ライフサイエンスコーパス: DIF

1 DIF analysis is not only proving very useful for differe

2 DIF may confound interpretation of subgroup differences.

3 DIF-1 (also known as interferon regulatory factor-2 bind

4 DIF-1 expression rescues breast cancer cells from NRIF3/

5 DIF-1 is a chlorinated alkyl phenone that is synthesized

6 DIF-1 is a transcriptional repressor that mediates its e

7 DIF-1 sensitivity may, therefore, not be characteristic

8 DIF-6, but not DIF-7 or PSI-2, appears to have an essent

9 Differentiation-inducing factor 1 (DIF-1) is a polyketide-derived morphogen which drives st

10 l inducer Differentiation inducing factor 1 (DIF-1), or are subjected to hyper-osmotic stress.

11 Differentiation-inducing factor-1 (DIF-1) is a polyketide that induces Dictyostelium amoeba

12 to this factor as DD1-interacting factor-1 (DIF-1).

13 However, a DIF-less mutant showed normal PdL activity during develo

14 In a DIF-1 induction assay the lrrB- mutant is profoundly def

15 ed to establish or rule out a diagnosis of a DIF-positive oral vesiculobullous disease.

16 removal of MybE or DimB reveals an alternate DIF-1 activation pathway, for pstU differentiation, that

17 (4) Although DIF-1 has little effect on its own synthesis in short-te

18 y was induced in cell suspension by cAMP and DIF acting in synergy.

19 Dorsal and DIF act downstream of Toll, whereas Relish acts downstre

20 ut not of the other cell types examined, and DIF-1 also protects these cells from H89-mediated apopto

21 ed by a telling synergy between c-di-GMP and DIF-1.

22 ation, based on conventional microscopic and DIF analysis, was tabulated.

23 entified as a transcriptional repressor, and DIF-1 knockdown leads to apoptosis of breast cancer cell

24 restalk region of the Dictyostelium slug and DIF-1 is a low molecular weight signalling molecule that

25 g to dissect growth dynamics under +DIF and -DIF in the model plant Arabidopsis (Arabidopsis thaliana

26 Differences between DIF-positive and -negative patients in demography, sites

27 negative direct immunofluorescence biopsies (DIF) in patients with clinically typical ocular mucous m

28 nduce stalk cell differentiation by blocking DIF-1 export, causing DIF-1 to build up within cells.

29 clinical and microscopic findings as CDG but DIF staining is negative.

30 in the absence of diagnosis confirmation by DIF.

31 The ecmA gene is not induced by DIF-1 in a mybE-strain.

32 result also indicates that the induction by DIF and cAMP as seen in cell suspensions is not essentia

33 yclic-AMP and this induction is inhibited by DIF-1.

34 extracellular cAMP, but surprisingly, not by DIF-1, a soluble molecule thought to be essential for th

35 l differentiation, is greatly overinduced by DIF in Dd-STATa null cells.

36 gtaC expression is directly regulated by DIF, and GtaC rapidly translocates to the nucleus in res

37 bitors, and this effect could be reversed by DIF-1.

38 hallmark of mutants aberrant in signaling by DIF-1, the polyketide that induces prestalk and stalk ce

39 that, in the presence of extracellular cAMP, DIF-1 causes DimB to associate with the ecmA promoter in

40 rentiation by blocking DIF-1 export, causing DIF-1 to build up within cells.

41 uld use caution with items that demonstrated DIF.

42 positive day/night temperature difference (+DIF).

43 (negative day-night temperature difference [-DIF]) inhibit hypocotyl growth in Arabidopsis (Arabidops

44 and two inducing stalk cell differentiation (DIFs 6 and 7) were resolved.

45 It also directs DIF-inducible gene expression.

46 Models disregarding DIF underestimate the actual alpha.

47 y typical ocular MMP disease with documented DIF results who were followed for at least 1 year at the

48 Dorsal, DIF, and Relish are NF-kappaB-related transcription fact

49 sis and auxin signaling were reduced during -DIF.

50 cription factor, which is required for every DIF-1 response investigated.

51 e to do so in vitro in response to exogenous DIF (a morphogen required for prestalk and stalk cell di

52 as rescued by complementation with exogenous DIF-1.

53 by the stalk differentiation-inducing factor DIF-1 and is restricted to a subset of prestalk cells (p

54 enes by the differentiation inducing factor (DIF).

55 alk inducer differentiation inducing factor (DIF-1), a chlorinated hexaphenone.

