ライフサイエンスコーパス: ARF

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

2 gative regulation of auxin response factors (ARFs).

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

4 that include several auxin response factors (ARFs).

5 the dissociation of Mule from its inhibitor ARF.

6 und that NS can enhance NPM stabilization of ARF.

7 omodulin explained the vancomycin-associated ARF.

8 recipients readmitted to the ICU because of ARF.

9 anscriptional activity in the absence of p14-ARF.

10 eviously suggested to function as inhibiting ARFs.

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

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

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

14 o rescue partially the phenotype of both the arf-1.1 and the ncs-1 null worms.

15 Over-expression of arf-1.1 in the AIY neurons was sufficient to rescue part

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

17 ith defects in four potential NCS-1 targets (arf-1.1, pifk-1, trp-1 and trp-2) showed qualitatively s

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

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

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

21 the viral replication is independent of its Arf activating function.

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

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

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

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

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

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

28 mouse models of BCR-ABL1 leukemia, Ikzf1 and Arf alterations synergistically promote the development

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

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

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

32 ecruitment to Golgi membranes relies on GBF1/Arf and ACBD3.

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

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

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

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

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

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

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

40 taneous immortalization while retaining both Arf and p53.

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

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

43 frequently lost in GBM, namely Ink4a, Ink4b, Arf and/or PTEN.

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

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

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

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

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

49 eports suggesting crucial roles for both p19(Arf) and DNA damage-signaling pathways in tumor suppress

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 ARF binds to and thereby inhibits the E3 ligase activity

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

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

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

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

79 IG2) that activate ADP-ribosylation factors (Arfs) by accelerating the replacement of bound GDP with

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

81 Although ARF can suppress tumor growth by activating p53 function

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

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

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

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

86 Accordingly, p19(Arf)-deficient mouse embryo fibroblasts (MEFs) arrest in

87 l Egr DNA-binding activity was suppressed in Arf-deficient but not wild-type (WT) MEFs, leading to Ce

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

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

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

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

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

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

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

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

96 However, concurrent deletion of Ink4a/Arf does not fully rescue the defects detected in Bmi-1(

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

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

99 Thus, our findings identify the Arf-Egr-C/EBPbeta axis as an important determinant of ce

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

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

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

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

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

105 gas was produced by ablation using a 193 nm ArF excimer laser.

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

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

108 of p53 restoration was not dependent on p19(Arf) expression but showed an inverse correlation with M

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

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

111 6 is constitutively linked to GIT1, a GAP of Arf family small G proteins, and that ARHGEF6 phosphoryl

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

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

114 These data suggest the importance of p19(Arf) for the cellular response to the low-level DNA dama

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

116 We report that the conserved Arf GAP Asap is required for cleavage furrow ingression

117 rotein-like (GLD), pleckstrin homology (PH), Arf GAP, and ankyrin repeat domains.

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

119 ts the functional relevance of reduced BRAG1 Arf-GEF activity as seen in the XLID-associated human mu

120 ynaptic transmission, independently of BRAG1 Arf-GEF activity or neuronal activity, but dependently o

121 ood, each of these mutations reduces BRAG1's Arf-GEF activity.

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

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

124 rminal DCB and HUS regulatory domains of the Arf-GEF Sec7 form a single structural unit.

125 hat four distinct mutations within BRAG1, an Arf-GEF synaptic protein, each led to X-chromosome-linke

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

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

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

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

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

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

132 Cytohesin Arf-GEFs are conserved plasma membrane regulators.

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

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

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

136 Arf guanine nucleotide exchange factors (Arf-GEFs) regulate virtually all traffic through the Gol

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

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

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

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

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

142 all traffic through the Golgi by activating Arf GTPase trafficking pathways.

143 basis for control of the cytoskeleton by the Arf GTPase-activating protein AGAP1 has not been charact

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

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

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

147 ADP ribosylation factor (Arf) GTPases are key regulators of membrane traffic at t

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

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

150 Arf guanine nucleotide exchange factors (Arf-GEFs) regul

151 recruiting two related brefeldin A-resistant Arf guanine nucleotide exchange factors, BRAG1 and BRAG2

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

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

154 , low-dose DNA damage responses in which p19(Arf) has a specific role.

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

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

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

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

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

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

161 s of Lnk and tumor suppressors Tp53 or Ink4a/Arf in mice triggers a highly aggressive and transplanta

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

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

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

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

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

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

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

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

170 We therefore examined the role of p19(Arf) in cellular responses to chronic, low-dose DNA-dama

171 to wild-type MEFs, suggesting a role for p19(Arf) in fine-tuning p53 activity.

172 senesce, revealing a selective role for p19(Arf) in senescence upon low-level, chronic DNA damage.

173 rf)-/- MEFs, suggesting that the role of p19(Arf) in the chronic DNA damage response may be partially

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

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

176 am of acute DNA damage is reported to be p19(Arf)-independent.

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

178 ARF inhibits the ability of NRF2 to transcriptionally ac

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

180 ARF interacts with and stabilizes the NB-associated UBC9

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

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

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

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

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

186 However, p19(Arf) is required for replicative senescence, a condition

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

188 for these seemingly disparate roles for p19(Arf) is that acute and chronic DNA damage responses are

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

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

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

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

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

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

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

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

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

198 a GTPase-activating protein (GAP) for ARL3 (Arf-like protein 3), a small GTPase.

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

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

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

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

203 eta signaling in the regulation of the Ink4a/Arf locus and highlight the potential of using small mol

204 pression of p16(Ink4a) (encoded by the Ink4a/Arf locus, also known as Cdkn2a) and a distinctive secre

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

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

207 naling can result in repression of the Ink4a/Arf locus, resulting in increased beta-cell replication

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

209 y through the direct repression of the Ink4a/Arf locus.

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

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

212 3T3 cells through a mechanism involving p19(Arf) loss.

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

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

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

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

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

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

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

220 ith an activated DNA damage response, as p19(Arf)-/- MEFs do not senesce after serial passage.

221 t to their response to acute DNA damage, p19(Arf)-/- MEFs exposed to chronic DNA damage do not senesc

222 w further that p53 pathway activation in p19(Arf)-/- MEFs exposed to chronic DNA damage is attenuated

223 is insufficient to promote senescence in p19(Arf)-/- MEFs, suggesting that the role of p19(Arf) in th

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

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

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

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

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

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

230 were also reduced in Ras(V12)-expressing p19(Arf) null mouse embryonic fibroblasts (MEFs), and overal

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

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

233 er, knockdown of miR-491-5p in primary Ink4a-Arf-null mouse glial progenitor cells exacerbated cell p

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

235 mation by Ras, whereas cells lacking p14/p19(Arf) or other tumor suppressors can be transformed.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 5A-mutated (smArf-deficient) full-length p19(Arf) proteins.

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

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

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

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

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

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

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

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

263 des important new prognostic information for ARF/RHD.

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

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

266 pression, providing new insight into how p19(Arf) serves as a tumor suppressor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

288 induced DSBs cooperate with loss of Ink4 and Arf tumor suppressors to generate high-grade gliomas tha

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

290 ation by oncogenic signals relies on the p19(Arf) tumor suppressor, while p53 activation downstream o

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

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

293 ARF was dormant during development, in uninjured adult f

294 Loss of Ink4a and Arf was sufficient to trigger IR-induced glioma developm

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

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

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

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

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