ライフサイエンスコーパス: ASF

1 ASF also induced weaker type-C self-association of galec

2 ASF and FET glycocoproteins were unambiguously detectabl

3 ASF participation was associated with significant increa

4 ASF/SF2 activates exon 3 inclusion, but SC35, acting thr

5 ASF/SF2 bound to a discrete region containing a purine-r

6 ASF/SF2 is an SR protein splicing factor that participat

7 ASF/SF2 modification is not altered when the inhibitor p

8 ASF/SF2 thus plays an important role in viral RNA expres

9 ASF/SF2, a member of the serine-arginine (SR) protein fa

10 ASF/SF2, a splicing factor known to prevent RLF, and GTP

11 ternative splicing factor/splicing factor 2 (ASF/SF2)-bound forms.

12 ternative splicing factor/splicing factor 2 (ASF/SF2).

13 ddition, the assay format for the galectin-3/ASF pair could be easily applied in screening for glycan

14 roduced clinical signs consistent with acute ASF.

15 This suggests that after ASF-induced nucleation, galectin-3 associates with itsel

16 we demonstrate that the SR proteins 9G8 and ASF/SF2 exhibit higher affinity for TAP/NXF1 when hypoph

17 e 10 phosphorylation and increased SRp20 and ASF/SF2 retention on mitotic chromosomes.

18 ification-regulated association of SRp20 and ASF/SF2 with chromatin.

19 t two SR protein splicing factors, SRp20 and ASF/SF2, associate with interphase chromatin, are releas

20 Although domain swaps between SRrp86 and ASF/SF2 showed that the RRMs primarily determined splici

21 ther inefficient splicing events tested, and ASF/SF2 depletion does not affect SMN1/2 splicing.

22 ncers and their binding proteins (U2AF65 and ASF/SF2) that had critical roles in splicing AR pre-mRNA

23 proteins enhance their ability to antagonize ASF/SF2.

24 itor of binding when a single ligand such as ASF is used will be as effective when used in studies wi

25 inities to multivalent glycoproteins such as ASF, independent of the quaternary structures of the gal

26 sequestering repeat-binding proteins such as ASF/SF2 and hnRNPA1, suggesting a toxic RNA pathogenesis

27 lalpha1-3GalNAc (TF-AuNP), (2) asialofetuin (ASF) containing both LacNAc (Galbeta1-4GlcNAc) and TF-an

28 ermining the IC(50) values for asialofetuin (ASF) and for bovine serum albumin derivatized with an av

29 -3 with the model glycoprotein asialofetuin (ASF), using a fluorescence anisotropy assay to measure t

30 Preincubation of PHUECs in asialofetuin (ASF), an ASGP-R ligand, significantly reduced invasion.

31 ity in the ITC binding data of asialofetuin (ASF), a glycoprotein that possesses nine LacNAc epitopes

32 several regions were indicated for baseline ASF, only 4q31.22-q32.2 and 11p15.4-p11.2 replicated the

33 y, we show a significant correlation between ASF/SF2 and CD3zeta protein levels in T cells from syste

34 nly weak and equivalent interactions between ASF/SF2 and other SR proteins with the 5' ends of SMN1 a

35 s, whereas biotinylated asialofetuin (biotin-ASF), a galectin-3 nanomolar binding partner, was bound

36 haScreen signal by competing with the biotin-ASF.

37 eactions inhibits RNA processing mediated by ASF/SF2, by SC35, or by RNPS1.

38 Collegiate ASF athletes may be at risk for clinically relevant incr

39 left ventricular remodeling among collegiate ASF athletes.

40 ubstantially larger population of collegiate ASF athletes is not known.

41 ore and after a single season of competitive ASF participation in 6 consecutive groups of first-year

42 e there are no vaccines available to control ASF after an outbreak, obtaining an understanding of the

43 The main problem for controlling ASF is the lack of vaccines.

44 The main problem in controlling ASF is the lack of vaccines.

45 inate swine and protect them from developing ASF.

