ライフサイエンスコーパス: ARF

1 he tumor suppressors p53, p16(Ink4a) and p19(Arf).

2 ity of auxin response transcription factors (ARFs).

3 that include several auxin response factors (ARFs).

4 k stratification of hematology patients with ARF.

5 omodulin explained the vancomycin-associated ARF.

6 he recruitment of coat proteins by GTP-bound ARFs.

7 plasma membrane GEF reported to activate all ARFs.

8 the transcription of genes encoding class A ARFs.

9 ecretion; activates ADP-ribosylation factor (ARF)1, 3, 4, and 5; and recruits ARF effectors to Golgi

10 mediate phenotype, consistent with NCS-1 and ARF-1.1 acting in the same pathway.

11 In contrast, double mutants of arf-1.1 and ncs-1 had an intermediate phenotype, consist

12 MIR160B) that targets AUXIN RESPONSE FACTOR (ARF)10 and ARF16 that are involved in establishment of d

13 atients (447 with acute respiratory failure [ARF]), 21.3% had a virus detected (56.4% rhinovirus/ente

14 lent complications were acute renal failure (ARF)(24.2%), septicemia (18.2%), and pneumonia (12.3%).

15 t with steroids or other immunosuppressants, ARF (25.5% vs. 16.3%; P = 0.004), and death in the ICU (

16 A subset of these, the conserved class A ARFs(5), are transcriptional activators of auxin-respons

17 report an incidence of 3%-7% progressing to ARF, a marker of poor prognosis.

18 Our results show that the Arf-activating property, but not the primary structure o

19 tracellular membrane traffic, and one of the Arf-activating proteins, GBF1, is a cellular factor requ

20 le that showed the exceptional efficiency of Arf activation by Brag2 on membranes.

21 Our data reveal a complex pattern of Arf activation in enterovirus-infected cells that may co

22 To further show that ARF activation regulates key signaling events leading to

23 ecinH3 attenuated the disease, reduced CLIC4/Arf activation, and restored BMPRII expression in the lu

24 of axon growth and regeneration through the ARF activator Efa6 in C. elegans, and by neurodevelopmen

25 Here we show that auxin response and ARF activity cell-autonomously control the asymmetric di

26 facilitates the activation of members of the ARF (ADP-ribosylation factor) family of small GTPases.

27 To test the ARF-AID system in a quantitative and sensitive manner, w

28 D degradation is substantially faster in the ARF-AID system.

29 binds to RB, leading to increased levels of ARF, an inhibitor of MDM2, and activation of p53.

30 rget of p53-independent tumor suppression by ARF and also suggest that the ARF-NRF2 interaction acts

31 of Mule, which subsequently dissociates from ARF and becomes activated.

32 y reconstituting the binding and kinetics of Arf and Brag2 in artificial membranes.

33 how additional frequent loss of CDKN2A/Ink4a/Arf and may be precursor lesions of aggressive malignant

34 ppressor protein Niam (Nuclear Interactor of ARF and Mdm2).

35 taneous immortalization while retaining both Arf and p53.

36 initiate GBM in mice in the context of Ink4a/Arf and Pten loss, and that these tumors are similar to

37 and VirA, which target small GTPases of the Arf and Rab families, consequently inhibiting several in

38 The Arf and Rab/Ypt GTPases coordinately regulate membrane t

39 omplementarily; however, the manner in which Arf and Rab/Ypt proteins perform interchangeable functio

40 During SD induction, auxin genes IAA, ARF and SAURs were down-regulated and circadian genes in

41 Considering the evolutionary conservation of ARFs and ARF-GEFs, this initial regulatory step of membr

42 ant entered the booting/heading stage, while ARFs and GRFs were downregulated suggesting these TF fam

43 Our studies further indicated that ARFs and HD-ZIP IIIs may play opposite roles in the regu

44 uires the coincidental presence of activated ARFs and specific membrane identifiers.

45 the puzzling dissimilarity of ARF6 to other ARFs and suggests the existence of other substrates regu

46 ; this results in silencing of Cdkn2a (Ink4a/Arf) and loss of p16 and p19 protein, consistent with ep

47 inct polypeptides, including full-length p19(Arf) and N-terminally truncated and unstable p15(smArf)

48 The ADP ribosylation factor (Arf) and the coat protein complex I (COPI) are involved

49 ncluding transcription factors, such as MYB, ARF, and LRR.

