ライフサイエンスコーパス: ACF

1 ACF (ATP-utilizing chromatin assembly and remodeling fac

2 ACF activity is stimulated by two defining features of t

3 ACF and colon adenocarcinomas were determined at 8 and 4

4 ACF and tumor efficacy endpoints were carried out on azo

5 ACF binds to both apoB RNA and apobec-1, the catalytic c

6 ACF binds to the protein carrier, transportin 2 in vivo,

7 ACF expression is predominantly nuclear, including mutan

8 ACF from low- and high-risk colons were not discriminate

9 ACF from sensitive A/J mice were considered at high risk

10 ACF generates and maintains nucleosome spacing by consta

11 ACF is a chromatin-remodeling complex that catalyzes the

12 ACF is measured periodically by computer-controlled vide

13 ACF provides fast degradation of the model contaminant m

14 ACF relocates to the cytoplasm after actinomycin D treat

15 ACF remain a potential biomarker for colorectal cancer,

16 ACF significantly inhibited growth and self-renewal pote

17 ACF treatment inhibited intratumoral expression of VEGF

18 ACF was found to prevent diet-induced obesity and insuli

19 ACF were identified in 97% of the Apc1638N/+ mice starti

20 ACF were predominantly located in the distal colon.

21 Between July 1, 2017, and June 30, 2018, ACF was conducted in 26 IDP camps and 963 host communiti

22 s detected by immunohistochemistry in all 22 ACF evaluated.

23 n extirpations in the Southeast (ACT n = 46, ACF n = 22) were most prevalent in upland rivers, with f

24 uated BRAF mutations by DNA sequencing in 53 ACF from patients with sporadic colorectal carcinomas an

25 We examined 55 ACF collected during screening colonoscopy from a total

26 r studies of ACF have raised questions about ACF.

27 Here, acriflavine (ACF), an inhibitor of HIF1alpha, induced the expression

28 -screening assay, we identified Acriflavine (ACF), a small molecule that inhibits the binding between

29 found that the HIF-1 inhibitor acriflavine (ACF) decreased survival and growth of CML cells.

30 persensitive to the Top2 poison acriflavine (ACF), activating the DNA damage checkpoint.

31 AutoN off the ATPase and thereby activating ACF.

32 by the fraction of cells remaining adherent (ACF) after a given time of exposure to shear stress in a

33 feeding of the FD diet resulted in advanced ACF formation and liver tumors in wild type mice.

34 s as key regions where Uls1 associates after ACF treatment.

35 At 2 days after ACF, LV end-diastolic dimension (LVEDD)/wall thickness w

36 Immediately after ACF induction, eccentric LV remodeling is mediated by in

37 From 4 to 15 weeks after ACF, interstitial collagen decreased by 30% and left ven

38 ese data, together with the finding that all ACF variants were co-expressed in rat liver nuclei (the

39 We found that altered ACF binding after chronic stress was correlated with alt

40 he nucleus, whereas wild-type chimeras or an ACF deletion mutant lacking the ANS were cytoplasmic.

41 targets ACF1 and ISWI, subunits of CHRAC and ACF nucleosome mobilizing complexes, to this specific si

42 ucts of nucleosome remodeling by SWI/SNF and ACF complexes using high-resolution microscopy combined

43 The APOBEC1-ACF complex edits and remains associated with the edited

44 We demonstrate that the APOBEC1-ACF holoenzyme mediates a multifunctional cycle.

45 proliferative state of dysplastic-appearing ACF.

46 elated chromatin remodeling ATPases, such as ACF and BRG1, and does not lead to complete disruption o

47 somes by an ATP-driven motor protein such as ACF or Chd1.

48 nical nucleosomes by a motor protein such as ACF.

49 Because ACF assembles nucleosomes uniformly on heterogeneous DNA

50 were larger compared to NH in core and belt ACFs, indicating neuroplasticity in the right hemisphere

51 The pol beta ACF was capable of substrate channeling for steps in vit

52 Some of the BER factors in the pol beta ACF were in a multi-protein complex as observed by sucro

53 At equilibrium, a continuously bound ACF complex can move the nucleosome back-and-forth many

54 A nucleosomes over macroH2A nucleosomes, but ACF, an ISWI complex implicated in gene repression, show

55 Chromatin assembly by ACF is also impaired upon mutation of an acidic region i

56 contributes to the overall cases averted by ACF.