56 Desmin intermediate filaments (DIFs) form an intricate meshwork that organizes myofiber

57 Thus, MybE is necessary for DIF-1 responsiveness and for the correct differentiation

58 etic selection to isolate genes required for DIF signal transduction, we found a mutant (dimC(-)) tha

59 ing diffusion-induced isotope fractionation (DIF) and implementing different parameterizations of loc

60 sure exhibits differential item functioning (DIF) by disease (atopic dermatitis versus psoriasis), ge

61 d significant differential item functioning (DIF) for 7 of 48 items (two mobility tasks, four reading

62 dy to examine differential item functioning (DIF) in 2 versions of the Experiences of Discrimination

63 ed to examine differential item functioning (DIF) on the Everyday Discrimination Scale by race/ethnic

64 gtaC(-) null cells showed some hallmark DIF signalling defects.

65 ory of patients should be accepted as having DIF-negative MMP, for clinical management purposes, with

66 on is induced by the chlorinated hexaphenone DIF-1.

67 Ignoring DIF-1 and not becoming prestalk should allow cells to ch

68 tained to perform direct immunofluorescence (DIF) and histologic analyses.

69 Direct immunofluorescence (DIF) testing is a useful adjunct for the diagnosis of im

70 CDG) are shown by direct immunofluorescence (DIF) to be immune mediated diseases.

71 atients, who have direct immunofluorescence (DIF)-negative biopsies, be excluded from a diagnosis of

72 cases of DG using direct immunofluorescent (DIF) in conjunction with histology and clinical evaluati

73 ) mutant, which is specifically defective in DIF-1 synthesis.

74 at of more severe central corneal disease in DIF-negative patients.

75 gs was demonstrated by a similar increase in DIF-associated PLD activity after stimulation of intact

76 hows that DimB binds to the ecmB promoter in DIF-induced cells.

77 dent phosphatase calcineurin plays a role in DIF-1 signaling to the DimB prestalk transcription facto

78 thylene application restored leaf growth in -DIF conditions, and constitutive ethylene signaling muta

79 ot respond typically to the prestalk inducer DIF-1.

80 nscriptional regulator required to integrate DIF-1 signaling and subsequent patterning in Dictyosteli

81 with the scale, including misfitting items, DIF by disease, age, and gender, disordered response thr

82 stablishing a definitive diagnosis for known DIF-positive diseases.

83 oxylin and eosin-stained slides of the known DIF-positive specimens without knowledge of the DIF resu

84 y differentiate normally in a mutant lacking DIF.

85 Large DIF was observed for 2 of 7 racial/ethnic discrimination

86 The authors also observed large DIF by race/ethnicity for 3 of 7 gender discrimination i

87 The large DIF by race/ethnicity in the index for racial/ethnic dis

88 The approximately twice larger DIF effect for chlorine than for carbon together with th

89 At the global level, DIF-1 causes a major shift in the phosphorylation/dephos

90 ifferentiation of prestalk-O cells by making DIF-1, and that this is one of the regulatory loops that

91 ation, and language of interview, meaningful DIF was observed for 3 (out of 10) items: "receiving poo

92 s requires the diffusible signaling molecule DIF-1, and provides an example of a spatial information-

93 ea, in Dictyostelium the signalling molecule DIF acts as a position-independent signal and was though

94 The signalling molecule DIF-1 is required for normal cell fate choice and patter

95 required to receive the signalling molecule DIF-1 that causes differentiation into prestalk cells.

96 on is induced using the stalk cell morphogen DIF.

97 ells to inhibition by the prestalk morphogen DIF-1.

98 associates with elongated normal and mutant DIFs assembled in vitro.

99 , including those with positive and negative DIF findings.

100 between patients with positive and negative DIF results.

101 The remaining specimens had negative DIF findings and consisted of numerous non-specific infl

102 rature cycles (cold photoperiod/warm night [-DIF]), most species exhibit reduced elongation growth.

103 DIF-6, but not DIF-7 or PSI-2, appears to have an essential carbonyl gr

104 mB, a marker of pstB differentiation, is not DIF inducible.

105 nsitive to the stalk cell-inducing action of DIF-1 but largely refractory to the repressive effect ex

106 r within the first minutes after addition of DIF-1, using a triple-label SILAC approach.

107 , wild-type cells respond to the addition of DIF-I by induction of the prestalk marker ecmA and repre

108 ng both chlorinations in the biosynthesis of DIF-1.

109 indings do not support the classification of DIF-negative patients, meeting the clinical criteria for

110 by regulating the cellular concentration of DIF-1.

