ライフサイエンスコーパス: SAG

1 SAG (sensitive to apoptosis gene) or ROC2/RBX2 is the se

2 SAG (sensitive to apoptosis gene) was cloned as an induc

3 SAG (sensitive to apoptosis gene) was first identified a

4 SAG (Sensitive to Apoptosis Gene), also known as RBX2 or

5 SAG and MAG patients were propensity matched using 38 ba

6 SAG is highly conserved during evolution, with identitie

7 SAG is localized in both the cytoplasm and the nucleus o

8 SAG protected cells from hypoxia-induced apoptosis when

9 SAG transactivation required both the intact binding sit

10 SAG was later found to be the second family member of RO

11 SAG-CUL5, but not RBX1-CUL1, negatively modulates beta-T

12 SAG/RBX2 and RBX1 are two family members of RING compone

13 SAG/RBX2/ROC2 protein is an essential RING component of

14 SAG:kn1 tobacco plants showed a marked delay in leaf sen

15 SAGs bypass normal antigen presentation by binding to cl

16 SAGs have been implicated in toxic shock syndrome and fo

17 7.4+/-3.7 microgram SAG/mL, ED90=29.1+/-11.1 SAG/mL.

18 eedback loop, in which on induction by AP-1, SAG promotes c-Jun ubiquitination and degradation, thus

19 These results suggest an HIF-1-SAG feedback loop in response to hypoxia, as follows: hy

20 Thus, AP-1/SAG establishes an autofeedback loop, in which on induct

21 Fs), UiO-66-X, X = SAG, NH-SAG, (NH-SAG)(2) (SAG: sulfonic acid groups), which have sub-1-nm windows

22 AG channels, and ~15 times of that of UiO-66@SAG channels.

23 II to the host receptor salivary agglutinin (SAG) were identified by surface plasmon resonance (SPR).

24 tooth surface receptor salivary agglutinin (SAG), as monitored by surface plasmon resonance, indicat

25 nal epitopes as well as salivary agglutinin (SAG)-binding activity.

26 Salivary agglutinin [SAG, encoded by the deleted in malignant brain tumors 1

27 n response to the hedgehog signaling agonist SAG, while myocardial differentiation and migration were

28 naling in response to the Smoothened agonist SAG and also inhibits signaling induced by an oncogenic

29 ant human SHH (rhShh) or smoothened agonist (SAG) increased levels of Ptch1, Gli1, Gli2, Gli3, Hes1 a

30 stration of Shh mimetic, smoothened agonist (SAG) restored BBB integrity and also abated the neuropat

31 d mice were treated with Smoothened Agonist (SAG), a Sonic Hedgehog (Shh) mimetic in order to fortify

32 s effectively as the known Smo full agonist, SAG.

33 gnaling ligand (recombinant Shh) or agonist, SAG and purmorphamine, prevented the induction of autoph

34 an impaired response to Smoothened agonist, SAG.

35 Interestingly, Smoothened agonist-SAG rescued OAF cell proliferation and osteogenic differ

36 l expression of certain Valpha regions among SAG-reactive T cells has suggested that the TCR alpha ch

37 Detection of an SAG gene by PCR correlated with positive results in func

38 -1 and MIC-2) or surface proteins (SAG-1 and SAG-2) during infection neutralized the marked decrease

39 and beta-TrCP1 are inversely correlated, and SAG-CUL5-betaTrCP1 forms a complex under physiological c

40 PAX6, CHML, and RDH11 at 7 weeks and CRX and SAG at 16 weeks.

41 , like ROC1/Rbx1/Hrt1, SAG binds to Cul1 and SAG-Cul1 complex has ubiquitin ligase activity to promot

42 ng-induced chlorophyll loss, cell death, and SAG expression were delayed in the pad4 mutant.

