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1                                              Ets DNA binding, selectivity, and regulation have been e
2                                              Ets family transcription factors regulate many aspects o
3                                              Ets homologous factor (EHF) is a key member of the trans
4                                              Ets homologous factor (EHF) is an Ets family transcripti
5                                              Ets Related Gene (ERG) is a component of normal and leuk
6                                              Ets transcription factors, which share the conserved Ets
7                                              Ets variant 2 (Etv2), a member of the E26 transforming-s
8                                              Ets-1 deubiquitination blocks its proteasomal destructio
9                                              Ets-2 acts as an independent preinduction repressor in n
10                                              Ets-2 binding to ARRE-2 in chromatin is stronger in naiv
11                                              Ets-2 silences directly constitutive or induced IL-2 exp
12                                              Ets-2, like its closely related homologue Ets-1, is a me
13 enediamines, such as derivatives 1(Me) and 1(Et), in both the solid-state and solution phases.
14 ) ethyl complexes, (PONOP)M(C2H5) (M = Ir (1-Et), Rh (2-Et)) and the iridium(I) propyl complex (PONOP
15 stal structure of a DNA complex of the Ets-2 Ets domain.
16 y available alane amine adduct (H(3)Al.NMe(2)Et) in toluene resulted in the formation of a conjugated
17 -SiR(3)(+)(C(6)F(5))(4)B(-) (SiR(3) = SiMe(2)Et, SiHEt(2)) and (Xantphos)Pd-SiR(3)(+)(BAr(f)(4)) (SiR
18 hos)Pd-SiR(3)(+)(BAr(f)(4)) (SiR(3) = SiMe(2)Et, SiHEt(2); Xantphos = 4,5-bis(diphenylphosphino)-9,9-
19 2; R(1) = Ph, R(2) = Naph, L3; R(1) = R(2) = Et, L4; R(1) = R(2) = Cy, L5; R(1) = R(2) = (t)Bu, L6),
20 s [P(3)O(8)NR(1)R(2)](2-) (2a: R(1) = R(2) = Et; 2b: R(1) = H, R(2) = (t)Bu) in greater than 70% yiel
21 nyl cluster, [(UO(2))(3)(Cy(7)Si(7)O(12))(2)(Et(2)O)(MeCN)(2)] (2), as yellow rods in 42% isolated yi
22 esence of catalytic systems Ti(acac)(2)Cl(2)-Et(2)AlCl and Co(acac)(2)(dppe)/Zn/ZnI(2) was performed
23 tion conditions with either the BF(3).OEt(2)/Et(3)SiH or TFA/BH(3).THF combinations.
24    Therefore, despite high levels of ERK1/2, Ets-1 target genes including DUSP6 and cyclins D1, D3, a
25 -(EtH)(+)), was prepared by protonation of 2-Et at -150 degrees C.
26 plexes, (PONOP)M(C2H5) (M = Ir (1-Et), Rh (2-Et)) and the iridium(I) propyl complex (PONOP)Ir(C3H7) (
27 d through an Ir(V) complex ((carb)PNP)Ir(H)3(Et) which reductively eliminates ethane with a very low
28                  The reaction of 2 with BF(3)Et(2)O affords the borylated derivative (3).
29 3) in DMF at 100 degrees C for 18 h or BF(3).Et(2)O at rt.
30 n of water, whereas in the presence of BF(3).Et(2)O bond migration took place preferentially.
31 uminyl by abstraction of pyridine with BF(3).Et(2)O unexpectedly led to a B/Al metathesis with the pr
32 ditions (HCl, montmorillonite K10, and BF(3).Et(2)O) were studied.