57 the effect in UHL compared to NH differed by ACF and ear of deafness.

58 ibution of nucleosome positions generated by ACF.

59 the remodelling of individual nucleosomes by ACF in real time, revealing previously unknown remodelli

60 t is converted into canonical nucleosomes by ACF.

61 Thus, chromatin assembly and remodeling by ACF can occur in the absence of histone modifications.

62 t inhibit substrate binding or remodeling by ACF.

63 The main causes for the reduced CCF/ACF amplitude ratio are differences in observation volum

64 se of complete binding, the ratio of the CCF/ACF amplitudes is expected to be 1.

65 hich two different FPs are linked, yield CCF/ACF amplitude ratios of ~0.5 or less for different FCCS

66 ate nucleosome mobilization per se by CHRAC, ACF or their catalytic subunit, ISWI.

67 xib (500 ppm) suppressed AOM-induced colonic ACF formation (P < 0.05 and < 0.001, respectively) and r

68 est that KJT can inhibit AOM-induced colonic ACF formation and might be a useful chemopreventive agen

69 As expected, sulindac inhibited colonic ACF formation (P < 0.001) and reduced the multiplicity o

70 ficantly suppressed the incidence of colonic ACF (P < 0.01 and < 0.001, respectively) and crypt multi

71 ndent inhibition of the incidence of colonic ACF.

72 The chromatin remodeling complex ACF helps establish the appropriate nucleosome spacing f

73 SWI-containing chromatin-remodelling complex ACF both fail to potentiate transcription.

74 and cellular thermal-shift-assays confirmed ACF binding to basigin in vitro and in live glioblastoma

75 ear stimulation in UHL, only posterior core ACFs showed larger ipsilateral responses, suggesting tha

76 do not necessarily translate to less costly ACF, as any savings from the test cost can be strongly o

77 apobec-1-deficient) hepatoma cells decreased ACF protein expression and induced a commensurate increa

78 Fluorinated phenylthiophenyl derivative, ACF, 2-[(2-amino-4-chloro-5-fluorophenyl)thio]-N,N-dimet

79 entage of purported, endoscopically detected ACF have not been confirmed on histologic review.

80 Dysplastic ACF, once postulated as the ACF destined for adenomatous

81 Hyperplastic ACF, dysplastic ACF, microadenomas, adjacent normal-appearing epithelium

82 Large and dysplastic ACF are putative precursors of colon cancer with neoplas

83 hylated in heteroplastic ACF than dysplastic ACF [35% (11 of 31) versus 7% (2 of 30), P = 0.01].

84 d a linear correlation, the most efficacious ACF inhibition being produced by the molecules with the

85 critically examine the evidence on employing ACF as an intermediate endpoint.

86 during initiation phase (wks. 3-21) enhanced ACF burden at 60 weeks, regardless of the diet in progre

87 ssion (wks. 22-60), a high-fat diet enhanced ACF formation compared to a control or energy restricted

88 NA editing activity coincident with enhanced ACF phosphorylation in vivo.

89 atic apoB mRNA editing activity by enhancing ACF nuclear localization/retention, facilitating the int

90 ing chromatin assembly and remodeling enzyme ACF to mobilize a mononucleosome, indicating that this s

91 te that the ATP-dependent remodeling enzymes ACF and Mi2beta can direct consecutive, opposing chromat

92 The new tracer [(18)F]ACF showed excellent brain penetration and selective loc

93 Synthesis of the novel PET tracer, [(18)F]ACF, as a probe for binding to SERT in the brain was suc

94 For preparation of the [(18)F]ACF, the NH(2) group of the initially coupled adduct was

95 The final product, [(18)F]ACF, was obtained after a borane and stannous chloride r

96 a significant increase of activating factor ACF, a component of the apoB mRNA editing complex.

97 An accessibility factor (ACF) that takes into account the role of the reactive, s

98 The ATP-dependent chromatin assembly factor (ACF) forms such structures in vitro and is required for

99 The ATP-dependent chromatin assembly factor (ACF) spaces nucleosomes to promote formation of silent c

100 ATP-dependent chromatin-assembly factor (ACF) uses the energy of ATP hydrolysis for the depositio

101 yme ATP-dependent chromatin assembly factor (ACF).

102 subunit 1 (APOBEC-1) complementation factor (ACF) family of related proteins.