43 ls treatment with recombinant Shh ligand and SAG, both Hh pathway agonists, stimulated HCV replicatio

44 sought to compare intermediate-term MAG and SAG outcomes with enhanced matching to reduce selection

45 mortality difference between matched MAG and SAG patients (2.4% vs. 2.2%, adjusted hazard ratio [AHR]

46 mposite outcome were similar between MAG and SAG patients at 1 year, but lower for MAG after 7 years.

47 Using the currently available SAG-MHC and SAG-TCR complex structures, models of various trimolecul

48 Several new structures of SAG-MHC and SAG-TCR complexes have significantly increased understan

49 Importantly, the fate of PF and SAG sutures can be reversed by manipulating Wnt signalin

50 uring the physiological patterning of PF and SAG sutures.

51 RBX1 and SAG are both overexpressed in human lung cancer; however

52 ation (P<.001) between clinical response and SAG sensitivity in vitro was observed only when strains

53 tigens, termed the surface antigen (SAG) and SAG-related surface antigens, that are developmentally r

54 to the family of surface antigens (SAGs) and SAG-related sequences of Toxoplasma gondii.

55 e propose the catalytic mechanism of SGE and SAG formation and that SA binds to the active site in tw

56 uncated splice variant of retinal S-antigen (SAG), known as regulators of the visual phototransductio

57 urface antigens, termed the surface antigen (SAG) and SAG-related surface antigens, that are developm

58 homology to the family of surface antigens (SAGs) and SAG-related sequences of Toxoplasma gondii.

59 Using the currently available SAG-MHC and SAG-TCR complex structures, models of variou

60 r define the interface between the bacterial SAG toxic shock syndrome toxin-1 (TSST-1) and the TCR, w

61 Bacterial SAGs can be classified into five distinct evolutionary g

62 which is unique relative to other bacterial SAGs owing to its structural divergence and its stringen

63 ed group of SAGs are the pyrogenic bacterial SAGs, which utilize a high degree of genetic variation o

64 Detailed biochemical difference between SAG and RBX1, and whether SAG mediates cross-talk betwee

65 ansferase (SA GTase) capable of forming both SAG and GS was purified, characterized, and partially se

66 MIF acts as a neurotrophin in promoting both SAG directional neurite outgrowth and neuronal survival

67 both plexinA1 and plexinA3 are expressed by SAG neurons, and plexinA1/plexinA3 double mutant mice sh

68 Furthermore, cell death induced by SAG deletion was accompanied by cell enlargement and abn

69 Importantly, growth suppression by SAG knockdown was partially rescued by simultaneous knoc

70 ties of Purkinje cells are also unchanged by SAG treatment, this lack of improvement in a region-spec

71 ses for high-affinity peptide/MHC binding by SAGs and for TCR Vbeta domain specificity of SAGs.

72 V beta families, as well as why only certain SAGs bind mouse V beta8.2.

73 s similarities seen with other characterized SAGs, although the CDR3 loop of Vbeta2.1 is probably inv

74 uditory systems and promotes mouse and chick SAG neurite outgrowth and neuronal survival, demonstrati

75 mediating redox-induced apoptosis, we cloned SAG, an evolutionarily conserved zinc RING finger gene t

76 op as well as with two universally conserved SAG residues (Leu(137) and Tyr(144) in TSST-1).

77 Consistently, SAG siRNA silencing reduced c-Jun polyubiquitination and

78 amination, nor has the mechanism controlling SAG delamination been elucidated.

79 omic information is retrieved from different SAGs, generating co-assembly that features >74% of genom

80 o the basis for the specificity of different SAGs for particular TCR beta chains, and for the observe

81 ur study, for the first time, differentiates SAG and RBX1 biochemically via their respective binding

82 p of Vbeta2.1 is probably involved in direct SAG-TCR molecular interactions, possibly contributing to

83 (PCR) analysis included recently discovered SAGs.