50 e investigated roles for members of the Rho, Arf, and Rab G-protein families in regulating WASP homol

51 gulators eIF4G1 and LARP1 are upregulated in Arf- and p53-null cells.

52 The requirement for GBF1 implies that Arfs are important for replication, but which of the dif

53 that expression of the tumor suppressor p14(ARF) (ARF) is upregulated in aggressive subtypes of MIBC

54 g, with 2,3,4,5,6-pentafluorophenyl favoring ArF-ArH interactions over 2,4,6-trifluorophenyl.

55 h more electron-releasing character favoring ArF-ArH interactions, and (ii) the fluorination pattern

56 tructural factors that determine whether the ArF-ArH interactions, and the resulting twisted, unaggre

57 Cofacial fluoroarene-arene (ArF-ArH) interactions cause twisting in the PE backbone,

58 this study, we report that a Golgi-localized Arf, Arl1, could suppress Ypt6 dysfunction via its effec

59 of genes involved in tuber-sprouting such as ARF, ARP, AIP and ERF.

60 Here, we identified ARF as a key regulator of nuclear factor E2-related fact

61 When activated, Arfs associate with membranes, where they regulate numer

62 or AuxRE variants, emphasizing that specific ARF-AuxRE binding strengths likely contribute to the com

63 d/or vitamin D deficiency were studied in an Arf(-/-) BCR-ABL acute lymphoblastic leukemia murine mod

64 ARF becomes stabilized upon binding to PPM1G and forms a

65 Thus, we reported a novel crosstalk of ARF/beta-catenin dysregulated YAP in Hippo pathway and a

66 GGA (Golgi-localized, gamma-ear-containing, ARF-binding protein), clathrin adaptors, and clathrin.

67 Golgi-localized, gamma-adaptin ear homology, Arf-binding) proteins and the AP-1 (assembly protein-1)

68 We previously showed that Mule/Huwe1/Arf-BP1 (Mule) controls murine intestinal stem and proge

69 xpression of CDKN2A (both p16(INK4a) and p19(ARF)) but not CDKN2B (p15(INK4b)).

70 Although ARF can suppress tumor growth by activating p53 function

71 f(M45A) strain are as resistant as wild-type Arf(+/+) cells to comparable oncogenic challenge and do

72 rected regulation of auxin response factors (ARFs) contribute to leaf development via auxin signaling

73 fibromas formation, additional loss of Ink4a/Arf contributes to atypical neurofibromas formation, and

74 Arfs control distinct steps in intracellular membrane tr

75 over, we demonstrated that a miRNA-regulated ARF, CrARF16, binds to the promoters of key TIA pathway

76 on, when combined with Vhl and Cdkn2a (Ink4a/Arf) deletion (VIM), produce kidney tumours that approxi

77 inding protein ITGB3BP (CENPR) and reflected ARF-dependent impairment of protein translation, which w

78 of of concept that tumors can respond, in an ARF-dependent manner, to p53 reactivation even if p53 in

79 erroptosis in a p53-independent manner while ARF depletion induces NRF2 activation and promotes cance

80 ll recognition of alternative reading frame (ARF)-derived peptides is uncertain.

81 In patients with ARF, detection of any respiratory virus was independentl

82 ologous studies have fueled a model in which ARF dimers bind with high affinity to distinctly spaced

83 In plants, ARF directly interacts with AID in the absence of auxin,

84 ically and functionally interrogate modes of ARF-DNA interaction.

85 le to the binding of the Us11 protein to the ARF domain in TRIM23.

86 tional K27-linked auto-ubiquitination of the ARF domain is essential for the GTP hydrolysis activity

87 ion and the folded PB1 interaction domain of ARFs drive protein assembly formation.

88 Using GEM microarray model, we found ARF dysregulates Hippo and Wnt pathways.

89 ion factor (ARF)1, 3, 4, and 5; and recruits ARF effectors to Golgi membranes.

