ライフサイエンスコーパス: ARF

1 ARF becomes stabilized upon binding to PPM1G and forms a

2 ARF binds to and thereby inhibits the E3 ligase activity

3 ARF inhibits the ability of NRF2 to transcriptionally ac

4 ARF interacts with and stabilizes the NB-associated UBC9

5 ARF is absent from previously engineered AID systems but

6 ARF plays a significant role in regulating ribosomal RNA

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

8 ARF was dormant during development, in uninjured adult f

9 ARF, malignant infiltration of the liver, and septicemia

10 In the present study, 23 and 25 ARF proteins were identified in C3 model- rice and C4 mo

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

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

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

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

15 the transcription of genes encoding class A ARFs.

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

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

18 inate gene induction jointly with activating ARFs and the Aux/IAAs.

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

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

21 plasma membrane GEF reported to activate all ARFs.

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

23 Although ARF can suppress tumor growth by activating p53 function

24 Although ARF, p53, and HDM2 also participate in the regulation of

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

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

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

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

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

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

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

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

33 e the nature and significance of ARF-DNA and ARF-Aux/IAA interactions, we analyzed structure-guided v

34 revealed that MADS-domain (such as FUL) and ARF proteins directly associate in planta.

35 en the homodimeric interfaces of AUX/IAA and ARF PB1 domains.

36 Most AUX/IAA and ARF proteins share highly conserved C-termini mediating

37 tic analysis, with ARFs in classes I-III and ARF-like proteins (ARLs) in class IV.

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

39 h p15(INK4b) has its own ORF, p16(INK4a) and ARF share common second and third exons with alternative

40 mor suppressors: p15(INK4b), p16(INK4a), and ARF (alternate reading frame).

41 itive Aux/IAA transcriptional repressors and ARF transcription factors produces complex gene-regulato

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

43 Thus, STAT3 and ARF may be prognostic markers to stratify high from low

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

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

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

47 t is remarkably specific to Golgi-associated ARF/ARL family GTPases during Shigella infection.

48 omodulin explained the vancomycin-associated ARF.

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

50 GN and its key members: cytosolic PKD2 binds ARF-like GTPase (ARL1) and shuttles ARL1 to the TGN.

51 Here, we show that PML IV specifically binds ARF, a key p53 regulator.

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

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

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

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

56 rthern Territory of Australia, we calculated ARF recurrence rates, rates of progression from ARF to R

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

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

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

60 ortance of charged amino acids in conferring ARF and Aux/IAA interactions have confirmed the PB1 doma

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

62 e human ARF promoter and activated conserved ARF-dependent Tp53 functions.

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

64 olecule Golgi-localized gamma-ear-containing ARF-binding protein 3 (GGA3) results in increased BACE1

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

66 s ARF binding to NPM, resulting in decreased ARF, increase MDM2 and decrease levels of p53 and the p5

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

68 ingle Aux/IAA repressing a pair of dimerized ARFs-sufficient for auxin-induced transcription.

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

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

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

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

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

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

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

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

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

78 n factor guanine nucleotide exchange factor (ARF-GEF) GNOM.

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

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

81 tors, the DNA binding auxin response factor (ARF) activators and the interacting auxin/indole acetic

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

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

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

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

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

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

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

89 ssor proteins and the AUXIN RESPONSE FACTOR (ARF) transcription factors.

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

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

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

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

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

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

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

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

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

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

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

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

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

103 ibosylation factor-guanine exchange factors (ARF-GEFs).

104 ated interactions of auxin response factors (ARF) and auxin/indole 3-acetic acid inducible proteins r

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

106 S-domain protein and Auxin Response Factors (ARFs) directly activating the expression of a miR172-enc

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

108 that include several auxin response factors (ARFs).

109 gative regulation of auxin response factors (ARFs).

110 g to derepression of auxin response factors (ARFs).

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

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

113 ity of auxin response transcription factors (ARFs).

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

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

116 (ICU) because of acute respiratory failure (ARF) has not been determined to date.