84 DSC SAGs encode features not previously identified in Parcub

85 The DSC SAGs are also distinguished by relative greater abundanc

86 Our results show that each SAG has a different, independent bias, yielding differen

87 tor cysteine-rich (SRCR) domains within each SAG molecule.

88 F receptor, CD74, is found on both embryonic SAG neurons and adult mouse spiral ganglion neurons.

89 Consistently, endogenous SAG is induced by 12-O-tetradecanoylphorbol-13-acetate (

90 properties of GaN microcrystals grown by ES-SAG.

91 utionary Selection Selective Area Growth (ES-SAG) has been proposed.

92 Finally, SAG forms in vivo complex with Cul-5 and VHL under hypox

93 Finally, SAG overexpression inhibited, whereas SAG siRNA silencin

94 th positive results in functional assays for SAG activity.

95 We report a critical role for SAG in controlling vascular and neural development by mo

96 Furthermore, SAG mainly binds to E2s UBCH10 and UBE2S known to mediat

97 Sul (CDS), Santo Augusto (STA), Sao Gabriel (SAG), and Vacaria (VAC).

98 lar canal formation, statoacoustic ganglion (SAG) development, and lateral line HC differentiation.

99 Statoacoustic ganglion (SAG) neurons project sensory afferents to appropriate ta

100 ak in the associated statoacoustic ganglion (SAG) neurons; both cell types can share a common lineage

101 e outgrowth from the statoacoustic ganglion (SAG) to the developing inner ear.

102 Neurons of the Statoacoustic Ganglion (SAG), which innervate the inner ear, originate as neurob

103 box 1 (RBX1) or sensitive to apoptosis gene (SAG), also known as RBX2, for activity.

104 Sensitive to apoptosis gene (SAG)/regulator of cullins-2-Skp1-cullin-F-box protein (S

105 d levels of some senescence-associated gene (SAG) transcripts as well as heightened salicylic acid le

106 The sustained activated genes (SAGs) included established pro-inflammatory signaling co

107 e expression of SENESCENCE ASSOCIATED GENES (SAGs), all hallmarks of leaf senescence.

108 p-regulation of senescence-associated genes (SAGs), ethylene and jasmonic acid biosynthetic genes, AP

109 oyed to isolate senescence-associated genes (SAGs), only a limited number of SAGs have been identifie

110 e expression of senescence-associated genes (SAGs).

111 The assembly of single-amplified genomes (SAGs) and metagenome-assembled genomes (MAGs) has led to

112 were recovered as single amplified genomes (SAGs) and metagenome-assembled genomes (MAGs).

113 eads from multiple Single Amplified Genomes (SAGs) belonging to evolutionary closely related cells.

114 e created over 900 single amplified genomes (SAGs) from 8 Tara Ocean samples across the Indian Ocean

115 d 12 Parcubacteria single amplified genomes (SAGs) from sediment samples collected within the Challen

116 examined 127 single-cell amplified genomes (SAGs) from uncultivated SUP05 bacteria isolated from a m

117 re analysed 3 single-cell amplified genomes (SAGs) of the choanoflagellate Monosiga brevicollis, whos

118 ilot library of 11 single amplified genomes (SAGs) was constructed from Gulf of Maine bacterioplankto

119 ata generated from single amplified genomes (SAGs).

120 of treatment with sodium antimony gluconate (SAG).

121 cts: UGT74F1 forms salicylic acid glucoside (SAG), while UGT74F2 forms primarily salicylic acid gluco

122 es primarily as the SA 2-O-beta-D-glucoside (SAG) and glucosyl salicylate (GS).

123 particular salivary agglutinin glycoprotein (SAG or gp340), and with ligands on other oral bacteria.

