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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
18 eedback loop, in which on induction by AP-1, SAG promotes c-Jun ubiquitination and degradation, thus
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
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
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
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
38 , like ROC1/Rbx1/Hrt1, SAG binds to Cul1 and SAG-Cul1 complex has ubiquitin ligase activity to promot
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
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
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.
56 r define the interface between the bacterial SAG toxic shock syndrome toxin-1 (TSST-1) and the TCR, w
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
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
65 both plexinA1 and plexinA3 are expressed by SAG neurons, and plexinA1/plexinA3 double mutant mice sh
68 ties of Purkinje cells are also unchanged by SAG treatment, this lack of improvement in a region-spec
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
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
86 F receptor, CD74, is found on both embryonic SAG neurons and adult mouse spiral ganglion neurons.
96 lar canal formation, statoacoustic ganglion (SAG) development, and lateral line HC differentiation.
98 ak in the associated statoacoustic ganglion (SAG) neurons; both cell types can share a common lineage
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
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
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
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
124 hose of TCR-peptide/MHC complexes reveal how SAGs circumvent the normal mechanism for T cell activati
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
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
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
142 vertebrates, locally expressed Fgf initiates SAG development by inducing expression of Neurogenin1 (N
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
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
154 tes ED50=2.4+/-2.6, ED90=6.4+/-7.8 microgram SAG/mL; unresponsive isolates ED50=7.4+/-3.7 microgram S
161 reveal wide diversity in the architecture of SAG-dependent T-cell signaling complexes, which neverthe
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
173 mice show defects in afferent projections of SAG neurons similar to those observed in plexinA1/plexin
177 entifies NF1 as a physiological substrate of SAG-CUL1-FBXW7 E3 ligase and establishes a ubiquitin-dep
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
186 iated genes (SAGs), only a limited number of SAGs have been identified, and information regarding the
190 s adhesion to SAG, with less of an effect on SAG-mediated bacterial aggregation, an innate defense me
194 ue TCR binding orientation relative to other SAG-TCR complexes, which results in the alpha3-beta8 loo
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
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
204 teins (MIC-1 and MIC-2) or surface proteins (SAG-1 and SAG-2) during infection neutralized the marked
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
211 endochondral ossification, whereas sagittal (SAG) remain patent life time, although both are neural c
215 bers of hair cells in the inner ear, smaller SAGs, defects in semicircular canals, and abnormal neuro
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
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
234 equired for maximum stabilization of the TCR-SAG-MHC complex and that the alpha chain increases the h
239 in the secondary heart field and found that SAG-treated embryos exhibited a much milder increase in
243 g cultured lung cancer cells, we showed that SAG knockdown suppressed growth and survival, inactivate
246 n a TCR beta chain (mouse V beta8.2) and the SAG staphylococcal enterotoxin B (SEB) at 2.4 A resoluti
250 -related-sequence (SRS) fold observed in the SAG family of surface antigens found in Toxoplasma gondi
253 inhibition of canonical Wnt signaling in the SAG suture, upon treatment with Wnt antagonists results
257 evening, the RAG breakfast, but neither the SAG meal nor fasting, resulted in a more confused feelin
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
269 d by unaltered expression of a subset of the SAGs, and cytokinin, abscisic acid, and salicylic acid b
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
286 the X-ray crystal structures of the group V SAG staphylococcal enterotoxin K (SEK) alone and in comp
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
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
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