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 a nuclear protein that upon cotransfection with a

13 ACF is measured periodically by computer-controlled vide

14 ACF provides fast degradation of the model contaminant m

15 ACF relocates to the cytoplasm after actinomycin D treat

16 ACF remain a potential biomarker for colorectal cancer,

17 ACF significantly inhibited growth and self-renewal pote

18 ACF treatment inhibited intratumoral expression of VEGF

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

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

21 ACF were predominantly located in the distal colon.

22 iously described auxiliary proteins (ABBP-1, ACF, and GRY-RBP) in that it does not contain any RNA re

23 s detected by immunohistochemistry in all 22 ACF evaluated.

24 mical expression of iNOS was evaluated in 42 ACF, 14 adenomas, and 25 carcinomas and their adjacent n

25 ression of beta-catenin was seen in 25 of 46 ACF with dysplasia and in 2 of 48 ACF with atypia.

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

27 n 25 of 46 ACF with dysplasia and in 2 of 48 ACF with atypia.

28 s; it was markedly reduced in 21 of 42 (50%) ACF and in 14 of 25 (56%) carcinomas.

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

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

31 r studies of ACF have raised questions about ACF.

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

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

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

35 AutoN off the ATPase and thereby activating ACF.

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

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

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

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

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

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

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

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

44 component holoenzyme containing apobec-1 and ACF.

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

46 ransfected cells, suggesting that CUGBP2 and ACF are bound in vivo.

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

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

49 proliferative state of dysplastic-appearing ACF.

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

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

52 nical nucleosomes by a motor protein such as ACF.

53 Because ACF assembles nucleosomes uniformly on heterogeneous DNA

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

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

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

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

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

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

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

61 ibution of nucleosome positions generated by ACF.

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

63 t is converted into canonical nucleosomes by ACF.

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

65 t inhibit substrate binding or remodeling by ACF.

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

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

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

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

70 Colonic ACF and tumors were evaluated histopathologically, and a

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

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

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

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

75 ndent inhibition of the incidence of colonic ACF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 We then examined ACF-catalyzed chromatin remodeling with completely purif

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 nt chromatin assembly and remodeling factor (ACF).

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

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

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

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

117 s across different auditory cortical fields (ACFs).

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

119 after the creation of an aortocaval fistula (ACF).

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

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

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

123 mically induced colonic aberrant crypt foci (ACF) and tumors, cyclooxygenase (COX)-2 activity, and ap

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

125 Aberrant crypt foci (ACF) are postulated to be the earliest precursor lesion

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 number of preneoplastic aberrant crypt foci (ACF).

142 ndergoing assessment of aberrant crypt foci (ACF).

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

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

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

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

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

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

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

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

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

152 lear (P = 0.0001) expressions increased from ACF to adenoma to carcinoma.

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

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

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

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

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

158 ssion of iNOS has not been reported in human ACF or multiple neoplastic lesions from the same patient

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

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

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

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

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

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

165 tein was not increased in hyperproliferative ACF.

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

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

168 In ACF with dysplasia, reduced membranous expression of bet

169 es, despite 3-fold higher LV ACE activity in ACF 1/1 versus ACF 1/0 mice.

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

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

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

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

174 LV angiotensin II was higher in ACF versus sham-operated mice but did not differ between

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

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

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

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

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

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

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

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

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

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

185 constants with their efficacy in inhibiting ACF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 chromatin assembly and ATPase activities of ACF.

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

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

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

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

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

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

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

209 l correlation with subsequent development of ACF.

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

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

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

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

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

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

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

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

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

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

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

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

222 evaluated for the spontaneous occurrence of ACF and tumors.

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

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

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

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

227 involves the NH(2)-terminal 380 residues of ACF.

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

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

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

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

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

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

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

235 ochemical activities are similar to those of ACF.

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

237 eas antisense knockout of either apobec-1 or ACF expression eliminated apoB RNA editing, establishing

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

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

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

241 Immunodepletion of CUGBP2 co-precipitates ACF, and these proteins co-localize the nucleus of trans

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

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

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

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

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

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

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

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

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

251 ed larger contralateral responses in several ACFs.

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

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

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

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

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

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

258 Heterokaryon assays confirmed directly that ACF shuttles in vivo.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 lows reliable quantitative assessment of the ACF.

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

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

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

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

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

289 ation, translocation and pausing, similar to ACF.

290 398 was shown to suppress mean colonic total ACF by 43% and multicrypt ACF by 63%; dietary CP-31398 a

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

292 old higher LV ACE activity in ACF 1/1 versus ACF 1/0 mice.

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.