90 F6) at the Golgi/TGN and recruits additional ARF effectors to the Golgi/TGN.

91 ntegrity and recruits numerous TGN-localized ARF effectors.

92 Mechanistically, ARF elevates nMET through binding to MET cytoplasmic dom

93 associated with Pten/Trp53 inactivation and ARF elevation hypothesizing the essential crosstalk of A

94 (TFs) (ERF, bHLH, WRKY, MYB, NAC, bZIP, and ARF), enzymes involved in cell wall metabolism (beta-gal

95 target in a variety of cancers arising from ARF epigenetic silencing, to loss of ARF function, as we

96 n-years) in the first year after the initial ARF episode, but low-level risk persisted for >10 years.

97 The ARFs ETTIN (ETT) and ARF4 promote organogenesis at the r

98 ivity of the atypical auxin response factor (ARF), ETTIN towards target genes without the requirement

99 Once on the replication membranes, all Arfs except Arf3 were no longer sensitive to inhibition

100 onic transducer, and a shear wave induced by ARF excitation is detected by the optical coherence tomo

101 We found that all Arfs expressed in human cells, including Arf6, normally

102 As a consequence, ARF expression sensitizes cells to ferroptosis in a p53-

103 MIBC, we demonstrate that tumors expressing ARF failed to respond to treatment with the platinum-bas

104 d cells, GBF1 activates small GTPases of the Arf family and coordinates multiple steps of membrane me

105 e data highlight key aspects of signaling by ARF family GAPs that contribute to previously underappre

106 Building on evolutionary data for the ARF family GTPases and their GTPase--activating proteins

107 wn to have uniquely broad specificity toward ARF family GTPases in in vitro assays.

108 at C9orf72-SMCR8-WDR41 acts as a GAP for the ARF family of small GTPases.

109 ctors (GEFs) on the ADP-ribosylation factor (ARF) family of small GTPases initiates intracellular tra

110 the active state, the BBSome is bound to an Arf-family GTPase (ARL6/BBS3) that recruits the BBSome t

111 s to generate MPNST in Nf1(Flox/Flox); Ink4a/Arf(Flox/Flox) and Nf1(Flox/-); Ink4a/Arf(Flox/Flox) pai

112 Ink4a/Arf(Flox/Flox) and Nf1(Flox/-); Ink4a/Arf(Flox/Flox) paired littermate mice to model tumors fr

113 , we identified that nMET signaling requires ARF for CRPC growth in Pten/Trp53 conditional knockout m

114 d that Arf1 appears to be the most important Arf for enterovirus replication.

115 nal regulators of the genes encoding class A ARFs from Arabidopsis thaliana and demonstrate that each

116 ng from ARF epigenetic silencing, to loss of ARF function, as well as tumors bearing oncogenic NF-kap

117 for replication, but which of the different Arfs function(s) during replication remains poorly under

118 shed cell lines expressing each of the human Arfs fused to a fluorescent tag and investigated their b

119 n depends on its highly-regulated and robust ARF GAP activity, requiring both the PH and the ARF GAP

120 GAP activity, requiring both the PH and the ARF GAP domains of ASAP1, and is modulated by phosphatid

121 AGAP2 (Arf GAP with GTP-binding protein-like domain, Ankyrin re

122 Arf GAP with Src homology 3 domain, ankyrin repeat, and

123 The Arf GTPase-activating protein (Arf GAP) with SH3 domain, ankyrin repeat and PH domain 1

124 For the ZA domain of Arf-GAP ASAP1, with a global correlational time of 24 ns

125 We previously showed that Arf-GAP with coil-coil, ANK repeat and PH domain-contain

126 n chromosome 6q13 comprising the genes small ARF GAP1 (SMAP1), an ARF6 guanosine triphosphatase-activ

127 te them, and the GTPase-activating proteins (ARF GAPs) that have the ability to both propagate and te

128 An ARF GEF known as General receptor for 3-phosphoinositide

129 s allowed the generation of hypotheses about ARF GEF protein function(s) as well as a better understa

130 that need to be coordinated in localizing an ARF GEF to an intracellular compartment to initiate a tr