46 ' splice site for BPV-1 RNA splicing in DT40-ASF cells, a genetically engineered chicken B-cell line

47 A expression in the chicken B-cell line DT40-ASF, expressing or not expressing ASF/SF2.

48 netically modified chicken B-cell line, DT40-ASF, we now show that ASF/SF2 inactivation results in a

49 ript, and deletion of this region eliminated ASF/SF2-mediated regulation of transcript stability.

50 epleted cells compared with cells expressing ASF/SF2, indicating a negative role for the SR protein.

51 line DT40-ASF, expressing or not expressing ASF/SF2.

52 Down-regulation of the splice factor ASF/SF2 by siRNA increases KLF6 SV1 messenger RNA levels

53 ong which p32, a cofactor of splicing factor ASF/SF-2, was identified.

54 tudies, similar to the known splicing factor ASF/SF-2.

55 ned at the C terminus of the splicing factor ASF/SF2 (ASF-CTD) and an RS domain deletion mutant prote

56 The cellular splicing factor ASF/SF2 also binds to this region and inhibits SM-RNA bi

57 We identify the essential splicing factor ASF/SF2 as a key component of the program, regulating a

58 the C9orf72 repeats, but the splicing factor ASF/SF2 can bind the r(GGGGCC)n repeat.

59 dependent on the SR protein splicing factor ASF/SF2 or to the creation of an exonic splicing silence

60 The human alternative splicing factor ASF/SF2, an SR (serine-arginine-rich) protein involved i

61 (also known as alternative splicing factor (ASF)).

62 ceral fat (AVF), abdominal subcutaneous fat (ASF), and abdominal total fat (ATF) were measured using

63 The control of African swine fever (ASF) has been hampered by the unavailability of vaccines

64 The control of African swine fever (ASF) has been hampered by the unavailability of vaccines

65 immunization.IMPORTANCE African swine fever (ASF) is endemic in Africa, parts of the Trans Caucasus,

66 panding distribution of African swine fever (ASF) is threatening the pig industry worldwide.

67 is available to control African swine fever (ASF).

68 eveloped signs of acute African swine fever (ASF).

69 Finally, ASF/SF2-depleted cells released from a mitotic block dis

70 le helix (H38) known as the "A-site finger" (ASF).

71 ce colonized with altered Schaedler's flora (ASF).

72 hen inoculated with altered Schaedler flora (ASF), a defined consortium of 8 bacteria with minimal ur

73 foods, GF cookies using alfalfa seed flour (ASF), at different substitution levels to common rice fl

74 ession patterns in the apical surface fluid (ASF) from aberrantly differentiated squamous metaplastic

75 elite, professional American-style football (ASF) players.

76 trategy, we monitored the progress curve for ASF/SF2 phosphorylation in the absence and presence of a

77 is a macrophage-tropic virus responsible for ASF, a transboundary disease that threatens swine produc

78 en implicated in two independent studies for ASF; further research is warranted to identify the genes

79 Analysis of DNA from ASF/SF2-depleted cells revealed that the nontemplate str

80 lso specifically bound by hnRNP A1, hnRNP H, ASF/SF2 and SRp40, but not by 9G8.

81 hicken B-cell line that expresses only human ASF/SF2 controlled by a tetracycline-repressible promote

82 genes are functional homologues of the human ASF/SF2 alternative splicing factor and they indicate a

83 a strong structural similarity to the human ASF/SF2 splicing factor and to the Arabidopsis atSRp34/p

84 Thus, our results identify ASF/SF2 as a novel factor in the regulation of alternati

85 Cardiomyocytes deficient in ASF/SF2 display an unexpected hypercontraction phenotype

86 ture of selective phosphate incorporation in ASF/SF2, region-specific phosphorylation in the RS domai

87 n ICAD-L restored apoptotic DNA laddering in ASF/SF2-depleted cells.

88 have recently shown that a docking motif in ASF/SF2 specifically interacts with a groove in SRPK1, a

89 ucture led us to identify a docking motif in ASF/SF2.

