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 is an SR protein splicing factor that participat

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

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

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

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

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

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

12 In 2020, ASF presents an acute and global animal health emergency

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 d effective vaccines to protect pigs against ASF has been hindered by lack of understanding of the co

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

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

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

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

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

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

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

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

34 haScreen signal by competing with the biotin-ASF.

35 A mathematical model of the wild boar ASF system is developed that captures the observed drop

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

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

38 left ventricular remodeling among collegiate ASF athletes.

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

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

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

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

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

44 odified virus were protected from developing ASF after challenge with the virulent parental virus.

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

48 ion from the phase-viscosity map to expected ASF flood test performance in micromodels.

49 ltaI177L is a novel efficacious experimental ASF vaccine protecting pigs from the epidemiologically r

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

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

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

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

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

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

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

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

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

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

60 African swine fever (ASF) is a devastating disease for domestic pigs.

61 African swine fever (ASF) is a severe viral disease that is currently spreadi

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

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

64 any available vaccines, African swine fever (ASF) outbreak containment relies on the control and cull

65 replication.IMPORTANCE African swine fever (ASF) poses a major threat to pig populations and food se

66 iota composition of the African swine fever (ASF) resistant warthogs (Phacochoerus africanus) from Af

67 tive vaccine to control African swine fever (ASF), and therefore, efficient disease control is depend

68 developed acute forms of acute swine fever (ASF).

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

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

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

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

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

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

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

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

77 importance of including animal source food (ASF) in diets to improve growth.

78 ould strictly avoid all animal source foods (ASF) and skip breakfast at least up to lunch time.

79 uma associated with American-style football (ASF) has been linked to brain pathology, along with phys

80 American-style football (ASF) has gained attention because of possible links betw

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

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

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

84 A survey of 3,913 former ASF players aged 24 to 89 was conducted for those who re

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

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

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

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

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

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

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

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

93 ed to determine the potential involvement in ASF resistance.

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

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

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

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

98 and the persistence of the virus observed in ASF outbreaks.

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

100 c encephalopathy (CTE) have been reported in ASF players, there are currently no established premorte

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

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

103 ission from individuals that survive initial ASF infection but eventually succumb to the disease are

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

105 ffect of breakfast skipping and avoidance of ASF for 55 days.

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

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

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

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

110 to inform decisions related to the design of ASF virus surveillance strategies in the US.

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

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

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

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

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

116 ere is no study that evaluated the effect of ASF fasting (avoidance of animal source foods and breakf

117 re research should investigate the effect of ASF fasting and breakfast skipping on micronutrient inta

118 ramatic change in the global epidemiology of ASF has resulted in concerns that the disease may contin

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

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

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

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

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

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

125 dy, we estimated the risk of introduction of ASF virus into the US through smuggling of pork in air p

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

127 ification guides the nuclear localization of ASF/SF2.

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

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

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

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

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

133 or stable association and phosphorylation of ASF/SF2.

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

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

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

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

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

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

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

141 ved the lethal challenge but showed signs of ASF.

142 Wild boar play a key role in the spread of ASF, yet despite their significance, little is known abo

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

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

145 ation density and in some situations prevent ASF from establishing in a population.

146 mptomatic head trauma in former professional ASF players and other contact sport athletes.

147 Sixty-six retired professional ASF players aged 29 to 75 years completed a health and w

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

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

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

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

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

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

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

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

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

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

158 1 phosphorylates the model human SR protein, ASF/SF2.

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

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

161 lkali-surfactant-foam enhanced oil recovery (ASF EOR) of heavy oil is affected by emulsion formation.

162 ly occasional incursions into other regions, ASF began spreading into Caucasian countries and Eastern

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

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

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

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

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

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

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

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

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

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

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

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

175 SF2/ASF promotes translation initiation by suppressing the a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 21 and miR-222, may also be regulated by SF2/ASF through a similar mechanism.

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

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

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

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

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

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

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

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

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

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

208 ic overexpression of the splicing factor SF2/ASF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 ated residues regulate the properties of SF2/ASF.

230 esult in the cytoplasmic accumulation of SF2/ASF.

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

232 igenic potential of cells overexpressing SF2/ASF.

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

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

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

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

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

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

239 -complementation assays with recombinant SF2/ASF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

264 We hypothesized that ASF-related symptomatic head trauma would predict worse

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

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

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

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

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

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

271 nsight into the key processes that drive the ASF dynamics and show that environmental transmission is

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

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

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

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

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

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

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

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

280 equencing technology in combination with the ASF-FAST software for the purpose of rapid and real-time

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

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

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

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

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

286 ess if these variations confer resilience to ASF we established an intranasal challenge model with a

287 found in warthog RELA were not resilient to ASF but a delay in onset of clinical signs and less vira

288 core microbiota from warthogs (resistant to ASF) and pigs (susceptible to ASF) showed 45 shared OTUs

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

290 (resistant to ASF) and pigs (susceptible to ASF) showed 45 shared OTUs, while 6 OTUs were exclusivel

291 n swine fever fast analysis sequencing tool (ASF-FAST), the analysis of output data was performed in

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

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

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

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

296 g the substitution levels of rice flour with ASF.

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

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

299 etected it in lymphoid tissue from pigs with ASF.

300 raising the substitution levels of rice with ASF.