131 ing cascade starts by the recruitment of the ARF-GEF cytohesins to the plasma membrane, which, in tur

132 n of one of the two SEC7 domains of the GNOM ARF-GEF dimer with its ARF1 substrate reduced the effici

133 data indicate a division of labor within the ARF-GEF family in mediating differential growth with GNO

134 Golgi-associated proteins revealed that the ARF-GEF GBF1 can selectively modulate the ER-Golgi traff

135 We show that ARF-GEF GNOM acts early, whereas BIG ARF-GEFs act at a l

136 dimers of Arabidopsis (Arabidopsis thaliana) ARF-GEF GNOM, which is involved in polar recycling of th

137 ich adherens junctions recruit the cytohesin Arf-GEF Steppke, which down-regulates junctional tension

138 n factor-guanine nucleotide exchange factor (ARF-GEF), to the Golgi.

139 ibed the regulation of Sec7, the trans-Golgi Arf-GEF, through autoinhibition, positive feedback, dime

140 We performed phylogenetic analyses of ARF GEFs in eukaryotes, defined by the presence of the S

141 This role requires ARF GEFs to be recruited from the cytosol to intracellul

142 uisition of a functionally diverse cohort of ARF GEFs to control it.

143 es, the guanine nucleotide exchange factors (ARF GEFs) that activate them, and the GTPase-activating

144 ow that ARF-GEF GNOM acts early, whereas BIG ARF-GEFs act at a later stage of apical hook development

145 The Arf-GEFs activate Arf GTPases and are therefore the key

146 The Golgi Arf-GEFs contain multiple autoregulatory domains, but th

147 were done with monomeric proteins, although ARF-GEFs form dimers in vivo.

148 In Saccharomyces cerevisiae, three conserved Arf-GEFs function at the Golgi: Sec7, Gea1, and Gea2.

149 tanding of the regulation of the early Golgi Arf-GEFs Gea1 and Gea2.

150 of ARF guanine-nucleotide exchange factors (ARF-GEFs), resulting in the recruitment of coat proteins

151 ng the evolutionary conservation of ARFs and ARF-GEFs, this initial regulatory step of membrane traff

152 ulatory mechanisms unique to the early Golgi Arf-GEFs.

153 ression of its target AUXIN RESPONSE FACTOR (ARF) genes; however, the function of miR160 in monocots

154 nique peripheral sites of the PH domain, the Arf GTPase and, unexpectedly, the Sec7 domain.

155 he activation of the ADP-ribosylation factor ARF GTPase by the SEC7 domain of ARF guanine-nucleotide

156 nces indicate that KNR6 can interact with an Arf GTPase-activating protein (AGAP) and its phosphoryla

157 The Arf GTPase-activating protein (Arf GAP) with SH3 domain,

158 RING E3 ligase and ADP-ribosylation factor (ARF) GTPase activity.

159 The Arf-GEFs activate Arf GTPases and are therefore the key molecular decision

160 biosynthetic sorting center of the cell, the Arf GTPases are responsible for coordinating vesicle for

161 Here, we investigated the roles of small Arf GTPases during enterovirus infection.

162 Arl/ARF GTPases regulate ciliary trafficking, but their tiss

163 ent knowledge of three protein families: the ARF GTPases, the guanine nucleotide exchange factors (AR

164 to the membrane primarily through binding to Arf GTPases, upon which it undergoes assembly to form co

165 that is dependent on the COP-II complex and ARF GTPases.

166 guanine nucleotide exchange factor for small Arf GTPases.

167 ing is regulated by ADP-ribosylation factor (ARF) GTPases and the development throughout eukaryotic e

168 Here we focused on ADP ribosylation factor (Arf) GTPases, which orchestrate a variety of regulatory

169 In yeast, Arf guanine nucleotide-exchange factor (GEF) Syt1p activ

170 tion factor ARF GTPase by the SEC7 domain of ARF guanine-nucleotide exchange factors (ARF-GEFs), resu

171 tion factor 1 (ARF1)-GTPase and its effector ARF-guanine-exchange factors (GEFs) of the Brefeldin A-i

172 icity and downstream effector events; 2) all ARFs have access to all membranes, but are restricted in

173 Although class A ARFs have tissue-specific expression patterns, how their

174 ADP-ribosylation factors (ARFs) have been reported to function in diverse physiolo

175 ntly of the E2F-regulated MDM2 inhibitor p14(ARF) Here, we report that the damage-induced noncoding (

176 etylase (HDA) and (2) auxin response factor (ARF)-histone acetyltransferase (HAT).