124 SAG family is as extensive as the T. gondii SAG family remains unresolved, but it is probable that a

125 re that has been described for the T. gondii SAGs, and each was predicted to have an amino-terminal s

126 e, we propose a Stochastic Average Gradient (SAG) fine-grained alignment method for optimizing the su

127 grafts (MAGs) versus single arterial grafts (SAGs) for patients with multivessel disease undergoing c

128 aled that the Streptococcus anginosus group (SAG) organisms may be important pathogens in pediatric p

129 On the other hand, SAG seemed to modulate the c-Jun levels.

130 ce exacerbates the problem of discerning how SAG acts to improve learning and memory.

131 hose of TCR-peptide/MHC complexes reveal how SAGs circumvent the normal mechanism for T cell activati

132 However, SAG combined with FGF2 potentiated the formation of MGPC

133 Indeed, like ROC1/Rbx1/Hrt1, SAG binds to Cul1 and SAG-Cul1 complex has ubiquitin lig

134 In cultured HSCs, SAG (an Hh agonist) up-regulated, whereas cyclopamine (a

135 d disruption of ySAG, yeast homolog of human SAG, and subsequent tetrad analysis revealed that ySAG i

136 Bacterially expressed and purified human SAG binds to zinc and copper metal ions and prevents lip

137 Importantly, SAG was found to be the second family member of Rbx (RIN

138 ay, strongly reducing luciferase activity in SAG treated NIH3T3 Shh-Light II cells, and inhibited the

139 led by an increase in chlorophyll content in SAG:kn1 leaves relative to leaves of the control plants

140 e sequencing to accurately correct errors in SAG reads, even from ultra-low coverage regions.

141 ablishment of proper afferent projections in SAG neurons, and this signaling likely occurs through a

142 generate appropriate afferent projections in SAG neurons; however, the ligands and coreceptors involv

143 ted in some 100-cell MDA products but not in SAGs, demonstrating that organisms containing bacterioch

144 Induced SAG then promotes HIF-1alpha ubiquitination and degradat

145 h SAG and BMP2 and found that BMP2 inhibited SAG-induced proliferation.

146 vertebrates, locally expressed Fgf initiates SAG development by inducing expression of Neurogenin1 (N

147 Through this interaction, SAGs activate T cells at orders of magnitude above antig

148 Interestingly, SAG expression increased tumor size, not because of acce

149 ue-restricted Ags, CHRNA1, GAD1, PLP1, KLK3, SAG, TG, and TSHR, was reduced.

150 that, besides important current limitations, SAGs can still provide interesting and novel insights fr

151 n overexpressed in several human cell lines, SAG protects cells from apoptosis induced by redox agent

152 This means SAG data can be used to perform accurate phylogenomic an

153 TPA-mediated SAG induction was significantly reduced in JB6-Cl.41 cel

154 present a model of the TSST-1-dependent MHC-SAG-TCR T-cell signaling complex that is structurally an

155 ructures, models of various trimolecular MHC-SAG-TCR complexes may be constructed that reveal wide di

156 responsive isolates ED50=7.4+/-3.7 microgram SAG/mL, ED90=29.1+/-11.1 SAG/mL.

157 tes ED50=2.4+/-2.6, ED90=6.4+/-7.8 microgram SAG/mL; unresponsive isolates ED50=7.4+/-3.7 microgram S

158 inding sites in a 1.3-kb region of the mouse SAG promoter.

159 Whether the S. neurona SAG family is as extensive as the T. gondii SAG family r

160 ~70, which are ~3 times of that of UiO-66-NH-SAG channels, and ~15 times of that of UiO-66@SAG channe

161 Particularly, the UiO-66-(NH-SAG)(2) channels exhibit ultrahigh proton selectivities,

162 works (MOFs), UiO-66-X, X = SAG, NH-SAG, (NH-SAG)(2) (SAG: sulfonic acid groups), which have sub-1-nm

163 nic frameworks (MOFs), UiO-66-X, X = SAG, NH-SAG, (NH-SAG)(2) (SAG: sulfonic acid groups), which have

164 Our results reveal a novel SAG/MHCII/TCR architecture in which vSAGs coerce a near-

165 oves both accuracy and contiguity of de novo SAG assemblies.

