in the ou

147 ffering by the inter-connectivities of their sup-spaces as one of the most important parameter determ

148 This sup-39-induced change was also observed when the e936 mu

149 or antagonist, desGly-NH2,d(CH2)5[D-Tyr2,Thr-sup-4]OVT, into the cPAGv reduced the percentage of time

150 duced in sup+ I cells (45 nM) as compared to sup- II cells (190 nNM) after 4 h in low serum.

151 Similar to sup-35, sup-37 loss-of-function mutations can suppress b

152 ort of this hypothesis, thapsigargin-treated sup+ I cells (0.2% serum) showed decreased Ca2+ entry up

153 ative tRNAs into efficient suppressor tRNAs (sup-tRNAs) by individually fine-tuning their sequence to

154 ficiency of the engineered suppressor tRNAs (sup-tRNAs) largely varies in a tissue- and sequence cont

155 by premature stop codons, suppressor tRNAs (sup-tRNAs) offer a more general strategy.

156 findings suggest that CSR1 is a potent tumor sup-pressor gene.

157 Seven heritable but unstable sup epi-alleles (the clark kent alleles) are associated

158 ) by approximately 31% relative to untreated sup- cells, concomitant with a 65% reduction in NF-kappa

159 Existing approaches to use sup-tRNAs therapeutically, however, require lifelong adm

160 When sup- II cells were placed under conditions that resulted

161 ere highly susceptible to apoptosis, whereas sup-II cells were resistant.