177 etylase (HDA) and (2) auxin response factor (ARF)-histone acetyltransferase (HAT).

178 predictive factors for 30-day mortality were ARF (HR = 3.64, 95% CI: 3.43-3.87, p < 0.001), malignant

179 The mouse p19(Arf) (human p14(ARF)) tumor suppressor protein, encoded

180 ternative to HVM for replacing in some cases ArF immersion technology combined with multi-patterning.

181 e 180-day mortality and acute renal failure (ARF), improving upon predictions that rely on preoperati

182 w that hypermethylation of p16/Ink4a and p19/Arf in CNT- and asbestos-induced inflammatory lesions pr

183 Consistently, loss of ARF in colon epithelial cells leads to up-regulation of

184 aberrant MET/nMET elevation correlates with ARF in human prostate cancer (PCa) specimens.

185 sults highlight a context-dependent role for ARF in modulating the drug response of bladder cancer.

186 nd tea-derived carbon dots can interact with ARF in nucleus that may further lead to the non-nuclear

187 the essential crosstalk of AKT/mTOR/YAP with ARF in prostate cancer.

188 Conditional ablation of Nf1 and Arf in the neural crest-derived SC lineage allows escape

189 Accumulation of ARF in the nucleolus is associated with poor outcome and

190 Intriguingly, increased expression of Arf in tumor stromal cells, as in tumor keratinocytes th

191 nce of cleaved transcripts of miRNA-targeted ARFs in C. roseus cells was confirmed by Poly(A) Polymer

192 sed the auxin response transcription factor (ARF) in an improved inducible degron system.

193 d translational efficiency following loss of ARF include many ribosomal proteins and translation fact

194 However, unlike GBF1, GARG activates all ARFs (including ARF6) at the Golgi/TGN and recruits addi

195 Whilst auxin affects canonical ARFs indirectly by facilitating degradation of Aux/IAA r

196 MPRII expression was restored by Arf6 siRNA, Arf inhibitor Sec7 inhibitor H3 (SecinH3), and inhibitor

197 ARF inhibits the ability of NRF2 to transcriptionally ac

198 nd unstable p15(smArf) ("small mitochondrial Arf") initiated from an internal in-frame AUG codon spec

199 Utilizing ribosome profiling, we show that ARF is a major suppressor of 5'-terminal oligopyrimidine

200 ARF is absent from previously engineered AID systems but

201 f p16/Ink4a is sustained and deletion of p19/Arf is detected, recapitulating human disease.

202 Arf is not expressed in most normal tissues of young mic

203 The gene encoding ARF is the most commonly deleted gene in human cancer.

204 In this system, acoustic radiation force (ARF) is produced by a remote ultrasonic transducer, and

205 as-filled hollow-core antiresonant fiber (HC-ARF) is reported spanning from 200 nm in the deep ultrav

206 The tumor suppressor P19(ARF) is strongly activated in the nerves of these mice a

207 expression of the tumor suppressor p14(ARF) (ARF) is upregulated in aggressive subtypes of MIBC.

208 exchange factor of ADP-ribosylation factors (Arfs), is critical for Rickettsia typhi (typhus group ri

209 In particular, ARF knockdown reduced non-nuclear localization of YAP wh

210 Mechanistically, ARF knockdown suppressed protein turnover of beta-cateni

211 , some genes encoding auxin response factor (ARF ), Leafy cotyledon1 (LEC1) and somatic embryogenesis

212 ADP-ribosylation factor (Arf)-like 4A (Arl4A), an Arf small GTPase, functions in

213 ADP-ribosylation factor (Arf)-like 4D (Arl4D), one of the Arf-like small GTPases,

214 Herein we report that the ARF-like (ARL) GTPase ARFRP1 functions upstream of two o

215 dicate that PI(4)P is needed to anchor Arl8 (Arf-like GTPase 8) and its effector homotypic fusion/vac