103 apobec-1 complementation factor (ACF) is an hnRNP family member which functions as the ob

104 Apobec-1 complementation factor (ACF) is the RNA binding subunit of a core complex that m

105 POBEC-1 and APOBEC-1 Complementation Factor (ACF).

106 ng subunit, apobec-1 complementation factor (ACF).

107 ng chromatin assembly and remodeling factor (ACF), Drosophila nucleosome assembly protein-1, plasmid

108 nt chromatin assembly and remodeling factor (ACF).

109 t chromatin assembly and remodelling factor (ACF) functions to generate regularly spaced nucleosomes,

110 t chromatin assembly and remodelling factor (ACF), an ISWI enzyme comprising a catalytic subunit, Snf

111 EC1) and a complementing specificity factor (ACF).

112 An accelerated catalytic Fenton (ACF) reaction was developed based upon a multicatalysis

113 s across different auditory cortical fields (ACFs).

114 luated the impact of an active case finding (ACF) intervention for TB and testing for HIV in IDP comm

115 Active case finding (ACF) may be valuable in tuberculosis (TB) control, but q

116 re studied in rats after aortocaval fistula (ACF) of 12 h, 2 and 5 days, and 4, 8, and 15 weeks.

117 (ACT), and Apalachicola-Chattahoochee-Flint (ACF) basins.

118 on azoxymethane-induced aberrant crypt foci (ACF) and colon adenocarcinomas in F344 rats.

119 ber of aberrant crypts, aberrant crypt foci (ACF) and crypts/focus in rats of the KJT + AOM group wer

120 Aberrant crypt foci (ACF) are collections of abnormal colonic crypts with het

121 Aberrant crypt foci (ACF) are postulated to be the earliest precursor lesions

122 ich support the role of aberrant crypt foci (ACF) as a putative precursor to colorectal adenomas and

123 had significantly less aberrant crypt foci (ACF) formation and significantly reduced colon cancer de

124 interact to accelerate aberrant crypt foci (ACF) formation and tumor development in beta-pol haploin

125 ncrease in premalignant aberrant crypt foci (ACF) formation over LOI(-) mice.

126 colonic microbiota and aberrant crypt foci (ACF) in C57BL/6N female mice fed various dietary interve

127 n of chemically induced aberrant crypt foci (ACF) in the colon of CF1 mice and intestinal adenomas in

128 the formation of colon aberrant crypt foci (ACF) induced by a s.c. injection of azoxymethane (C2H6N2

129 re was no difference in aberrant crypt foci (ACF) or tumor burden when animals were treated with AOM

130 alignant lesions called aberrant crypt foci (ACF) that are localized to the distal three centimeters

131 icted that hyperplastic aberrant crypt foci (ACF), a putative precancerous lesion found in the colon,

132 e (AOM)-induced colonic aberrant crypt foci (ACF), against AOM and dextran sulfate sodium (DSS)-induc

133 atures of preneoplastic aberrant crypt foci (ACF), gene expression analysis was performed on ACF from

134 Aberrant crypt foci (ACF), the earliest identified neoplastic lesions in the

135 lation changes in human aberrant crypt foci (ACF), the earliest putative precursor to CRC.

136 number of preneoplastic aberrant crypt foci (ACF).

137 ndergoing assessment of aberrant crypt foci (ACF).

138 of AOM-induced colonic aberrant crypt foci (ACF).

139 DNA fingerprints of 44 aberrant crypt foci (ACF; the earliest identified neoplastic lesion in the co

140 Aberrant crypt foci (ACFs) were similarly increased significantly by approxim

141 IF1alpha in adipose tissue was essential for ACF to improve the SOCS3-STAT3-adiponectin pathway to co

142 Colons were evaluated for ACF, and colonic mucosae were assayed for COX and NOS is

143 an unanticipated physiological function for ACF beyond apoB RNA editing.

144 Moreover, this proposed mechanism for ACF may be relevant to the function of other chromatin-r

145 when designing cost-effective strategies for ACF.

146 h colorectal adenomas, and the technique for ACF detection using high-magnification chromoendoscopy h

147 The pol beta affinity-capture fraction (ACF) was found to contain several BER factors including

148 es that predict cancer risk, LCM-LA RNA from ACF was hybridized to cDNA arrays.

