ライフサイエンスコーパス: ARF

1 ARF binds to and thereby inhibits the E3 ligase activity

2 ARF expression also frequently colocalized with the expr

3 ARF inhibits the ability of NRF2 to transcriptionally ac

4 ARF interacts with and stabilizes the NB-associated UBC9

5 ARF is a multifunctional tumor suppressor that acts as b

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

7 ARF was dormant during development, in uninjured adult f

8 ARF(-/-) cells exhibit overexpression of Mad2, BubR1, an

9 ARF(-/-) MEFs exhibit mitotic defects including misalign

10 als, including up to six ARF and at least 18 ARF-like (ARL) proteins.

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

12 RP1 at the sites of unrepaired SBs activates ARF transcription through a protein signalling cascade,

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

14 Although ARF can suppress tumor growth by activating p53 function

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

16 r data identify the DNA-binding domain as an ARF dimerization domain, suggest that ARF dimers bind co

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

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

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

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

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

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

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

24 The CDKN2A locus, which houses the INK4a and ARF tumor suppressor genes, is frequently altered in NSC

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

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

27 Concordant expression of CAI2 with p16 and ARF in normal tissue along with the ability of CAI2 to i

28 p16 and ARF, two important tumor-suppressor genes on chromosome

29 to more rapid proliferation, CAI2, p16, and ARF expression all increased dramatically.

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

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

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

33 thic hemolytic anemia, thrombocytopenia, and ARF.

34 auxin concentrations, IAAs are degraded and ARFs become free to regulate auxin-responsive genes.

35 identify functionally redundant Arabidopsis ARF guanine-nucleotide exchange factors (ARF-GEFs) BIG1-

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

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

38 omodulin explained the vancomycin-associated ARF.

39 In the absence of auxin, ARF transcription factors are repressed by interaction w

40 subunit, DDX5, as a critical target of basal ARF function.

41 NA-contacting residues are conserved between ARFs, and we discover that monomers have the same intrin

42 The interaction between ARFs and IAAs is thus central to auxin signalling and oc

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

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

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

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

47 recycles via a distinct pathway mediated by ARF-6 (ADP-ribosylation factor-6).

48 to secretory trafficking pathway mediated by ARF-GEFs confers specificity of cargo delivery to the di

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

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

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

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

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

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

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

56 gi-associated, gamma adaptin ear containing, ARF binding protein 1 (GGA1) as a suppressor of release

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

58 y and consequently activating E2F1-dependent ARF transcription.

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

60 EBNA1(ARF) encodes a KSHV LANA-like glutamine- and glutamic ac

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

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

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

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

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

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

67 enomas from Arf(+/+) mice robustly expressed ARF, while ARF expression was markedly reduced in malign

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

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

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

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

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

73 (ARF3) belongs to the auxin response factor (ARF) family that regulates the expression of auxin-respo

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

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

76 In plants, the AUXIN RESPONSE FACTOR (ARF) transcription factor family regulates gene expressi

77 n are mediated by the auxin response factor (ARF) transcription factors and the Aux/IAA (IAA) transcr

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

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

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

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

82 1D24 interacts with ADP ribosylation factor (ARF)6, a small GTPase crucial for membrane trafficking.

83 sis ARF guanine-nucleotide exchange factors (ARF-GEFs) BIG1-BIG4 as regulators of post-Golgi traffick

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

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

86 d to transcriptional auxin response factors (ARF).

87 interactions between AUXIN RESPONSE FACTORS (ARFs) and Aux/IAA repressors play a central role in auxi

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

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

90 distinct DNA-binding auxin response factors (ARFs), yet the mechanistic basis for generating specific

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

92 that include several auxin response factors (ARFs).

93 gative regulation of auxin response factors (ARFs).

94 Host ADP-ribosylation factors (ARFs) act as in vitro allosteric activators of CTA1, but

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

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

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

98 (ECMO) for severe acute respiratory failure (ARF) in adults is growing rapidly given recent advances

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

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

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

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

103 des important new prognostic information for ARF/RHD.

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

105 mal approach to organizing ECMO programs for ARF in adult patients.