216 Arl8b is an Arf-like GTPase that specifically localizes to lysosomes

217 Arf-like protein 13b (ARL13b) is a small GTPase that fun

218 eotide-exchange factor (GEF) Syt1p activates Arf-like protein Arl1p, which was accompanied by accumul

219 The conserved ARF-like small GTPase ARL-8 is localized to SVPs and dir

220 is unconventional egress is regulated by the Arf-like small GTPase Arl8b and can be blocked by the Ra

221 ion factor (Arf)-like 4D (Arl4D), one of the Arf-like small GTPases, functions in the regulation of c

222 cle regulators that are encoded by the Ink4a/Arf locus, deletion of this locus only partially rescues

223 d in the nucleus and recruited to the INK4AB/ARF locus.

224 Although disruption of the CDKN2A (INK4A/ARF) locus has been reported in end-stage disease, infor

225 n developing Schwann cells with global Ink4a/Arf loss and identified paraspinal plexiform neurofibrom

226 However, Arf loss and p53 loss produce differing outcomes-loss of

227 Knockout of p53 largely phenocopies ARF loss, with increased protein synthesis and expressio

228 Although Arf(M45A) mice manifest the latter defects, smArf alone

229 rast, smArf-deficient cells from mice of the Arf(M45A) strain are as resistant as wild-type Arf(+/+)

230 ARF, malignant infiltration of the liver, and septicemia

231 ippo pathway and a new approach to stimulate ARF-mediated signaling to inhibit nuclear YAP using nano

232 A multiomics approach revealed a Cdkn2a.Arf-mediated, p53-independent mechanism by which EZH2 in

233 Constitutive PB mutagenesis in Arf(-/-) mice provided a collection of spontaneous tumor

234 tributed to repeated cooption of the tasiRNA-ARF module during evolution.

235 er initiation through Auxin Response Factor (ARF) MONOPTEROS (MP) and recruitment of chromatin remode

236 ucible variant of the auxin response factor (ARF) MONOPTEROS (MP) is sufficient to restore patterning

237 overexpression in p53 (-/-) and INK4a (-/-)/Arf (-/-) mouse embryonic fibroblasts (MEFs), which fail

238 The single Arf mRNA encodes two distinct polypeptides, including fu

239 Mutations in the ARF N terminus that reduced binding also reduced GAP act

240 s p19(Arf) within the nucleolus, require p19(Arf) N-terminal amino acids that are not present within

241 Surprisingly, depletion of Arf6, a class 3 Arf, normally implicated in plasma membrane events, also

242 suppression by ARF and also suggest that the ARF-NRF2 interaction acts as a new checkpoint for oxidat

243 n abrogates cytoplasmic assemblies, promotes ARF nuclear localization, and results in an altered tran

244 Our data suggest a model in which ARF nucleo-cytoplasmic partitioning regulates auxin resp

245 assessed by swapping it with the Sec7d from ARF nucleotide-binding site opener (ARNO)/cytohesin-2, a

246 ducing smArf alone are as oncogenic as their Arf-null counterparts in generating acute lymphoblastic

247 Apart from being prone to tumor development, Arf-null mice are blind, and their male germ cells exhib

248 iation force optical coherence elastography (ARF-OCE) system that uses an integrated miniature ultras

249 The ARF of carbohydrates with an electron-donor group (EDG)

250 anomeric alkoxyl radical beta-fragmentation (ARF) of carbohydrates possessing an electron-withdrawing

251 ss response via a genetically intact MYC-p19(ARF)-p53 axis.

252 lecularly defined BL [mBL]) revealed the MYC-ARF-p53 axis as the primary deregulated pathway.

253 which has the potential to signal toward the Arf pathway.

254 f auxin, and we found that expression of the ARF PB1 (Phox and Bem1) domain suppresses constitutive d

255 rammed death through a surprising mechanism: ARF physically interacts with and antagonizes activation

256 ARF plays a significant role in regulating ribosomal RNA

257 features (AUC = 0.82; 95% CI: 0.66-0.94) in ARF prediction improved performance over preoperative fe

258 th tumor initiation and progression; loss of Arf promotes tumor progression but not initiation.