149 nal along with the autocorrelation function (ACF) were used to quantify liposome entrapment efficienc

150 of the auto- and cross-correlation function (ACF and CCF) amplitudes.

151 osition (PseAAC), auto-correlation function (ACF) and Bi-gram position-specific scoring matrix (Bi-gr

152 more frequently methylated in heteroplastic ACF than dysplastic ACF [35% (11 of 31) versus 7% (2 of

153 sms to the activities of yeast RSC and human ACF, which are representative members of two major class

154 In this first study of human ACF with this approach, the finding of altered DNA finge

155 The human ACF chromatin-remodeling complex (hACF) contains the ATP

156 Hyperplastic ACF, dysplastic ACF, microadenomas, adjacent normal-appe

157 tions and serrated histology in hyperplastic ACF supports the idea that these lesions are an early, s

158 Hyperproliferative ACF had significantly increased mRNA levels of EGFR (6.0

159 In hyperproliferative ACF, 44% possessed significant increases in four EGFR si

160 tein was not increased in hyperproliferative ACF.

161 nvolved in RNA binding and is used to import ACF into the nucleus as cargo.

162 Importantly, ACF exhibited significantly less-severe effects on non-C

163 These alterations in ACF binding and nucleosome positioning were associated w

164 expression in CRC, this was not the case in ACF, suggesting the insufficiency of methylation changes

165 the nuclear accumulation of beta-catenin in ACF, confirming that beta-catenin is a critical target o

166 of the loci harboring methylation changes in ACF were also altered in CRC samples, though the magnitu

167 ally methylated regions (DMRs) identified in ACF, 537 (66%) were hypermethylated and 274 (34%) were h

168 FD resulted in a significant increase in ACF formation in wild type (WT) animals exposed to 1,2-d

169 s associated with a 2- to 3-fold increase in ACF phosphorylation relative to that in control primary

170 itude of change at these sites was lesser in ACF.

171 We therefore studied methylation in ACF from patients with familial adenomatous polyposis (F

172 Our findings suggest that methylation in ACF is an early event in the pathogenesis of a subset of

173 more costly, tests such as Xpert MTB/RIF in ACF in a high-burden setting?

174 tests such as smear and Xpert-like tests in ACF, relating to the accuracy of the reference standard

175 AOM-induced ACF became apparent at approximately 4-6 weeks and conti

176 e degree as it protected against AOM-induced ACF formation.

177 and Msh6 independently suppress AOM-induced ACF, and combination of the two mutant alleles had a mul

178 A element previously hypothesized to inhibit ACF activity does not inhibit substrate binding or remod

179 constants with their efficacy in inhibiting ACF.

180 us loss of Apc may be sufficient to initiate ACF in these mice and that these mice may be suitable mo

181 fication chromoendoscopy, we collected large ACF with endoscopic features of dysplasia and separately

182 Moreover, in a murine CML model, ACF decreased leukemia development and reduced LSC maint

183 ipsilateral responses, suggesting that most ACFs in the left hemisphere had greater resilience again

184 mean colonic total ACF by 43% and multicrypt ACF by 63%; dietary CP-31398 at 150 and 300 ppm suppress

185 files have been generated for 10 KRAS-mutant ACF and 10 CRCs harboring a KRAS mutation, as well as ma

186 )-tetrahydrofuran yielded the nonradioactive ACF (yield 25%).

187 BRAF mutation was present in only 2% of ACF and 6% of sporadic HPs.

188 At the RNA level, 38% of ACF were hyperproliferative, with proliferating cell nuc

189 Ras was activated in 46% of ACF (3.2 +/- 0.4-fold; P < 0.05), but K-ras mutations we

190 At the protein level, 46% of ACF were hyperproliferative (PCNA, 3.2 +/- 1.2-fold).

191 Methylation was present in 34% (21 of 61) of ACF, including both FAP and sporadic types, but was more

192 abnormality identified in 16% (10 of 61) of ACF.

193 t K-ras mutations were present in only 7% of ACF.

194 Nuclear accumulation of ACF is transcription-dependent, temperature-sensitive, a

195 chromatin assembly and ATPase activities of ACF.

196 wo-dimensional phosphoamino acid analysis of ACF immunopurified from hepatocyte nuclear extracts demo

197 Strong associations of ACF methylation with K-ras mutation (P = 0.007) and with

198 ch is necessary for the efficient binding of ACF complex to DNA.

