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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 methylation, also contains a hypermethylated sup allele.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 with ALK- ALCL who are phosphorylated STAT3<sup/>.

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

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

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

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

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

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

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

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

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

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

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

76 egative bacterium Pseudomonas aeruginosa (PA sup)].

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

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

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

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

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

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

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

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

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

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

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

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

89 -17 to facilitate lin-12 signalling and that sup-17 does not act downstream of lin-12.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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