90 Two N-terminal RNA recognition motifs in ASF/SF2 control access to the RS domain and guide the di

91 The relative increase in PP after PPVL in ASF and specific pathogen-free mice was not significantl

92 specific mapping of phosphorylation sites in ASF/SF2 as a function of the protein phosphatase PP1.

93 vels were increased approximately sixfold in ASF/SF2-depleted cells compared with cells expressing AS

94 rescued viral RNA expression and splicing in ASF/SF2-depleted cells is mediated through the phosphati

95 reover, in a murine model of hepatic injury, ASF transplantation was associated with decreased morbid

96 Activation of cells lacking ASF/SF2 through anti-immunoglobulin M-B-cell receptor cr

97 mulated the association of U1 snRNPs but not ASF/SF2 with substrate RNA.

98 ough the observed K(a) values for binding of ASF to the galectins and two truncated forms are only 50

99 n flanking sequences induce conformations of ASF/SF2 that increase the lifetime of phosphates in the

100 thway and reveal the central contribution of ASF/SF2-regulated CaMKIIdelta alternative splicing to fu

101 f exogenous PKCI-r mRNA in cells depleted of ASF/SF2.

102 Depletion of ASF/SF2 from the cells by tetracycline greatly decreased

103 We first show that in vivo depletion of ASF/SF2 results in a hypermutation phenotype likely due

104 es a specific region within the RS domain of ASF/SF2 by using a fully processive catalytic mechanism,

105 but, surprisingly, the effector RS domain of ASF/SF2 is dispensable for cell survival in MEFs.

106 n the N-terminal portion of the RS domain of ASF/SF2 while Clk/Sty was able to transfer phosphate to

107 t mass spectral analysis of the RS domain of ASF/SF2, a prototypical SR protein.

108 he N-terminal half of the basic RS domain of ASF/SF2, which is destined to be phosphorylated, is boun

109 hese data indicate a novel, direct effect of ASF/SF2 on PKCI-r mRNA stability.

110 topes shows that the first LacNAc epitope of ASF binds with approximately 6000-fold higher affinity t

111 Furthermore, the expression of ASF/SF2 reversed the silencing of exon IIIc caused by th

112 A is associated with increased expression of ASF/SF2.

113 3) fetuin (FET), the sialylated glycoform of ASF.

114 al for the recognition and nuclear import of ASF/SF2.

115 Furthermore, inactivation of ASF/SF2 also blocks DNA fragmentation normally induced b

116 Strikingly, inhibition of ASF/SF2 expression had no significant effect on PKCI-r s

117 Strikingly, siRNA-mediated knockdown of ASF/SF2 caused retention of HP1 proteins on mitotic chro

118 ification guides the nuclear localization of ASF/SF2.

119 Here we tested if the mechanism of ASF/SF2 phosphorylation by SRPK is evolutionarily conser

120 se results suggest that the docking motif of ASF/SF2 is a key regulatory element for sequential phosp

121 Phosphorylation of ASF/SF2 at a single site in the C-terminal end of the RS

122 s docking motif restricts phosphorylation of ASF/SF2 by SRPK1 to the N-terminal part of the RS domain

123 Strikingly, phosphorylation of ASF/SF2 is sensitive to changes in Tyr, but not Ser/Thr,

124 or stable association and phosphorylation of ASF/SF2.

125 t on splicing through the phosphorylation of ASF/SF2.

126 Surprisingly, in the presence of ASF, this remained low even at high galectin-3 concentra

127 een implicated in mRNA export, prevention of ASF/SF2 from shuttling had little impact on mRNA export.

128 ults support a model by which recruitment of ASF/SF2 to nascent transcripts by RNA polymerase II prev

129 coordination in the biological regulation of ASF/SF2 is unknown.

130 further show that Clk/Sty causes release of ASF/SF2 from speckles by phosphorylating the C-terminal

131 of the galectins for the first epitope(s) of ASF are in the nanomolar range, with a gradient of decre

132 ved the lethal challenge but showed signs of ASF.

133 ablates the interaction of either hnRNPA1 or ASF/SF2 with the repeat.

134 ut nine known glycan-based binding sites per ASF molecule.

