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 encodes a novel zinc RING finger protein that consis

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 h that a small increase in the affinity of a SAG for MHC can overcome a large decrease in the SAG's a

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

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

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

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

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

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

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

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

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

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

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

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

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

35 -1 and MIC-2) or surface proteins (SAG-1 and SAG-2) during infection neutralized the marked decrease

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

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

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

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

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

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

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

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

44 uring the physiological patterning of PF and SAG sutures.

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

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

47 at there is an interplay between TCR-SAG and SAG-MHC interactions in determining mitogenic potency, s

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

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

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

51 AG-1 but not the tachyzoite-specific antigen SAG-2 but are different from the cysts formed by avirule

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

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

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

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

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

57 Bacterial SAGs can be classified into five distinct evolutionary g

58 the three-dimensional structure of bacterial SAGs, and of their complexes with MHC class II molecules

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

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

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

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

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

64 ethylene were the strongest inducers of both SAGs and visible yellowing.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 (PCR) analysis included recently discovered SAGs.

82 DSC SAGs encode features not previously identified in Parcub

83 The DSC SAGs are also distinguished by relative greater abundanc

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

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

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

87 IDS, excluding a requirement for Mtv-encoded SAGs in the pathogenesis of this disorder.

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

89 properties of GaN microcrystals grown by ES-SAG.

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

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

92 Finally, SAG overexpression inhibited, whereas SAG siRNA silencin

93 th positive results in functional assays for SAG activity.

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

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

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

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

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

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

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

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

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

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

104 dopsis thaliana senescence-associated genes (SAGs) in attached and/or detached leaves was compared in

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

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

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

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

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

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

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

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

113 ata generated from single amplified genomes (SAGs).

114 of treatment with sodium antimony gluconate (SAG).

115 FN-gamma; n = 9), sodium antimony gluconate (SAG; n = 8), or amphotericin B lipid complex (ABLC; n =

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 aluate the actual contribution of individual SAG residues to stabilizing the beta-SEC3 complex, as we

138 Individual SAGs differed from the norms in different ways, however,

139 s varied more in their effects on individual SAGs.

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

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

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

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

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

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

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

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

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

149 Mechanistically, SAG appears to inhibit and/or delay metal ion-induced cy

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

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

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

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

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

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

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

157 Four new SAGs were isolated as part of this work, one of which sh

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

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

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

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

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

163 These studies open the way to the design of SAG variants with altered binding properties for TCR and

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

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

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

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

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

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

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

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

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

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

174 The role of SAG during embryogenesis remains unknown.

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

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

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

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

179 ate the relationship between the affinity of SAGs for TCR and MHC and their ability to activate T cel

180 simple relationship between the affinity of SAGs for the TCR and their biological activity: the tigh

181 ch toward the identification and analysis of SAGs.

182 istry, immunology, and structural biology of SAGs.

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

184 opose that there are five distinct groups of SAGs.

185 chment in light was also a strong inducer of SAGs, but not of visible yellowing.

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

187 extending the known TCR recognition site of SAGs.

188 SAGs and for TCR Vbeta domain specificity of SAGs.

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

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

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

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

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

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

195 lly unique relative to those formed by other SAGs.

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

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

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

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

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

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

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

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

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

205 e mesophile control, Chlamydomonas raudensis SAG 49.72.

206 ng site for its highly glycosylated receptor SAG.

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

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

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

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

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

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

213 features can not be addressed with a single SAG.

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

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

216 Some SAGs responded quickly to treatments, which may indicate

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

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

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

220 beta8.2Jbeta2.1Cbeta1) and the superantigen (SAG) staphylococcal enterotoxin C3 (SEC3) has been recen

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

222 Superantigens (SAGs) activate T cells by simultaneously binding the Vbe

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

224 Superantigens (SAGs) are a class of immunostimulatory proteins of bacte

225 Superantigens (SAGs) bind simultaneously to major histocompatibility co

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

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

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

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

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

231 find that there is an interplay between TCR-SAG and SAG-MHC interactions in determining mitogenic po

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

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

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

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

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

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

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

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

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

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

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

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

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

245 The SAG promoter activity, as measured by luciferase reporte

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

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

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

249 In the SAG and ABLC groups, levels of IFN-gamma and IL-10 mRNA

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

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

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

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

254 for MHC can overcome a large decrease in the SAG's affinity for the TCR.

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

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

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

258 cysteines which are also found in all of the SAG and SRS proteins of T. gondii.

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

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

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

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

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

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

265 , 44, and 81 showed strong inhibition of the SAG-induced Hedgehog signaling activation in NIH3T3 Shh-

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

267 ithelium prefigure their position within the SAG.

268 Most of the SAGs responded to most of the treatments in a similar fa

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

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

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

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

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

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

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

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

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

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

279 reductions in streptococcal cell adhesion to SAG and to two strains of A. naeslundii were observed wh

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 lows: hypoxia induces HIF-1 to transactivate SAG.

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

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

285 uced levels was significantly increased upon SAG silencing.

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

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

288 domain specificity of SEK and other group V SAGs.

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

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

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

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

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

294 reby providing a basis for understanding why SAGs having other residues at these positions show diffe

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 om a well-characterized CD4 T cell line with SAGs by mutational analysis of its Vbeta domain.