33 used phenazines was developed via PIFA-BF(3).Et(2)O-mediated oxidative coupling of di-heteroarylated
34                                        BF(3).Et(2)O-mediated synthesis of multisubstituted indenes fr
35 l)benzo[e]indoles, upon treatment with BF(3).Et(2)O/Et(3)N, afforded a new type of fluorescent boron
36 ain-specific homeobox/POU domain protein 3b, Ets variant gene 1, substance P, somatostatin, vasoactiv
37 able Th(III) complex in the salts [K(THF)(5)(Et(2)O)][Th(OC(6)H(2)(t)Bu(2)-2,6-Me-4)(4)] and [Li(THF)
38 L = {(ArNH)(ArN)-C=N-C=(NAr)(NHAr)}; Ar =2,6-Et(2)-C(6)H(3)] with a commercially available alane amin
39  the formation of the cluster species [Fe(8) Et(12) ](2-) , a rare example of a structurally characte
40                       Attempts to generate a Et(2)O-free version of 1 resulted instead in a dinuclear
41 ducts in the presence or absence of an added Et(3)N, respectively.
42                                 In addition, Ets-1 is located in both the nucleus and cytoplasm of re
43 le for Etv2 that is mediated by two adjacent Ets motifs in the proximal promoter.
44                                     Although Ets-1 negatively regulates the expression of Blimp1, a k
45 ar import mechanism of NRF-2 is unique among Ets factors.
46 g of c-Jun (an AP-1 factor) and Etv5/ERM (an Ets factor) to these regions in lens chromatin.
47                                     Etv2, an Ets-transcription factor, governs the specification of t
48     We sought to define the role of Etv5, an Ets-family transcription factor, in TH17 cell developmen
49 tion site 1 (Fli-1) transcription factor, an Ets family member, is implicated in the pathogenesis of
50            Ets homologous factor (EHF) is an Ets family transcription factor expressed in many epithe
51                                   SPIB is an Ets transcription factor that is expressed exclusively i
52 o motif as a hybrid bioisostere of CF(3) and Et (BITE) in a series of modified barbiturate inhibitors
53 n, and cyclization with acetic anhydride and Et(3)N.
54 Cl] in the presence of hydrazine hydrate and Et(3)N affords a Cn(-) complex of copper(I), [(Cn(-))Cu(
55 riptive embryology, skeletogenesis in Sp and Et has long been known to occur by distinct means.
56                                     PU.1 and Ets-1 represent archetypes for studying site discriminat
57 wo sequence-divergent ETS homologs, PU.1 and Ets-1, to DNA sites harboring a hemi- and fully methylat
58 egulatory regions contain arrays of AP-1 and Ets-binding sites.
59 ibility to dimethyl sulfate for PU.1/DNA and Ets-1/DNA complexes, indicating that the dynamics of PU.
60                                  The IRF and Ets families of transcription factors regulate the expre
61 ducible transcription factors, NF-kappaB and Ets-1, to the locus.
62 2 mRNA expression, Ets-2 protein levels, and Ets-2 binding to ARRE-2 decrease upon cell activation fo
63 y demonstrated important roles for Mesp1 and Ets variant 2 (Etv2) during lineage specification, but t
64 s-1 precedes rapid nuclear entry of NFAT and Ets-1 deficiency results in impaired nuclear entry, but
65                                    Usp9x and Ets-1 levels are coincidently elevated in melanoma with
66                           Both Ets1, another Ets family member, and Fli-1 drive transcription from th
67 treatment with alkyl metal reagents, such as Et(2) Zn and Bu(2) Mg.
68 ently with even weak terminal bases, such as Et(3)N.
69 strained spacing-Ets and Homeobox as well as Ets and E-box.
70 mposite elements (AICEs) and with TF PU.1 at Ets-IRF composite elements (EICEs), it is unclear how th
71  of Etv2 at midgestation, binding of Etv2 at Ets-binding sites in the Fli1 promoter is replaced by Fl
72 tions of E4 cardiomyocytes prove optimal at ~Et,E4 both in vivo and in vitro.