135 The human SR (serine-arginine) protein ASF/SF2 relies on the processive phosphorylation of the

136 Here, we identify the RNA-binding protein ASF/SF2 as a critical, allele-specific, disease-relevant

137 t, mediated by the splice regulatory protein ASF/SF2.

138 The SR (arginine-serine rich) protein ASF/SF2 (also called human alternative splicing factor),

139 The prototypical SR protein ASF/SF2 (human alternative splicing factor) contains two

140 ne-serine (RS)-rich domain of the SR protein ASF/SF2 is phosphorylated by SR protein kinases (SRPKs)

141 ion of the RS domain (RS1) of the SR protein ASF/SF2, a modification that promotes nuclear entry of t

142 , which was predicted to bind the SR protein ASF/SF2.

143 describe a novel function for the SR protein ASF/SF2.

144 ide evidence that a prototypical SR protein, ASF/SF2, is unexpectedly required for maintenance of gen

145 a heart-specific knockout of one SR protein, ASF/SF2, produces cardiomyopathy and misregulation of sp

146 1 phosphorylates the model human SR protein, ASF/SF2.

147 The mammalian serine-arginine (SR) protein, ASF/SF2, contains multiple contiguous RS dipeptides at t

148 his, SELEX-binding sites for the SR proteins ASF/SF2, 9G8, and SRp20 were able to stimulate polyadeny

149 translational turnover of splicing regulator ASF/SF2, which directly binds and regulates these target

150 Indicative of a direct role, ASF/SF2 prevented R loop formation in a reconstituted in

151 SF2 (ASF) bound chemokine mRNA in unstimulated cells, whereas

152 n of complexes of TRAF5-TRAF2, Act1 and SF2 (ASF).

153 e C terminus of the splicing factor ASF/SF2 (ASF-CTD) and an RS domain deletion mutant protein (ASFDe

154 ife of CXCL1 mRNA, whereas depletion of SF2 (ASF) prolonged it.

155 Overexpression of SF2 (ASF) shortened the half-life of CXCL1 mRNA, whereas depl

156 TRAF2-TRAF5 and the RNA-binding protein SF2 (ASF).

157 mRNA in unstimulated cells, whereas the SF2 (ASF)-mRNA interaction was much lower after stimulation w

158 Significantly, compared to ASF/SF2, ASF-CTD increased the reaction rate during the early sta

159 SF2/ASF and another SR protein, SC35, are both able to stimu

160 SF2/ASF and SRp40 activate the ESE and are required for effi

161 SF2/ASF promotes translation initiation by suppressing the a

162 serine/arginine-rich splicing factor 1) (SF2/ASF, splicing factor 2/alternative splicing factor), an

163 ings identify for the first time that an SF2/ASF binding site also can serve as a 3' ss in a transcri

164 usly attributed either to the loss of an SF2/ASF-dependent exonic splicing enhancer or to the creatio

165 ne/arginine-rich (SR) proteins SRp20 and SF2/ASF and the CELF protein CUG-BP1.

166 ified as hnRNP A1, hnRNP H, hnRNP F, and SF2/ASF by site-specific cross-linking and immunoprecipitati

167 kidney cells demonstrated that SRp20 and SF2/ASF increase exon inclusion but that CUG-BP1 causes exon

168 ch (SR) proteins SC35, SRp40, SRp55, and SF2/ASF involved in alternative RNA splicing were predicted

169 The activities of hnRNP A1 and SF2/ASF on N1 splicing were examined by adding purified prot

170 ice sites, and tethering of hnRNP A1 and SF2/ASF proteins between competing splice sites mimicked the

171 nd that the relative ratios of SRp20 and SF2/ASF to CUG-BP1 in different cells determine the degree o

172 We identified binding of SRp20 and SF2/ASF to the exonic enhancers and CUG-BP1 to the exonic si

173 which are recognized by SC35, SRp55, and SF2/ASF) or GGTTGTTGAGG (nucleotides 27-37 from the 5' end,

174 otif (including PSF/SFPQ, Tra2-beta1 and SF2/ASF).

