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 protocols tailored to the clinical diagnosis may enh

4 DIF results were positive in 14% of lesional biopsies, i

5 DIF results were positive in less than half of cases of

6 DIF was split across SA and RRB.

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

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

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

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

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

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

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

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

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

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

17 (DIF) between genders was found in Item 18 (DIF contrast, 0.40 logits; p = 0.04).

18 Of 2050 DIF biopsies submitted, 367 (17.9%) were positive; IgG,

19 or more of the tests was present in 6 of 24 DIF- patients (25%) compared with 22 of 49 DIF positive

20 4 DIF- patients (25%) compared with 22 of 49 DIF positive (DIF+) patients (44.9%).

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

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

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

24 An additional DIF biopsy of another mucosal site or of affected or una

25 All DIF- patients (24/73 [31.8%]) had either ocular-only dis

26 ody testing using a 6-antibody panel for all DIF biopsies is likely unnecessary.

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

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

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

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

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

32 histopathology/dermatopathology findings and DIF testing panel tailored truncations by clinical indic

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

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

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

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

37 To explore the relationship between TFP and DIF, we first applied traditional double fixed-effects m

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

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

40 preliminary structural relationship between DIF and TFP using double fixed-effects models combined w

41 e the complex nonlinear relationship between DIF and TFP.

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

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

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

45 in the absence of diagnosis confirmation by DIF.

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

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

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

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

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

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

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

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

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

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

56 Results of 2050 consecutive DIF skin biopsies submitted to the laboratory between Ap

57 Current DIF test panels are based on historical clinical descrip

58 lidated by using 220,800 manually delineated DIF image patches from 106 images of 46 different patien

59 uld use caution with items that demonstrated DIF.

60 iopsy; 64% of patients (14/22) demonstrated +DIF on initial biopsy and an additional 36% of patients

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

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

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

64 It also directs DIF-inducible gene expression.

65 Models disregarding DIF underestimate the actual alpha.

66 e logs-data types typically used to document DIFs.

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

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

69 sis and auxin signaling were reduced during -DIF.

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

71 However, hand mannerisms evidenced DIF across all 5 algorithms, with generally greater diff

72 Measurement bias was identified by examining DIF and differential test functioning (DTF), within a gr

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

74 as rescued by complementation with exogenous DIF-1.

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

76 enes by the differentiation inducing factor (DIF).

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

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

79 Digital Inclusive Finance (DIF), as a classical financial model, plays an important

80 discuss potential fields of application for DIF inhibitors, ranging from non-V600E oncoproteins and

81 By contrast, for DIF+ nonocular MMP patients, all the individual tests, a

82 autoantibody detection is inappropriate for DIF- ocular-only MMP patients, resulting in missed diagn

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

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

85 eral acceptability of triaging specimens for DIF testing based on histopathology findings remained wi

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

87 Drilling-induced fractures (DIFs) form when hoop stress around a borehole exceeds te

88 A noticeable differential item functioning (DIF) between genders was found in Item 18 (DIF contrast,

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

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

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

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

93 , followed by differential item functioning (DIF), exploratory factor analysis (EFA) and confirmatory

94 o evidence of differential item functioning (DIF).

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

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

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

98 l and identified several intervals with high DIF susceptibility.

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

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

101 atologists submit direct immunofluorescence (DIF) biopsies on a daily basis, using an assay detecting

102 sition pattern in direct immunofluorescence (DIF) microscopy is a recognizable feature and confirmati

103 e chart review of direct immunofluorescence (DIF) studies in buccal mucosal biopsies was performed.

104 Direct immunofluorescence (DIF) testing has been an important ancillary tool for th

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

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

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

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

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

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

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

112 sts in recognition of u-serrated patterns in DIF images and facilitate the diagnosis of EBA.

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

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

115 nly MMP patients but showed limited value in DIF- multisite ocular MMP patients.

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

117 for various DIF testing practice, including DIF testing triage by histopathology/dermatopathology fi

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

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

120 r the definition of the RAF dimer interface (DIF) by crystallography, this review focuses on the impl

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

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

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

124 y differentiate normally in a mutant lacking DIF.