111 To assess the contribution of DIF to successful diagnosis, three pathologists examined

112 consider the advantages and disadvantages of DIF adjustment (omitting items, constructing separate me

113 The effect of DIF on the overall isotope signal attenuation was greate

114 IF-1 and with the known inhibitory effect of DIF-1 on chemotaxis to cAMP.

115 re hypersensitive to the inducing effects of DIF and readily form stalk cells in monolayer assay, the

116 o regulate the cell type-specific effects of DIF.

117 pon pharmacological or genetic inhibition of DIF-1 biosynthesis.

118 ound that cerulenin, a specific inhibitor of DIF-1 biosynthesis, abolished the induction of stalk cel

119 This interaction of DIF-1, IRF-2BP1, and EAP1 occurs through the conserved C

120 Small interfering RNA (siRNA) knockdown of DIF-1 selectively leads to apoptosis of breast cancer ce

121 cells is caused by a high perceived level of DIF-1 signalling, leading to nuclear localization of Dim

122 they do not accumulate measurable levels of DIF-I, a morphogen that was previously implicated in pre

123 We suggest that both these manifestations of DIF hypersensitivity in the null strain result from the

124 to the prespore cells as the major source of DIF-1.

125 , suggesting that gtaC regulates a subset of DIF responses.

126 This revealed a new world of DIF-1-controlled signaling, with changes in components o

127 of prestalk development is not dependent on DIF-1 and suggest that the morphogen participates mainly

128 diseases did not yield positive findings on DIF testing.

129 gly, an even larger number of genes are only DIF inducible in mybE- cells, some genes are only induci

130 sitive for respiratory viruses by culture or DIF, 86 (92%) were positive by RT-PCR, including 66 HRSV

131 breast cancer cells from NRIF3 expression or DIF-1 knockdown, while expression of FASTKD2 leads to ap

132 results were negative by viral isolation or DIF.

133 pond to DIF as they are phenocopied in other DIF signalling mutants.

134 the mutant were distinct from those of other DIF signalling mutants, suggesting that gtaC regulates a

135 alk cell-inducing chlorinated alkyl phenone, DIF-1.

136 yostelium cells to the signalling polyketide DIF-1 causes DimB, a bZIPtranscription factor, to accumu

137 c gene, ecmA, is inducible by the polyketide DIF-1 in a monolayer assay and requires the DimB and Myb

138 s in vitro, can be induced by the polyketide DIF-1 or by the cyclical dinucleotide c-di-GMP.

139 A polyketide, DIF-1, which induces stalk-like cells in vitro, was isol

140 owever, the known stalk-inducing polyketide, DIF-1, could not replace conditioned medium and induce t

141 y 48% of the specimens demonstrated positive DIF findings and consisted of pemphigus vulgaris, mucous

142 ften biopsy of these lesions yields positive DIF results.

143 r, show that purified prespore cells produce DIF-1 at more than 20 times the rate of prestalk cells.

144 utant responds to DIF-1 but does not produce DIF-1; (2) the dimA(-) mutant produces DIF-1 but does no

145 oduce DIF-1; (2) the dimA(-) mutant produces DIF-1 but does not respond to DIF-1; and (3) the dimA(-)

146 tempted to find out which cell type produces DIF-1, a diffusible signal molecule inducing the differe

147 The required DIF-1 polyketide could also be endogenous, as shown by t

148 The differentiation-inducing signals (DIFs) currently known in Dictyostelium appear unable to

149 Since DIF-1 is the most potent inhibitor of RhT activity, and

150 mens) or direct immunofluorescence staining (DIF) (65 specimens).

151 Using standard DIF analysis, 11 of the CDG cases were diagnosed as beni

152 We found that DIF-1 did not affect the expression of the tagB or carB

153 Our results indicate that DIF-1 plays a key role in breast cancer cell survival an

154 photobleaching of living cells, we show that DIF inhibits the nuclear export of Dd-STATc.

155 hing and molecular analyses, we suggest that DIF-induced dimerisation of Dd-STATc functionally masks

156 activity during development, suggesting that DIF does not control PdL in vivo.

157 breast cancer cells, further suggesting that DIF-1 plays a key role in NRIF3/DD1-mediated apoptosis.

158 We found that -DIF altered leaf growth patterns, decreasing the amplitu

159 The DIF also contained F-actin, vinculin, talin, paxillin, a

160 The DIF and Relish complex is detectable in whole animal ext

161 The DIF contained PLD1, RhoA, and ARF, and the level of each

162 The DIF results were recorded.

163 The DIF-1 complex was found to repress FASTKD2, a putative p

164 er DimA activity is required to activate the DIF response pathway in certain cells or is a component

165 Thus, regulation of FASTKD2 by NRIF3 and the DIF-1 complex acts as a novel death switch that selectiv

166 e activity is counterbalanced in vivo by the DIF-1-regulated activity of PTP3, a Tyr922 phosphatase.