175 HPV16 infection upregulates hnRNP A1 and SF2/ASF, both key factors in alternative splicing regulation

176 CUGBP1, hnRNPH, hnRNPA1, hnRNPA2B1, and SF2/ASF.

177 he basis of their functional antagonism; SF2/ASF enhances U1 snRNP binding at all 5'SSs, the rise in

178 trate that hnRNP A/B proteins antagonize SF2/ASF-dependent ESE activity and promote exon 7 skipping b

179 An anti-SF2/ASF antibody specifically immunoprecipitates the approxi

180 (SR) protein SRSF1 (previously known as SF2/ASF) is a splicing regulator that also activates transla

181 s mediated by direct interaction between SF2/ASF and the primary miR-7 transcript to facilitate Drosh

182 Both SF2/ASF and hnRNPA1 control the selection of competing 5'-sp

183 the mTOR pathway in cells transformed by SF2/ASF and found that this splicing factor activates the mT

184 mTORC1 activation by SF2/ASF bypasses upstream PI3K/Akt signaling and is essentia

185 R by rapamycin blocked transformation by SF2/ASF in vitro and in vivo.

186 However, splicing activation by SF2/ASF is dependent on the N1 exon enhancer element whereas

187 21 and miR-222, may also be regulated by SF2/ASF through a similar mechanism.

188 which in SMN1 is recognized directly by SF2/ASF.

189 extract complemented by SC35 but not by SF2/ASF.

190 lates IL-2 production and that decreased SF2/ASF expression in SLE T cells contributes to deficient I

191 g RNA-mediated suppression of endogenous SF2/ASF and Tra2beta significantly reduces exon 10 splicing.

192 Exogenous SF2/ASF dramatically enhances normal exon 10 splicing and ef

193 (Ser2-P) RNAPII, and the splicing factor SF2/ASF at the minigene.

194 lar concentration of the splicing factor SF2/ASF augments the efficiency of NMD and ultimately shifts

195 ous work showed that the splicing factor SF2/ASF binds to this FP region and stimulates splicing of i

196 The splicing factor SF2/ASF is an oncoprotein that is up-regulated in many cance

197 Furthermore, splicing factor SF2/ASF ultraviolet (UV) cross-linked to the exon 2'/2 junct

198 ng factor 2/alternative splicing factor (SF2/ASF) enhances the expression of CD3zeta chain by limitin

199 ng factor 2/alternative splicing factor (SF2/ASF) expression in differentiated mouse erythroleukemia

200 ng factor 2/alternative splicing factor (SF2/ASF) to be important in the expression of CD3zeta chain.

201 ic overexpression of the splicing factor SF2/ASF.

202 e that the antagonistic splicing factors SF2/ASF and hnRNPA1 act as potent regulators of G alpha(s) i

203 y binds to FACT and the splicing factors SF2/ASF and U2AF65.

204 Here, we show that splicing factors SF2/ASF, Tra2beta, and a 50-kDa nuclear protein bind in vitr

205 Finally, SF2/ASF expression is up-regulated and correlates with exon

206 r results uncover an additional role for SF2/ASF and indicate that the efficiency of the pioneer roun

207 found multiple high score ESE motifs for SF2/ASF, SC35, and SRp40 in exon 3 of G alpha(s).

208 PI3K/Akt signaling and is essential for SF2/ASF-mediated transformation, as inhibition of mTOR by ra

209 Furthermore, SF2/ASF stimulates exon 16 inclusion in both in vitro comple

210 We confirmed that human SF2/ASF is methylated at residues R93, R97, and R109, which

211 ed TAP binding correlates with increased SF2/ASF binding, but not increased REF/Aly or Y14 binding.