73 g the highly reactive bromenium source BDSB (Et(2)SBr.SbCl(5)Br), can lead to concise asymmetric tota
74 osome 11p13, is an intergenic region between Ets homologous factor (EHF) and Apaf-1 interacting prote
75  A formally iron(0) ate complex [ (iPr)BIPFe(Et)(CH(2)=CH(2))](-) was identified as the principle res
76                                         Both Ets and Gata factors have been shown to have important r
77                     Both GABP and PU.1 bound Ets sites in the Lbr promoter in vitro, and in vivo with
78  1/p-X-C6H4OH (rho = -3.3 for X = OMe, t-Bu, Et, and Me; rho = +1.5 for X = F, Cl, and CF3).
79 derivatives of cyanoacetic acid catalyzed by Et(3)N is presented.
80 in catalytic CO(2) and Ph(2) CO reduction by Et(3) SiH and hydrogenation of 1,1-diphenylethylene usin
81  radicals linked by iodides and separated by Et(4) N(+) counter-ions.
82 1) does not rescue the expression of IL-2 by Ets-1-deficient Th cells.
83  unique bipartite mode of ERK2 engagement by Ets-1 and involves two suboptimal noncanonical docking i
84 e the highly specific recognition of ERK2 by Ets-1, and enable the optimal localization of its dynami
85 e promoter may be predominantly regulated by Ets at the dorsal midline and are expressed in a ring.
86                           In naive Th cells, Ets-2 mRNA expression, Ets-2 protein levels, and Ets-2 b
87                                 Versus a CGC(Et)Ti + SNSCr tandem catalyst, Ti-C0-Cr(SNS) yields poly
88 y titanium olefin polymerization center (CGC(Et)Ti) covalently linked to a chromium bis(thioether)ami
89 ly, those achieved by tandem mononuclear CGC(Et)Ti and SNSCr catalysts under identical reaction condi
90                  In contrast, the tandem CGC(Et)Ti + SNSCr system yields 91.0% n-propyl branches unde
91             The R groups were CF3, CHO, COMe/Et, CO2Me, CONMe2/Et2, H, and 1-propynyl.
92 r via two identical, but inverted, composite Ets/E-box motifs enclosing the core promoter.
93 scription factors, which share the conserved Ets DNA-binding domain, number nearly 30 members in huma
94 , we report that Fli1 binds to the conserved Ets-binding sites within promoter and enhancer regions o
95  We demonstrate that Etv2 binds to conserved Ets-binding sites within the promoter region of the Fli1
96 oter region of SAM-pointed domain-containing Ets-like factor (SPDEF), a driver of mucous differentiat
97 he promoter of SAM-pointed domain-containing Ets-like factor (SPDEF), a known factor for goblet cell
98                                  Conversely, Ets-2 silencing allows for constitutive IL-2 expression
99 ation by creating signaling-incompetent Dome:Et/Lat heterodimers.
100                           Tissue elasticity, Et, increases daily for heart to 1-2 kPa by embryonic da
101 ibute utility theory (MAUT), and Elimination Et Choix Traduisant la REalite (ELECTRE III).
102 manner that recapitulates that of endogenous Ets-1 expression in the neural crest.
103                    Fli-1 binds to endogenous Ets binding sites in the distal region of the CCL5 promo
104  We have identified regions flanking the ERG Ets domain responsible for autoinhibition of DNA binding
105 increases membrane permeability to ethidium (Etd(+)) and Ca(2+) by activating P2X7 receptors (P2X7Rs)