166 In control mice, sensory afferents of SAG neurons terminate at the vestibular sensory patches,

167 reveal wide diversity in the architecture of SAG-dependent T-cell signaling complexes, which neverthe

168 ere we report functional characterization of SAG by the use of yeast genetics approach.

169 combinant protein catalyzed the formation of SAG and GS, and exhibited a broad specificity to simple

170 Consistently, chemical inducers of SAG reduced beta-TrCP1 level.

171 Hypoxia induction of SAG was largely HIF-1alpha dependent.

172 cence was also delayed in detached leaves of SAG:kn1 plants.

173 Here we report that the levels of SAG and beta-TrCP1 are inversely correlated, and SAG-CUL

174 gh frequency of SEG/SEI and a high number of SAG genes per bacterium.

175 Here, we report that overexpression of SAG, but not RBX1, correlates with poor patient prognosi

176 n, underscoring the therapeutic potential of SAG in controlling HAND pathogenesis.

177 mice show defects in afferent projections of SAG neurons in the inner ear.

178 mice show defects in afferent projections of SAG neurons similar to those observed in plexinA1/plexin

179 The role of SAG during embryogenesis remains unknown.

180 ited upon small interfering RNA silencing of SAG or ROC1.

181 Several new structures of SAG-MHC and SAG-TCR complexes have significantly increas

182 entifies NF1 as a physiological substrate of SAG-CUL1-FBXW7 E3 ligase and establishes a ubiquitin-dep

183 t beta-TrCP1 is a physiological substrate of SAG-UBCH10C/UBE2S.

184 ch toward the identification and analysis of SAGs.

185 istry, immunology, and structural biology of SAGs.

186 NA demethylation regulates the expression of SAGs and thus leaf senescence remain elusive.

187 The best-characterized group of SAGs are the pyrogenic bacterial SAGs, which utilize a h

188 opose that there are five distinct groups of SAGs.

189 iated genes (SAGs), only a limited number of SAGs have been identified, and information regarding the

190 In contrast, in dml3 the promoters of SAGs were hypermethylated and their transcript levels we

191 body or 3' UTR regions to activate a set of SAGs.

192 extending the known TCR recognition site of SAGs.

193 SAGs and for TCR Vbeta domain specificity of SAGs.

194 observed influence of the TCR alpha chain on SAG reactivity.

195 s adhesion to SAG, with less of an effect on SAG-mediated bacterial aggregation, an innate defense me

196 egions of AgI/II adhere to distinct sites on SAG.

197 e appears to be strong selective pressure on SAGs to maintain binding to diverse T cells.

198 tes the G(q) pathway, possibly via EAT-16 or SAG-1.

199 ue TCR binding orientation relative to other SAG-TCR complexes, which results in the alpha3-beta8 loo

200 lly unique relative to those formed by other SAGs.

201 ds in a markedly different way than do other SAGs.

202 Our SAG fine-grained alignment algorithm is much faster than

203 When overexpressed, SAG remarkably reduced both basal and TPA-induced c-Jun

204 roEL and GroEL/GroES complexes, our parallel SAG-based fine-grained alignment can achieve higher prec

205 Bank (PDB ID:1KP8) showed that our parallel SAG-based fine-grained alignment method could achieve cl

206 that surface antigen proteins, in particular SAG-1, of Toxoplasma gondii are important to this parasi

207 etermine whether BMP signaling could prevent SAG-induced proliferation, we treated explants with SAG

208 und that outflow tract co-cultures prevented SAG-induced proliferation.

209 he Arabidopsis senescence-inducible promoter SAG (senescence associated gene)12 was observed during e

210 mouse epidermis driven by the K14 promoter, SAG inhibited TPA-induced c-Jun levels and activator pro

211 G proteins, and thus we named these proteins SAG-unrelated surface antigens (SUSA).

212 teins (MIC-1 and MIC-2) or surface proteins (SAG-1 and SAG-2) during infection neutralized the marked

213 e mesophile control, Chlamydomonas raudensis SAG 49.72.