199 The binding of ACF, translocation of DNA and exiting of translocation p

200 Finally, molecular characterization of ACF has been studied on only a limited basis.

201 e taken as indicative of the overall cost of ACF.

202 rcinogen; however, FD reduced development of ACF in beta-pol haploinsufficient mice.

203 At 2 weeks (before development of ACF), there were marked changes in a number of 4D-ELF si

204 l correlation with subsequent development of ACF.

205 sidue motif (ANS) in the auxiliary domain of ACF that functions as an authentic nuclear localization

206 r export signal is involved in the export of ACF and the edited apoB mRNA together, to the site of tr

207 elieved, and identify epigenomic features of ACF that may provide new targets for cancer chemoprevent

208 Enhanced formation of ACF in p21-deficient mice supports a tumor suppressor fu

209 After formation of ACF or adenomas, the mice were injected (i.p.) with ERRP

210 y be an initiating event in the formation of ACF, with inflammatory cell cytokine expression contribu

211 eries (ITS) analyses to assess the impact of ACF on TB case notifications.

212 all molecular mechanism of the inhibition of ACF by the 3-nitroflavones under study appears to involv

213 n/retention, facilitating the interaction of ACF with APOBEC-1 and thereby increasing the probability

214 Small interfering RNA knockdown of ACF in either rat (apobec-1-expressing) or human (apobec

215 reatment significantly reduced the number of ACF from 25.0 +/- 3.0 (controls) to 14.9 +/- 1.6 (ERRP-t

216 Although the number of ACF increased with age (P < 0.0001), the average number

217 ce developed significantly higher numbers of ACF than wild-type mice in response to AOM, and these we

218 evaluated for the spontaneous occurrence of ACF and tumors.

219 In the presence of ACF and ATP, the nucleosomes exhibit gradual translocati

220 The prevalence of ACF has not correlated with colorectal adenomas, and the

221 ever, FD attenuated onset and progression of ACF and prevented liver tumorigenesis in beta-pol haploi

222 found that the transcriptional properties of ACF-assembled chromatin containing unmodified histones w

223 Recent, larger-scale, multicenter studies of ACF have raised questions about ACF.

224 rkers under development, additional study of ACF is needed before reliable, clinical application can

225 c nucleosome arrays, and the ISWI subunit of ACF is an ATPase that is related to helicases.

226 Acf1, the large subunit of ACF, is essential for the full activity of the complex.

227 the in vivo function of the Acf1 subunit of ACF/CHRAC in Drosophila.

228 by ISWI, the smaller of the two subunits of ACF.

229 ever, the functions and potential targets of ACF beyond apoB mRNA editing are unknown.

230 ochemical activities are similar to those of ACF.

231 ), gene expression analysis was performed on ACF from two mouse strains with differing tumor sensitiv

232 Periodic ACF can both improve control and save medium-term health

233 thematical model of TB dynamics and periodic ACF (PACF) in the HIV era, simplified by assuming consta

234 Significantly, phosphorylated ACF was restricted to nuclear extracts where it co-sedim

235 the presence of Uls1 at these sites prevents ACF-dependent Top2 accumulation.

236 Thus, we propose ACF, a US Food and Drug Administration (FDA)-approved dr

237 one NAP1 and the ATP-dependent motor protein ACF.

238 By using a purified ACF-dependent system for chromatin assembly, we found th

239 Recombinant ACF bound an AU-rich region in the IL-6 3'-untranslated

240 h NVP-AEW541 abrogated this effect, reducing ACF to a level 30% lower even than found in exposed LOI(

241 ctor receptor (EGFR) signaling in regulating ACF proliferation.

242 Furthermore, the chromatin remodeler ACF can overcome this effect.

243 e in an ATP-dependent reaction that requires ACF following transcription factor binding to chromatin.

244 harbor BRAF mutations and that non-serrated ACF would not.

245 ould be found more often in the non-serrated ACF.

246 ed larger contralateral responses in several ACFs.

247 , P = 0.002], especially dysplastic sporadic ACF [75% (3 of 4) versus 8% (2 of 24), P = 0.004].

248 dic types, but was more frequent in sporadic ACF [53% (18 of 34) versus 11% (3 of 27), P = 0.002], es

249 We also studied ACF rats after BK2 receptor (BK2R) blockade (2 days) or

250 and organizing community outreach to support ACF.