259 that block the activation of Golgi-localized Arf proteins and COPI vesicle formation, proANP secretio

260 ors to regulate expression levels of class A ARF proteins and modulate auxin signalling output throug

261 dose-response assays suggest that different ARF proteins might show distinct comparative affinities

262 5A-mutated (smArf-deficient) full-length p19(Arf) proteins.

263 S (DCGS), and acute rejection-free survival (ARFS) rates for RDP compared with historical controls on

264 ARF recurrence was highest (incidence, 3.7 per 100 perso

265 (GAP) for ARF6, as the most highly enriched ARF regulator in hair cells.

266 Furthermore, redundant abaxial-enriched ARF repressors suppress WOX1 and PRS expression, also th

267 al binding affinities of A-class and B-class ARFs, respectively, suggesting a mechanistic basis for t

268 In patients with ARF, respiratory virus detection was independently assoc

269 ns, and (ii) the fluorination pattern of the ArF ring, with 2,3,4,5,6-pentafluorophenyl favoring ArF-

270 emonstrate that the tumor suppressor protein ARF sensitizes cancer cells to programmed death through

271 how that the Cdkn2a alternate reading frame (Arf) serves as a gatekeeper tumor suppressor in mice tha

272 We believe that the inherent complexity of ARF signaling and its regulation by GEFs and GAPs will r

273 pletion of Arf1, but not other class 1 and 2 Arfs, significantly increased the sensitivity of replica

274 ibosylation factor (Arf)-like 4A (Arl4A), an Arf small GTPase, functions in cell morphology, cell mig

275 Members of the ADP-ribosylation factor (ARF) small GTPase family regulate membrane trafficking a

276 tes these findings by revealing that loss of ARF strongly correlates with sustained expression of inf

277 gest that differential binding affinities of ARF subfamilies underlie diversity in cis-element functi

278 in all clinical research studies evaluating ARF survivors after discharge.

279 for use in all clinical research evaluating ARF survivors after hospital discharge.

280 search evaluating acute respiratory failure (ARF) survivors' outcomes after hospital discharge has su

281 conserved noncanonical Arabidopsis thaliana ARF that adopts an alternative auxin-sensing mode of tra

282 n microscopic BCCs activates p53 in part via Arf (that is, the oncogene-induced stress pathway) but n

283 tors (ArfGEFs) that regulate the activity of Arf, they govern vesicle formation, COPI trafficking and

284 ity of AUXIN RESPONSE transcription FACTORs (ARFs), through their binding to cis-regulatory elements

285 Moreover, the ability of ARF to induce p53-independent tumor growth suppression i

286 rt the relevance of high-affinity binding of ARF transcription factors to uniquely spaced DNA element

287 The auxin response factor (ARF) transcription factor family regulates auxin-respons

288 pacities of different auxin response factor (ARF) transcription factors to various dsDNA targets, inc

289 that acts through the AUXIN RESPONSE FACTOR (ARF) transcription factors(2-4).

290 auxin, acting through AUXIN RESPONSE FACTOR (ARF) transcription factors, is critical for embryo patte

291 that IAV infection enhances a model cellular ARF translation, which potentially has important implica

292 We examined results from the ARF Trial Network study to assess the association of pla

293 Here, we describe a mechanism by which the ARF tumor suppressor binds PPM1G to negatively regulate

294 ctors, coupled with inactivation of the INK4/ARF tumor suppressors, are hallmarks of T-lineage acute

295 The mouse p19(Arf) (human p14(ARF)) tumor suppressor protein, encoded in part from an

296 g protein (GAP) for ADP-ribosylation factor (ARF)-type GTPases.

297 ng is effectuated by auxin response factors (ARFs) whose activity is repressed by Aux/IAA proteins un

298 Interactions of p19(Arf) with Mdm2, or separately with nucleophosmin (NPM, B

299 (NPM, B23) that localizes and stabilizes p19(Arf) within the nucleolus, require p19(Arf) N-terminal a

300 normal renal function developing unexplained ARF without hypovolemia after administration of vancomyc