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

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

119 comes for people with acute rheumatic fever (ARF) and rheumatic heart disease (RHD) and the effect of

120 ns the signaling protein Exchange Factor for ARF-6 (EFA-6) is a potent intrinsic inhibitor of axon re

121 guanine nucleotide exchange factor (GEF) for ARF small GTPases, causes a robust migration response.

122 des important new prognostic information for ARF/RHD.

123 nation by its E3 ligase Ubiquitin Ligase for ARF and elongated its half-life, whereas knockdown of NS

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

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

126 tudy, we developed acoustic radiation force (ARF) orthogonal excitation optical coherence elastograph

127 t to the resultant acoustic radiation force (ARF) that acts to translate particles, and experimentall

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

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

130 We identified the alternative reading frame (ARF) protein as a key protein associating with NS and fu

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

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

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

134 Kinase (Syk) prevents its dissociation from ARF, thereby inhibiting Mule E3 ligase activity and TNF-

135 recurrence rates, rates of progression from ARF to RHD to severe RHD, RHD complication rates (heart

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

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

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

139 d InaC as a bacterial factor that binds host ARF and 14-3-3 proteins and modulates F-actin assembly a

140 ted in binding of zebrafish E2f to the human ARF promoter and activated conserved ARF-dependent Tp53

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

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

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

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

145 ic thiostrepton and (ii) an FOXM1 inhibiting ARF-derived peptide-recapitulate the findings of genetic

146 eviously suggested to function as inhibiting ARFs.

147 the dissociation of Mule from its inhibitor ARF.

148 CD24 competitively inhibits ARF binding to NPM, resulting in decreased ARF, increase

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

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

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

152 p16 cyclin-dependent kinase inhibitor INK4a/ARF gene.

153 histone H3S28 phosphorylation at the INK4AB/ARF locus and contributes to the rapid transcriptional a

154 (INK4A), and p14(ARF), encoded by the INK4AB/ARF locus, are crucial regulators of cellular senescence

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

156 ntegrity and recruits numerous TGN-localized ARF effectors.

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

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

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

160 ulation, the suppression is relieved by Mule/ARF-BP1-mediated Miz1 ubiquitination and subsequent degr

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

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

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

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

165 The context-dependent activation of ARF did not affect growth and development but inhibited

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

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

168 recipients readmitted to the ICU because of ARF.

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

170 antagonistic pleiotropic characteristics of ARF as both tumor and regeneration suppressor imply that

171 tudy provides insights on characteristics of ARF/ARL genes in rice and foxtail millet, which could be

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

173 We also report that CARF (Collaborator of ARF) is a new target of miR-335 that regulates its growt

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

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

176 ereas knockdown of NS led to the decrease of ARF levels.

177 radation of the Aux/IAAs and derepression of ARF-based transcription.

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

179 at by adjusting the expression of a group of ARF repressors, of which SlARF10A is a primary target, s

180 ral mechanism for functional inactivation of ARF and reveal an important cellular context for genetic

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

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

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

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

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

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

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

188 ation clinically would require modulation of ARF -p53 axis activation.

189 To parse the nature and significance of ARF-DNA and ARF-Aux/IAA interactions, we analyzed struct

190 und that NS can enhance NPM stabilization of ARF.

191 tant as a simplified platform for studies of ARF function and demonstrate that repressing ARFs regula

192 Recent structural analyses of ARFs and Aux/IAAs have raised questions about the functi

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

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

195 vidences also demonstrate the involvement of ARFs in conferring tolerance to biotic and abiotic stres

196 f the Aux/IAAs, and studies of a subgroup of ARFs that function as transcriptional activators.