214 follow-up 6.5 years) for patients receiving SAGs and MAGs.

215 ng site for its highly glycosylated receptor SAG.

216 and the transcript abundances of the related SAGs in WT.

217 In undamaged retinas, SAG or rhShh had no apparent effect upon the Muller glia

218 he other hand, like its family member, ROC1, SAG promoted VHL-mediated HIF-1alpha ubiquitination and

219 ulation of free and glucoside-conjugated SA (SAG) in response to pathogen infection is compromised in

220 ion of three distinct interactions: TCR-SAG, SAG-MHC, and MHC-TCR.

221 endochondral ossification, whereas sagittal (SAG) remain patent life time, although both are neural c

222 also confirm that the co-assembly of several SAGs improves the general genomic recovery.

223 features can not be addressed with a single SAG.

224 fast high in either rapidly (RAG) or slowly (SAG) available glucose.

225 bers of hair cells in the inner ear, smaller SAGs, defects in semicircular canals, and abnormal neuro

226 Additional in vitro experiments suggested SAG treatment was not associated with the establishment

227 lysis of Staphylococcus aureus superantigen (SAG) genes was undertaken in isolates from a major hospi

228 receptor (TCR) to a bacterial superantigen (SAG) results in stimulation of a large population of T c

229 Superantigens (SAGs) aberrantly alter immune system function through si

230 Superantigens (SAGs) are a class of immunostimulatory and disease-causi

231 Superantigens (SAGs) bind simultaneously to major histocompatibility co

232 Superantigens (SAGs) elicit massive T-cell proliferation through simult

233 Superantigens (SAGs) interact with host immune receptors to induce a ma

234 isease is caused by bacterial superantigens (SAGs) secreted from Staphylococcus aureus and group A st

235 o binding sites for bacterial superantigens (SAGs): a low-affinity site on the alpha chain and a high

236 ung tumorigenesis and suggest that targeting SAG-CRL E3 ligases may be an effective therapeutic appro

237 bination of three distinct interactions: TCR-SAG, SAG-MHC, and MHC-TCR.

238 measured, producing an energy map of the TCR-SAG interaction.

239 equired for maximum stabilization of the TCR-SAG-MHC complex and that the alpha chain increases the h

240 Thus, the overall stability of the TCR-SAG-MHC complex is determined by the combination of thre

241 interacts with the MHC beta chain in the TCR-SAG-MHC complex.

242 Here we demonstrate that SAG, a chlorobenzothiophene-containing Hh pathway agonis

243 We found that SAG is overexpressed in murine KrasG12D-driven lung tumo

244 in the secondary heart field and found that SAG-treated embryos exhibited a much milder increase in

245 We report here that SAG was subjected to hypoxia induction at the levels of

246 We report here that SAG/ROC2/Rbx2 is a novel transcriptional target of activ

247 Results indicate that SAG treatment reduced viral burden in the CNS immediatel

248 g cultured lung cancer cells, we showed that SAG knockdown suppressed growth and survival, inactivate

249 Previous studies showed that SAG prefers to bind with CUL5, as well as CUL1, whereas

250 The SAG promoter activity, as measured by luciferase reporte

251 n a TCR beta chain (mouse V beta8.2) and the SAG staphylococcal enterotoxin B (SEB) at 2.4 A resoluti

252 the association of sequence diversity at the SAG-binding gene of S. mutans, and DMBT1 CNV.

253 hol had been drunk the previous evening, the SAG meal resulted in better memory.

254 -related-sequence (SRS) fold observed in the SAG family of surface antigens found in Toxoplasma gondi

255 Two of five flavobacteria in the SAG library contained proteorhodopsin genes, suggesting

256 inhibition of canonical Wnt signaling in the SAG suture phenocopies craniosynostosis.