106  L alone or in combination with ethionamide (Et), amikacin (A), and Z given for 2 or 7 months.
107 , five compounds [R = butyl (Bu), R = ethyl (Et), R = methoxymethyl (MeOMe), R = methyl (Me), and R =
108  Ewing Sarcoma pathogenesis is driven by EWS/Ets fusion oncoproteins, of which EWS/Fli1 is the most c
109                                Driven by EWS/Ets, or rarely variant, oncogenic fusions, Ewing Sarcoma
110   Erf is a gene for a ubiquitously expressed Ets DNA-binding domain-containing transcriptional repres
111    In naive Th cells, Ets-2 mRNA expression, Ets-2 protein levels, and Ets-2 binding to ARRE-2 decrea
112  kinase substrates, the transcription factor Ets-1 has no canonical docking motifs, yet it is efficie
113       We found that the transcription factor Ets-1 is highly expressed in KS spindle cells and is upr
114 cific expression of the transcription factor Ets-1, located within one of these loci on chromosome 8,
115 memory, Th cells by the transcription factor Ets-2 that binds to the antigen receptor response elemen
116                             This metal-free, Et(3)N-catalyzed cascade reaction proceeded with exclusi
117  hexanes, followed by recrystallization from Et(2)O/MeCN, results in the formation of the uranyl clus
118 S rats and SS rats with only one functioning Ets-1 gene (ES rats) demonstrated similar increases in B
119 H, Me) are superior to bulkier groups (e.g., Et, pTol), and a Mes substituent is even prohibitively l
120 ing sites that were also enriched for Gata1, Ets, and Runx1 motifs.
121  nature of the remote substituent along Me > Et > iPr and oligomer molecular weights increase.
122   Dynamic (1)H NMR characterization of 1-(H)(Et)(+) establishes site exchange between the Ir-H and Ir
123 hylene through formation of ((carb)PNP)Ir(H)(Et)(C2H4) and by H2 through formation of ((carb)PNP)Ir(H
124 ethane from Ir(III) complex ((carb)PNP)Ir(H)(Et)(H2) is calculated to proceed through an Ir(V) comple
125  by H2 through formation of ((carb)PNP)Ir(H)(Et)(H2).
126 f putative binding sites for SoxE, homeobox, Ets, TFAP2 or Fox proteins results in loss or reduction
127    Ets-2, like its closely related homologue Ets-1, is a member of the Ets family of DNA binding tran
128                                  HTy and HTy-Et also altered the transcription of specific genes invo
129 -Xantphos)Ni(I) -Me and (tBu-Xantphos)Ni(I) -Et complexes undergo fast insertion of CO(2) at 22 degre
130                                Facile Pt(II)-Et functionalization was determined to occur via a low e
131 are either missing or operate differently in Et.
132 2-cryptand), 1-Tb, reacts with dinitrogen in Et(2)O at -35 degrees C to form the end-on bridging dini
133                      The overall increase in Et over land is about twofold of the decrease in Es.
134 ificantly (p < 0.01), caused by increases in Et and Ei, which are partially counteracted by Es decrea
135 tration, contraction wave speed is linear in Et as theorized for excitation-contraction coupled to ma
136 croglia are not required for the increase in Etd(+) uptake by astrocytes induced by FGF-1, although t
137 1 and carbenoxolone) prevent the increase in Etd(+) uptake by astrocytes, whereas Gap19, a selective
138 ear evidence for the allosteric mechanism in Ets-2.
139 esence of an autoinhibitory module, which in Ets-1 allosterically inhibits the DNA binding activity.
140  by preventing Akt activity and inactivating Ets-1 function in NSCLC cells.
141 rs involved in IE gene expression, including Ets, AP-1, CREB, and C/EBP, which lead to the transient
142 HV latent vFLIP gene is sufficient to induce Ets-1 expression in an NF-kappaB-dependent fashion.
143                                 ET-1 induced Ets-like kinase-1 (Elk-1), signal transducer and activat
144                                     Instead, Ets-1 physically and functionally interacts with the nuc
145 ether, these results uncover new inputs into Ets-1, revealing critical links in the cranial neural cr
146 : NRF-2alpha, which binds to DNA through its Ets domain, and NRF-2beta, which contains the transcript
147                              Up to 2.5 mug/L Et-Ph3P(+) was quantified in a small stream from the Hes
148 n the back reaction rapidly leads to labeled Et-S-CoM, which enables intermediate formation to be det
149 ely acting receptor, Eye Transformer/Latran (Et/Lat).