212 iR-7) can form a negative feedback loop: SF2/ASF promotes miR-7 maturation, and mature miR-7 in turn

213 e-site mutations were smaller, had lower SF2/ASF motif scores, a decreased availability of decoy spli

214 The consequent decrease in nuclear SF2/ASF levels prevents it from modulating the alternative s

215 Consequently, depletion of SF2/ASF allowed exon 1B to splice to the distal 3' ss but ha

216 sitive charge regulate the activities of SF2/ASF and emphasizes the significance of localization cont

217 ggest that tissue-specific expression of SF2/ASF and hnRNPA1 governs the expression of alternative is

218 control the subcellular localization of SF2/ASF and that both the positive charge and the methylatio

219 s show that the C-terminal RS domains of SF2/ASF and Tra2beta are required for normal exon 10 splicin

220 These results underscore a function of SF2/ASF in pri-miRNA processing and highlight the potential

221 ature miR-7 in turn targets the 3'UTR of SF2/ASF to repress its translation.

222 activity is mediated by interactions of SF2/ASF with both mTOR and the phosphatase PP2A, two key reg

223 te Drosha cleavage and is independent of SF2/ASF's function in splicing.

224 ore importantly, we reveal a function of SF2/ASF, independent of T-cell receptor/CD3 signaling, where

225 ated residues regulate the properties of SF2/ASF.

226 esult in the cytoplasmic accumulation of SF2/ASF.

227 ncorporates information from both of our SF2/ASF-specific matrices and that accurately predicts the e

228 igenic potential of cells overexpressing SF2/ASF.

229 The SR protein SF2/ASF has been initially characterized as a splicing facto

230 The SR protein SF2/ASF is an oncoprotein that functions in pre-mRNA splicin

231 of mRNAs bound by the shuttling protein SF2/ASF.

232 ESEs in response to the human SR protein SF2/ASF.

233 ESEs responsive to the human SR proteins SF2/ASF, SC35, SRp40 and SRp55, and to predict whether exoni

234 tifs recognized by the human SR proteins SF2/ASF, SRp40, SRp55 and SC35.

235 -complementation assays with recombinant SF2/ASF.

236 e well-known exonic splicing regulators, SF2/ASF and hnRNP A1, to the splicing of an exon primarily c

237 trix, along with our previously reported SF2/ASF score matrix, was used to search the sequences of tw

238 Thus, we propose that SRp20, SF2/ASF, and CUG-BP1 act antagonistically to regulate IR alt

239 of two prototypical SR proteins, SRSF1 (SF2/ASF) and SRSF2 (SC35), using splicing-sensitive arrays a

240 A-processing: the splicing factor SRSF1 (SF2/ASF), the RNA helicase p68 (DDX5), and the heterogeneous

241 We previously characterized SRSF1 (SF2/ASF)-dependent exon skipping of the CaMKIIdelta gene dur

242 Cross-linking experiments show that SF2/ASF and hnRNP A1 compete to bind pre-mRNA, and we conclu

243 We have also provided evidence that SF2/ASF and hnRNPA1 play a role in 3'-splice site selection

244 Here we show that SF2/ASF and one of its upregulated microRNAs (miR-7) can for

245 The data suggest that SF2/ASF has both essential and regulatory roles, whereas Tra

246 Here we demonstrate that SF2/ASF levels are decreased in patients with SLE and more s

247 Here we demonstrate that SF2/ASF promotes translation initiation of bound mRNAs and t

248 Our results demonstrate that SF2/ASF regulates IL-2 production and that decreased SF2/ASF

249 ecular Cell, Michlewski et al. show that SF2/ASF, a splicing factor, stimulates translation initiatio

250 transcription factor transactivates the SF2/ASF promoter.

251 hen the 3' splice site is weak, both the SF2/ASF RS domain and U2AF(35) are required for splicing.

252 In contrast to Tra2beta, the SF2/ASF RS domain remains essential in the presence of a str

253 The abrogation of the SF2/ASF-dependent ESE is the basis for inefficient inclusion

254 In contrast to SF2/ASF and in agreement with other systems, hnRNP A1 repres

255 These findings suggest the model whereby SF2/ASF functions as an adaptor protein to recruit the signa

256 esults suggest that clinical tumors with SF2/ASF up-regulation could be especially sensitive to mTOR

257 er translation initiation complexes with SF2/ASF, translationally active ribosomes, and the translati

258 isolated several times independently, showed ASF/SF2-related differential expression.