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

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

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

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

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

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

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

132 en for direct immunofluorescence microscopy (DIF) and indirect immunofluorescence microscopy (IIF) on

133 To warrant inclusion in containment models, DIFs must be systemic rather than incidental.

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

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

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

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

138 on is induced using the stalk cell morphogen DIF.

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

140 tients found a high sensitivity of a mucosal DIF biopsy for diagnosis of MMP, and lower sensitivity o

141 In 6 patients with a negative mucosal DIF, a skin biopsy confirmed diagnosis of MMP.

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

143 , including those with positive and negative DIF findings.

144 between patients with positive and negative DIF results.

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

146 g follow-up, even in the setting of negative DIF.

147 and is recommended in patients with negative DIF results and high clinical suspicion.

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

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

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

151 Diagnostic accuracy of DIF, IIF SSS, and immunoblot for BP180 and BP230.

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

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

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

155 testing agreed on many practical aspects of DIF testing, including matters not queried previously.

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

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

158 by regulating the cellular concentration of DIF-1.

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

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

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

162 The overall estimated effect of DIF on total DTF was not large.

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

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

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

166 Weak evidence of DIF was found for nine items.

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

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

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

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

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

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

173 metrics was used to examine the magnitude of DIF and DTF.

174 The magnitude of DIF was only moderate to large for 2 items: hand manneri

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

176 Histopathologic findings and the results of DIF biopsies using the standard 6-antibody panel were ev

177 ference was found between the sensitivity of DIF on a perilesional buccal biopsy and a normal buccal

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

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

180 sus was found against tailored truncation of DIF panel based on the clinical indication in the first

181 tunity for high-value, cost-conscious use of DIF.

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

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

184 diseases did not yield positive findings on DIF testing.

185 linical diagnoses not optimally supported on DIF: lichen planus, porphyria, and connective tissue dis

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

187 In addition, an optional DIF test on a skin biopsy specimen and one or more perfo

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

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

190 results were negative by viral isolation or DIF.

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

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

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

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

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

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

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

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

199 olitary ocular involvement showed a positive DIF of only the oral mucosa.

200 Of those, 2 had a positive DIF on repeat biopsy.

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

202 Perilesional biopsies gave higher positive DIF than lesional biopsies (P = .029).

203 are associated with an increase in positive DIF results.

204 ften biopsy of these lesions yields positive DIF results.

205 s (25%) compared with 22 of 49 DIF positive (DIF+) patients (44.9%).

206 model, Extreme Gradient Boosting, to predict DIF from conventional wireline logs.

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

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

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

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

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

212 cognition is still of limited use in routine DIF microscopy.

213 of 89.3% in the classification of u-serrated DIF image patches, an expert level of diagnostic accurac

214 No single item showed DIF consistently across all modules.

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

216 For race, 8 items had a significant DIF, 6 of which involved SA.

217 S-2 diagnostic items (11%) had a significant DIF.

218 For sex, 5 items showed significant DIF.

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

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

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

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

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

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

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

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

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

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

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

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

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

232 The DIF results were recorded.

233 The DIF was considered positive when there was deposition of

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

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

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

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

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

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

240 -positive specimens without knowledge of the DIF results.

241 A structural perspective of the DIF, how dimerization impacts inhibitor activation and t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 urvey containing 54 statements pertaining to DIF testing was created and distributed to assess consen

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

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

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

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

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

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

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

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

268 y translocates to the nucleus in response to DIF.

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

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

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

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

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

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

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

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

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

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

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

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

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

282 limited auxin and ethylene signaling under -DIF.

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

284 outcome was degree of consensus for various DIF testing practice, including DIF testing triage by hi

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

286 compared with control participants, whereas DIF- multisite ocular MMP differed for 1 ELISA and 3 of

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

288 Recent unresolved key issues include whether DIF testing and test panels should be triaged or truncat

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

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

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

292 Most items with DIF had greater difficulty and poorer discrimination in

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