150 activated or memory Th cells; in the latter, Ets-2 participates in a change of the IL-2 promoter arch
151 tituents slow the reaction in the order Me &lt; Et < (i)Pr < (t)Bu.
152 t also Akt activity is essential to maintain Ets-1 in an active state.
153 dT lesions, with the alkyl group being a Me, Et, nPr, iPr, nBu, iBu or sBu, at a defined site and exa
154 dT lesions, with the alkyl group being a Me, Et, nPr, iPr, nBu, iBu, (R)-sBu and (S)-sBu, are recogni
155 dG lesions, with the alkyl group being a Me, Et, nPr, iPr, nBu, iBu, or sBu, in several human cell li
156                      Cyclophanes bearing Me, Et, and MeO cap substituents and beta-Me, Et, or Ph arm
157 e, Et, and MeO cap substituents and beta-Me, Et, or Ph arm substituents are obtained, and a modified
158 dipp)][B(Ar(F))4] (1R[B(Ar(F))4]; R = H, Me, Et; Ar(F) = C6H3-3,5-(CF3)2; Idipp = C[N(C6H3-2,6-iPr2)C
159 f the form WN(NR2)3 [R = combinations of Me, Et, (i)Pr, (n)Pr] have been synthesized as precursors fo
160 es the conversion of N2 to N(SiR3)3 (R = Me, Et) at room temperature, representing the highest turnov
161 plexes (DNICs) [((R)DDB)Fe(NO)2](+) (R = Me, Et, Iso; (R)DDB = N,N'-bis(2,6-dialkylphenyl)-1,4-diaza-
162                                The size (Me, Et, iPr, and tBu) and position (meta and para) of the al
163  of spiroindolenines from 2-substituted (Me, Et) indoles and 2-(pyrrolidin-1-yl)benzaldehydes has bee
164 strocytes that show enhanced Px1 HC-mediated Etd(+) uptake.
165 tivity is dependent on a likely Fgf-mediated Ets transcription factor-binding site.
166                             Within a minimal Ets-1 enhancer region, mutation of putative binding site
167 expression was easily rescued under modelled Ets-factor gain of function, as occurs in TERT promoter
168      FeMoco and an analogous small-molecule (Et(4) N)[(Tp)MoFe(3) S(4) Cl(3) ] cubane have both been
169  leads to the intermediate, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]Mo(Cl)(NHSiMe3) (V), and XOSiMe3 as a co-p
170 IV) terminal imido complex, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]Mo(NSiMe3) (3), with a 1:2 mixture of iPrO
171 n of the Mo(IV) dichloride, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]MoCl2 (1), and the generation of 1 equiv e
172 the intermediate, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]Mo(Cl)(NHSiMe3) (V), and XOSiMe3 as a co-product.
173 al imido complex, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]Mo(NSiMe3) (3), with a 1:2 mixture of iPrOH and Me3S
174 o(IV) dichloride, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]MoCl2 (1), and the generation of 1 equiv each of HN(
175 (2)(N-Et-HPTB)(NO)(DMF)(3)](BF(4))(3) (1) (N-Et-HPTB is the anion of N,N,N',N'-tetrakis(2-(l-ethylben
176 x 1 ([Mn2 (O2 CCH3 )(N-Et-HPTB)](ClO4 )2 , N-Et-HPTB=N,N,N',N'-tetrakis(2-(1-ethylbenzimidazolyl))-2-
177 de a dinitrosyl diiron(II) complex, [Fe(2)(N-Et-HPTB)(NO)(2)(DMF)(2)](BF(4))(3) (2) with [{FeNO}(7)](
178 ed mononitrosyl diiron(II) complex, [Fe(2)(N-Et-HPTB)(NO)(DMF)(3)](BF(4))(3) (1) (N-Et-HPTB is the an
179 xed-valent diiron(II, III) complex, [Fe(2)(N-Et-HPTB)(OH)(DMF)(3)](BF(4))(3) (3).