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

198 In accordance, loss of STAT3 and p14(ARF) expression in patient tumours correlates with incre

199 sor proteins p15(INK4B), p16(INK4A), and p14(ARF), encoded by the INK4AB/ARF locus, are crucial regul

200 LCL proliferation induces p16(INK4A) and p14(ARF)-mediated cell senescence.

201 valuation of epigenetic heterogeneity at p14(ARF) and BRCA1 gene-promoter loci in liquid biopsies obt

202 /mouse double minute (MDM) 2/MDM4/CDKN2A-p14(ARF) pathways, in cells that present features associated

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

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

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

206 nverse relationship between MAGE-A11 and p14-ARF correlated with p14-ARF inhibition of the MAGE-A11-i

207 dation of MAGE-A11 promoted by the human p14-ARF tumor suppressor contributes to low levels of MAGE-A

208 A11 is targeted for degradation by human p14-ARF, a tumor suppressor expressed from an alternative re

209 r levels of MAGE-A11 associated with low p14-ARF increase AR and E2F1 transcriptional activity and pr

210 ct on HDM2 in the absence or presence of p14-ARF and cooperated with HDM2 to increase E2F1 transcript

211 anscriptional activity in the absence of p14-ARF.

212 een MAGE-A11 and p14-ARF correlated with p14-ARF inhibition of the MAGE-A11-induced increase in andro

213 TP53 mutations, genomic loss of CDKN2A (p16(ARF)), evidence of increased numbers of DNA double stran

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

215 encoded tumor suppressors p16(INK4a) and p19(ARF), which are required for growth arrest and myeloid d

216 ing the p16(INK4A)-cyclin D1-CDK4-Rb and p19(ARF)-Mdm2-p53 cell cycle pathways.

217 Mechanistically, we identify p19(ARF) as a direct Stat3 target.

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

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

220 Thus, we propose that in the absence of p53, ARF can be stabilized by NS and nucleophosmin to serve a

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

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

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

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

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

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

227 osylation factor family of small G-proteins (ARFs) and the protein kinase D (PKD) family of serine/th

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

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

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

231 ion, monomeric Aux/IAAs were able to repress ARF activity in both yeast and plants.

232 ARF function and demonstrate that repressing ARFs regulate auxin-induced genes and fine-tune their ex

233 Further the repressing ARFs coordinate gene induction jointly with activating A

234 evels of the ARF10/16/17 family of repressor ARF transcription factors.

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

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

237 Expression analysis of rice ARFs and ARLs in different tissues, stresses and abscisi

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

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

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

241 led that promoter architecture could specify ARF activity and that ARF19 required dimerization at two

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

243 Furthermore, overexpression of NS suppressed ARF polyubiquitination by its E3 ligase Ubiquitin Ligase

244 ding sequences of the human tumor suppressor ARF into the zebrafish genome.

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

246 tivity yields a class of 22-nucleotide tasiR-ARF variants associated with the processing of arf3 tran

247 short-interfering RNAs (siRNAs) termed tasiR-ARFs.

248 However, contrary to tasiR-ARFs' essential function in development, DCL4 proteins e

249 cting siRNAs (tasiRNAs) in addition to tasiR-ARFs, with expanded potential targets.

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

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

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

253 the first year, almost 10 times higher than ARF recurrence.

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

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

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

257 These findings suggest that ARF-1.1 interacts with NCS-1 in AIY neurons and potentia

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

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

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

261 Aux/IAA transcriptional repressors, and the ARF transcription factors.

262 Loss of Stat3 signalling disrupts the ARF-Mdm2-p53 tumour suppressor axis bypassing senescence

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 rnative auxin-sensing mechanism in which the ARF ARF3/ETTIN controls gene expression through interact

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

281 tingly, beta-arrestin2 can interact with the ARF guanine nucleotide exchange factor ARNO, although th

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

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

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

285 Similar to ARF, PML IV enhances global SUMO-1 conjugation, particul

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

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

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

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

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

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

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

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

294 ity rates for 572 individuals diagnosed with ARF and 1248 with RHD in 1997 to 2013 (94.9% Indigenous)

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

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

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

298 k stratification of hematology patients with ARF.

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

300 (I-IV) based on phylogenetic analysis, with ARFs in classes I-III and ARF-like proteins (ARLs) in cl