257 inhibition of canonical Wnt signaling in the SAG suture, upon treatment with Wnt antagonists results

258 Instead, the SAG gene family is a common trait that presumably has an

259 a chain through a zinc bridge that links the SAG and class II molecules.

260 evening, the RAG breakfast, but neither the SAG meal nor fasting, resulted in a more confused feelin

261 TG was identified in the first intron of the SAG gene.

262 tra hair cells, whereas morphogenesis of the SAG is adversely affected to different degrees.

263 he interface occurs in a novel region of the SAG molecule.

264 This new member of the SAG superfamily was designated SporoSAG.

265 onical Wnt signaling, whereas patency of the SAG suture is achieved by constantly activated canonical

266 ion requires simultaneous interaction of the SAG with the V beta domain of the T cell receptor (TCR)

267 , 44, and 81 showed strong inhibition of the SAG-induced Hedgehog signaling activation in NIH3T3 Shh-

268 to be GPI anchored but are unrelated to the SAG proteins, and thus we named these proteins SAG-unrel

269 ithelium prefigure their position within the SAG.

270 d by unaltered expression of a subset of the SAGs, and cytokinin, abscisic acid, and salicylic acid b

271 Most of the SAGs, apart from alphaproteobacteria, were phylogenetica

272 Many of these SAGs are closely related to environmental sequences obta

273 We have also cloned three SAGs from randomly selected enhancer trap lines, demonst

274 ive cross-talk between CRL5 and CRL1 through SAG mediated ubiquitylation of beta-TrCP1.

275 Thus, SAG appears to control cell cycle progression in yeast b

276 Thus, SAG is a cellular protective molecule that appears to ac

277 Thus, SAG, in a manner depending on the availability of F-box

278 In human tissues, SAG is ubiquitously expressed at high levels in skeletal

279 on that could inhibit S. mutans adherence to SAG was also confirmed to be within the C(1) and C(2) do

280 ncreased inhibition of S. mutans adhesion to SAG, with less of an effect on SAG-mediated bacterial ag

281 e functional contribution of TCR residues to SAG recognition, binding by 24 single-site alanine subst

282 al loss of a Thm1 allele impairs response to SAG.

283 lows: hypoxia induces HIF-1 to transactivate SAG.

284 HIF-1 bound to this site and transactivated SAG expression.

285 s well as G2/M checkpoint control genes upon SAG withdrawal.

286 uced levels was significantly increased upon SAG silencing.

287 the X-ray crystal structures of the group V SAG staphylococcal enterotoxin K (SEK) alone and in comp

288 Group V SAGs are characterized by the alpha3-beta8 loop, a uniqu

289 domain specificity of SEK and other group V SAGs.

290 In vivo, SAG-treated embryos showed up-regulated BMP2 expression

291 nally, SAG overexpression inhibited, whereas SAG siRNA silencing enhanced, respectively, the TPA-indu

292 basal and TPA-induced c-Jun levels, whereas SAG small interfering RNA (siRNA) silencing increased su

293 potentiated the formation of MGPCs, whereas SAG combined with IGF1 stimulated the nuclear migration

294 difference between SAG and RBX1, and whether SAG mediates cross-talk between CRL5 and CRL1 are previo

295 e ySAG deletion is fully rescued by wildtype SAG, but not by several hSAG mutants.

296 Treatment of chick embryos with SAG at HH14, just before the peak in secondary heart fie

297 uced proliferation, we treated explants with SAG and BMP2 and found that BMP2 inhibited SAG-induced p

298 mice was rescued by a single treatment with SAG, an agonist of the Sonic hedgehog pathway, administe

299 rebellar morphology following treatment with SAG.

300 tal-organic frameworks (MOFs), UiO-66-X, X = SAG, NH-SAG, (NH-SAG)(2) (SAG: sulfonic acid groups), wh