106 hermore explain the critical requirement for ARF inactivation in cancer cells, which are frequently d

107 s suggests a multimerization requirement for ARF protein repression, leading to a refined auxin-signa

108 However, no role for ARF in cell division has previously been proposed.

109 Our results define an unexpected role for ARF in chromosome segregation and mitotic checkpoint fun

110 Our findings suggest a vital role for ARF in DNA damage signalling, and furthermore explain th

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

112 Our finding of a role for ARF in NSCLC is consistent with the observation that ben

113 emonstrate a novel, p53-independent role for ARF in the mitotic checkpoint.

114 The best-characterized role for ARF is in stabilizing p53 in response to cellular stress

115 r ARL2 that displayed crossover activity for ARFs as well.

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

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

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

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

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

121 ously undescribed alternative reading frame (ARF) proteins in their repeat regions.

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

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

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

125 ween E6, focal adhesion kinase, and the GIT1 ARF-GAP protein for binding to paxillin are required but

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

127 However, ARF has tumor suppressive functions outside this pathway

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

129 Similar detailed analyses of other Aux/IAA-ARF regulatory modules will be required to fully underst

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

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

132 protein interaction module that functions in ARF-ARF dimerization and facilitates DNA binding has rec

133 ra B phenocopies mitotic defects observed in ARF(-/-) MEFs.

134 ours of vascular reflow) or glycerol-induced ARF.

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

136 eviously suggested to function as inhibiting ARFs.

137 the dissociation of Mule from its inhibitor ARF.

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

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

140 ein, as the pivotal factor required for INK4-ARF silencing and CIMP in CRCs containing activated KRAS

141 so directs transcriptional silencing of INK4-ARF in human embryonic stem cells.

142 (INK4B), and p16(INK4A), encoded by the INK4-ARF locus.

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

144 BRAF(V600E)/TP53(Null) or BRAF(V600E)/INK4A-ARF(Null) lung cancer cells triggered a G1 cell-cycle ar

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

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

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

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

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

150 in the folded conformation required for its ARF-mediated activation.

151 rescues mitotic phenotypes in cells lacking ARF.

152 utamic acid-rich protein, whereas KSHV LANA1(ARF) encodes a serine/arginine-like protein.

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

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

155 and p66Shc as important regulators mediating ARF activation.

156 w an important role for p66Shc in modulating ARF activation, cell growth, and migration in HER2-posit

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

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

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

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

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

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

163 tients who were readmitted to ICU because of ARF over a 5-year period.

164 recipients readmitted to the ICU because of ARF.

165 lation near the RING domain or by binding of ARF.

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

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

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

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

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

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

172 /IV and reveal the molecular determinants of ARF-IAA interactions.

173 and other oncogenes induce the expression of ARF, thus stabilizing p53 activity and arresting cell pr

174 he additional tumor-suppressive functions of ARF and offer a molecular explanation for the common up-

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

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

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

178 port that the short mitochondrial isoform of ARF (smARF), previously identified as an alternate trans

179 Consistent with this, loss of ARF results in aneuploidy in vitro and in vivo.

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

181 To address the role of ARF in Kras-driven NSCLC, we compared the susceptibility

182 However, the specific role of ARF in pulmonary tumorigenesis remains unclear.

183 he cellular DNA damage response, the role of ARF protein in this process is unclear.

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

185 und that NS can enhance NPM stabilization of ARF.

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

187 To identify other molecular targets of ARF, we focused on known interacting proteins of DDX5 in

188 Although the C termini of ARF and Aux/IAA proteins facilitate their homo- and hete

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

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

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

192 suggested that CAI2 may regulate p16 and/or ARF.

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

194 d EBNA3C jointly suppress p16(INK4A) and p14(ARF), enabling continuous cell proliferation.

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

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

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

198 antigen 3C (EBNA3C) repression of CDKN2A p14(ARF) and p16(INK4A) is essential for immortal human B-ly

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

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

201 EST/NRSF-repressive complexes to repress p14(ARF) and p16(INK4A) expression.

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

203 the CIMP genes are the tumor suppressors p14(ARF), p15(INK4B), and p16(INK4A), encoded by the INK4-AR

204 ificantly decreased Sin3A binding at the p14(ARF) promoter (P < 0.05).