251 a subset of colorectal carcinomas, and that ACF from FAP patients and patients with sporadic colorec

252 These data demonstrate that ACF is a metabolically regulated phosphoprotein and sugg

253 These data demonstrate that ACF with distinct tumorigenic potential have distinguish

254 Heterokaryon assays confirmed directly that ACF shuttles in vivo.

255 We find that ACF senses linker DNA length through an interplay betwee

256 system for chromatin assembly, we found that ACF hydrolyses about 2#150;4 molecules of ATP per base p

257 These findings collectively indicate that ACF/CHRAC functions in the assembly of periodic nucleoso

258 icient embryo extracts further indicate that ACF/CHRAC is a major chromatin assembly factor in Drosop

259 tively on two ACF molecules, indicating that ACF functions as a dimer of ATPases.

260 y times before dissociation, indicating that ACF is a highly processive and bidirectional nucleosome

261 We also observed that ACF assembles nucleosomes in localized arrays, rather th

262 Here we show that ACF becomes committed to the DNA template upon initiatio

263 By performing ChIP-seq, we show that ACF leads to a general increase in Top2 binding across t

264 The impact of the intervention showed that ACF can greatly increase TB case notifications.

265 nt in vitro stem cell assays, we showed that ACF, but not TKIs, targets the stem cell potential of CM

266 In summary, we have shown that ACF with up-regulated PCNA possess increased EGFR signal

267 Taken together, these data suggest that ACF plays a crucial role, which is independent of apobec

268 These findings suggest that ACF regulates liver regeneration following PH at least i

269 Results suggest that ACF using a moderate-accuracy test could in fact cost mo

270 henotypes of flies lacking Acf1 suggest that ACF/CHRAC promotes the formation of repressive chromatin

271 e site of apoB mRNA editing), suggested that ACF variants might compete with one another for APOBEC-1

272 to implant and proliferate, suggesting that ACF plays a key role in cell growth and differentiation.

273 The ACF was a component of a multistakeholder collaboration

274 Dysplastic ACF, once postulated as the ACF destined for adenomatous transformation, have been r

275 At optimized testing conditions, the ACF of activated cells was consistently found to be thre

276 In contrast, the ACF remodeler, belonging to ISWI family, only produces r

277 Together, our findings identify the ACF chromatin-remodeling complex as a critical component

278 ich these two substrate cues function in the ACF remodeling reaction is not well understood.

279 terminal domain dependent manner, and in the ACF-bound nucleosome, lengthening the linker DNA reduces

280 stablish that persistent upregulation of the ACF (ATP-utilizing chromatin assembly and remodeling fac

281 strate altered fingerprints for 23.3% of the ACF and 95.7% of the cancers.

282 he average number of crypts per focus of the ACF did not increase significantly.

283 nly chemoprotective during initiation of the ACF, but also therapeutic in the postinitiation progress

284 lows reliable quantitative assessment of the ACF.

285 dant pair for production of OH-radicals, the ACF system contains Pd/H2 as catalyst/reductant pair for

286 osomes approximately 10-fold slower than the ACF remodeling complex.

287 With the ACF chromatin remodeling factor, HMGN2 does not directly

288 tin-remodeling factor and contrasts with the ACF remodeling factor, which stimulates the removal of l

289 We compared methylation to ACF histopathology, K-ras proto-oncogene mutation, loss

290 ation, translocation and pausing, similar to ACF.

291 398 was shown to suppress mean colonic total ACF by 43% and multicrypt ACF by 63%; dietary CP-31398 a

292 eosome movement depends cooperatively on two ACF molecules, indicating that ACF functions as a dimer

293 In vivo, ACF also regulated the SOCS3-STAT3-adiponectin pathway,

294 equent to PU.1 binding to chromatin, whereas ACF will not support erasure.

295 J mice were considered at high risk, whereas ACF from resistant AKR/J mice were considered at low ris

296 The mechanism by which ACF mobilizes nucleosomes remains poorly understood.

297 st that a tracking mechanism exists in which ACF assembles chromatin as an ATP-driven DNA-translocati

298 mount of APOBEC-1 co-immunoprecipitated with ACF and inhibited in vitro editing activity.

299 1 was effectively co-immunoprecipitated with ACF from nuclear, but not cytoplasmic extracts.

300 nt targeting sequence (ANS) contained within ACF.