167 However, the DIF was small relative to baseline changes in item diffi

168 genetic selection to isolate mutants in the DIF-1 response pathway.

169 -positive specimens without knowledge of the DIF results.

170 at puberty 1) as important components of the DIF-1 complex mediating both complex stability and trans

171 compromised cAMP-mediated inhibition of the DIF-1 mediated ecmB induction.

172 in Dictyostelium only in the presence of the DIF-1 polyketide or its metabolites.

173 est that they are directly downstream of the DIF-1 signal.

174 Of the DIF-positive cases, only pemphigus vulgaris could be dia

175 The formation of the DIF-Relish heterodimer is particularly interesting becau

176 we specifically tested the functions of the DIF;Relish (a ; sign represents the peptide linker) link

177 Unexpectedly, it also required the DIF-1 polyketide.

178 edge of how cells receive and respond to the DIF-1 signal.

179 ts ethylene biosynthesis and constrains the -DIF-induced phase shift in rhythmic growth.

180 genes that depend on MybE and DimB for their DIF-1 inducibility.

181 Thus, DIF-1 regulates DimB activity to generate a gradient of

182 Thus, DIF-1 synthesis appears to be required for the induction

183 the nuclei of Dictyostelium cells exposed to DIF, the chlorinated hexaphenone that directs prestalk c

184 tes in the nucleus when cells are exposed to DIF-1, and ChIP analysis shows that, in the presence of

185 r Pyk2, a tyrosine-specific TKL, exposure to DIF-1 does not activate STATc.

186 o, Dd-STATa null cells are hypersensitive to DIF for expression of ST/lacZ, a marker for the earliest

187 e defects are due to a failure to respond to DIF as they are phenocopied in other DIF signalling muta

188 A, which is required for cells to respond to DIF-1.

189 utant produces DIF-1 but does not respond to DIF-1; and (3) the dimA(-) mutant exhibits cell autonomo

190 es exist: (1) the dmtA(-) mutant responds to DIF-1 but does not produce DIF-1; (2) the dimA(-) mutant

191 cAMP receptor that we observe in response to DIF-1 and with the known inhibitory effect of DIF-1 on c

192 tes that are dephosphorylated in response to DIF-1 are phosphorylated in response to extracellular cA

193 y to regulate diverse targets in response to DIF-1 is partly due to their ability to form homo- and h

194 isation of both DimA and DimB in response to DIF-1 suggest that they are directly downstream of the D

195 y translocates to the nucleus in response to DIF.

196 e direct regulators of cellular responses to DIF-1.

197 o position -364 eliminated responsiveness to DIF and cAMP, but normal PdL activity in prestalk cells

198 In response to -DIF, the phase of ethylene emission advanced 2 h, but to

199 nditions that clinically resembled typically DIF-positive vesiculobullous diseases did not yield posi

200 ed imaging to dissect growth dynamics under +DIF and -DIF in the model plant Arabidopsis (Arabidopsis

201 tants displayed reduced leaf movement under +DIF, similar to wild-type plants under -DIF.

202 ntain robust leaf movement amplitudes under -DIF, indicating that ethylene signaling becomes limiting

203 on in the basal part of the hypocotyl under -DIF was restored by both 1-aminocyclopropane-1-carboxyli

204 Indeed, petioles of plants under -DIF had reduced ACC content, and application of ACC to t

205 der +DIF, similar to wild-type plants under -DIF.

206 romoter activity was strongly reduced under -DIF but could be restored by auxin application in an ACC

207 n of several ACC Synthase was reduced under -DIF but could be restored by auxin application.

208 ally suppressed in the petiole region under -DIF conditions.

209 limited auxin and ethylene signaling under -DIF.

210 We show that, under -DIF, lower auxin biosynthesis activity limits the signal

211 With the exception of pemphigus vulgaris, DIF is essential for establishing a definitive diagnosis

212 etter understanding of the mechanism whereby DIF directs cell type divergence.

213 Treatment of cells with DIF-1 or exposure to hyper-osmotic stress induces a decr

214 ssion of dmtA; this is again consistent with DIF-1 production by prespore cells.

215 Even with DIF analysis, 7 cases could not be definitively assigned

216 se hydrodynamic dispersion (with and without DIF) and aerobic fringe degradation on the evolution of