259 preferentially interact with itself, SRp20, ASF/SF2, SRp55, and, to a slightly lesser extent, SC35.

260 he 2.9 A crystal structure of the core SRPK1:ASF/SF2 complex reveals that the N-terminal half of the

261 evated levels of RNA-binding proteins SRSF1 (ASF/SF2), SRSF9 (SRp30c), and HuR that are known to regu

262 cellular SR splicing factors (SRSFs) SRSF1 (ASF/SF2), SRSF2 (SC35), and SRSF3 (SRp20).

263 ex with its heterologous mammalian substrate ASF/SF2 and processively phosphorylates the same sites a

264 rylation on a specific SR protein substrate, ASF/SF2, is modulated by autophosphorylation but also th

265 rine/arginine-rich (SR) protein superfamily (ASF/SF2 and SC35) act antagonistically to regulate exon

266 two canonical members of the SR superfamily, ASF/SF2 and SRp75.

267 We demonstrate that ASF/SF2 and SC35 are each required for cell viability, b

268 Despite the fact that ASF-substituted GF cookies had inferior sensory attribut

269 cken B-cell line, DT40-ASF, we now show that ASF/SF2 inactivation results in a G2-phase cell cycle ar

270 We show for the first time that ASF/SF2 binds specifically to the 3'-UTR of CD3zeta and

271 report demonstrates for the first time that ASF/SF2 is required under physiological conditions for t

272 The ASF protrudes from the large subunit just above the A-si

273 he p32 protein, previously identified as the ASF/SF2 splicing factor-associated protein, copurified w

274 endent G-quadruplex structures that bind the ASF/SF2 protein.

275 etry, revealing 22 different proteins in the ASF from squamous NHTBE cells.

276 ntains 10 Psis and 6 are concentrated in the ASF helix (3 of the ASF Psis are conserved among eukaryo

277 etic depletion analysis that the Psis in the ASF helix and adjoining helices are not crucial for cell

278 analysis revealed 174 unique proteins in the ASF of squamous NHTBE cells compared with normal mucocil

279 are concentrated in the ASF helix (3 of the ASF Psis are conserved among eukaryotes).

280 Many of the ASF virus genes lack similarity to known genes and have

281 factor and they indicate a diversity of the ASF/SF2-like alternative splicing factors in monocot pla

282 The X-ray structure of the ASF/SF2-SRPK1 complex revealed several features of the c

283 Therefore, ASF/SF2, and perhaps other SR proteins, affects gene exp

284 These ASF proteins may be used to detect abnormal lesions in t

285 Three ASF/SF2-like alternative splicing genes from maize were

286 Thus, ASF/SF2 represents a new class of substrates that use un

287 doexon of a sequence selected for binding to ASF/SF2 or its replacement with beta-globin exon 2 only

288 Significantly, compared to ASF/SF2, ASF-CTD increased the reaction rate during the

289 training, promising results were limited to ASF and ATF primarily on 7q36.2 (including NOS3) in blac

290 lectin-3 mutant (R186S) that bound poorly to ASF but required much higher concentration ( approximate

291 Similar to ASF/SF2-like genes in other organisms, the maize pre-mRN

292 -mRNA substrate in the presence of Tra2beta, ASF/SF2 and SRp40, whereas hnRNP A1 specifically inhibit

293 onic splicing enhancers, each containing two ASF/SF2 (alternative splicing factor/splicing factor 2)

294 has only inhibitory activity, increased upon ASF/SF2 depletion.

295 Our results validate ASF/SF2 as a fundamental splicing regulator in the repro

296 f Fox allows hnRNP H1 to better compete with ASF/SF2 for binding to exon IIIc.

297 g the substitution levels of rice flour with ASF.

298 e also found that HP1 proteins interact with ASF/SF2 in mitotic cells.

299 Moreover, colonization of GF mice with ASF 2 days after PPVL led to a significant increase in i

300 raising the substitution levels of rice with ASF.