205 EBNA3C bound strongly to the p14(ARF) promoter through SPI1/IRF4/BATF/RUNX3, establishing

206 p14-ARF prevented MAGE-A11 interaction with the E2F1 oncopro

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

208 down-regulation of MAGE-A11 promoted by p14-ARF was independent of HDM2, the human homologue of mous

209 protect against degradation promoted by p14-ARF.

210 e 2, an E3 ubiquitin ligase inhibited by p14-ARF.

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

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

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

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

215 anscriptional activity in the absence of p14-ARF.

216 some was mediated by an interaction with p14-ARF and was independent of lysine ubiquitination.

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

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

219 signal located in but independent of the p16/ARF exon 3.

220 peding up-regulation of both the p21 and p19(ARF) cell-cycle regulators.

221 ediated by the well-known p16(INK4a) and p19(ARF) pathways.

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

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

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

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

226 red a G1 cell-cycle arrest regardless of p19(ARF) status.

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

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

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

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

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

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

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

234 recycling of WLS requires the COPI regulator ARF as well as ERGIC2, an ER-Golgi intermediate compartm

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

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

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

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

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

240 sed in the treatment of patients with severe ARF, with a focus on ECMO.

241 ~30 members in mammals, including up to six ARF and at least 18 ARF-like (ARL) proteins.

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

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

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

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

246 l mitochondrial form of the tumor suppressor ARF (smARF).

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

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

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

250 We show that, in contrast to other tasiR-ARF biogenesis mutants, dcl4 null alleles have an unchar

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

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

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

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

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

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

257 induced by DNA strand breaks (SBs) and that ARF protein accumulates in response to persistent DNA da

258 transcriptional target of p53, arguing that ARF induces the p53 checkpoint to arrest cell proliferat

259 Thus, we propose that ARF regulates Drosha mRNA translation to prevent aberran

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

261 We show that ARF DNA-binding domains also homodimerize to generate co

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

263 as an ARF dimerization domain, suggest that ARF dimers bind complex sites as molecular calipers with

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

265 -Ras and integrin recycling and suggest that ARF-regulated trafficking of R-Ras is required for R-Ras

266 We further provide evidence that ARFs have the potential to oligomerize, a property that

267 The ARF family of regulatory GTPases, within the RAS superfa

268 The ARF tumor suppressor is part of the CDKN2A locus and is

269 The ARF tumour suppressor protein, the gene of which is freq

270 The ARF-GEF-defective mutants gnom-like 1 (gnl1-1) and gnom

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

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

273 on sequence is also the binding site for the ARF tumor suppressor, which inhibits ubiquitination of p

274 use embryonic fibroblasts (MEFs) lacking the ARF tumor suppressor contain abnormal numbers of chromos

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

276 1-3 as GAPs for six different members of the ARF family were determined and found to display wide var

277 ogression by regulating the stability of the ARF tumor suppressor.

278 enesis are abnormal when the function of the ARF-GEF gene GNOM is lost as well as when auxin efflux a

279 t of DNA breaks and predate evolution of the ARF/Mdm2 axis.

280 cancer cells and suggest that targeting the ARF/Rho/MLC signaling axis might be a promising strategy

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

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

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

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

285 growth factor stimulation can activate this ARF isoform to regulate migration as well as proliferati

286 ctivation as well as the recruitment of this ARF isoform to the EGFR.

287 by regulating the recycling of R-Ras through ARF activation.

288 Thus, ARF alone is unable to activate disordered CTA1 at physi

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

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

291 Arf(+/+) mice robustly expressed ARF, while ARF expression was markedly reduced in malignant adenoca

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

293 oncentrations, IAA repressors associate with ARF proteins and recruit corepressors that prevent auxin

294 ind complex sites as molecular calipers with ARF-specific spacing preference, and provide an atomic-s

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

296 rame protein (CARF) associates directly with ARF, p53, and/or human double minute 2 protein (HDM2), a

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

298 Interaction with ARF is required for in vivo toxin activity, as enzymatic

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