180                 Complex 1 ([Mn2 (O2 CCH3 )(N-Et-HPTB)](ClO4 )2 , N-Et-HPTB=N,N,N',N'-tetrakis(2-(1-et
181                           Reaction of [Fe2(N-Et-HPTB)(CH3COS)](BF4)2 (1) with (NO)(BF4) produces a no
182 -Et-HPTB)(O2CPh)(NO)2](BF4)2 (1a) and [Fe2(N-Et-HPTB)(DMF)2(NO)(OH)](BF4)3 (2a), are characterized by
183 heme mononitrosyl diiron(II) complex, [Fe2(N-Et-HPTB)(NO)(DMF)3](BF4)3 (2).
184   Two non-heme iron-nitrosyl species, [Fe2(N-Et-HPTB)(O2CPh)(NO)2](BF4)2 (1a) and [Fe2(N-Et-HPTB)(DMF
185 c (MAZ) compounds of the type EtZn-(R''-Zn)n-Et (R'' = ethyl and propyl branched alkylene groups) wer
186 2-2,6)NCMe}2CH](-); R = Pr(i) ((Dip)Nacnac), Et ((Dep)Nacnac)) using 1,3-cyclohexadiene.
187 elevant to an emerging role of PU.1, but not Ets-1, as a pioneer transcription factor in vivo.
188 robustly bound fully methylated DNA, but not Ets-1, which was substantially inhibited.
189 pled to site discrimination by PU.1, but not Ets-1.
190                                     Notably, Ets-1 is induced by BRAF or MEK kinase inhibition, resul
191 as embryonically lethal, a single-nucleotide Ets motif mutant was viable, and steady-state hematopoie
192 ASO designs comprised of short S-cEt (S-2'-O-Et-2',4'-bridged nucleic acid) gapmer ASOs, approximatel
193  synthesized in the presence of N-Fmoc and O-Et protected phosphoserine and phosphotyrosine to prepar
194 [e]indoles, upon treatment with BF(3).Et(2)O/Et(3)N, afforded a new type of fluorescent boron complex
195 in the presence of stoichiometric amounts of Et(3)N in dichloroethane at 80 degrees C.
196       If 1-Gd is dissolved in THF instead of Et(2)O under N(2), the irreversible formation of an (N(2
197 ith 2 months of EtZA followed by 5 months of Et or EtZ.
198 to the molecular mechanism and regulation of Et/Lat in Drosophila that may inform our understanding o
199 ed by autocrine IL-6 and inhibits accrual of Ets-1, Set1 methyltransferase and trimethylation of hist
200 cognition sequence and the mode of action of Ets post-translational modifications.
201 ely blocks the transcriptional activation of Ets-1, which inhibits its target gene, dual specificity
202 ization did not occur with the ETS domain of Ets-1, a close structural homolog of PU.1, 2:1 complex f
203 f DNA site recognition by the ETS domains of Ets-1 and PU.1, which represent the extremes in amino ac
204                         This nuclear exit of Ets-1 precedes rapid nuclear entry of NFAT and Ets-1 def
205 ogram, including the sustained expression of Ets transcription factors such as ETV1 Together, our dat
206 oapoptotic genes and decreased expression of Ets-1 and other hematopoietic genes.
207 ble the autoinhibited and DNA bound forms of Ets-1.
208                                 Mutations of Ets or E-box sites in either DNA motif abolished the act
209        In contrast, the C-terminal region of Ets-1, including its Pointed (PNT) domain, engages in a
210  mediated predominantly by the regulation of Ets-domain dynamics with only modest structural changes.
211 ge effects are dependent on de-repression of Ets transcription factors.
212                            The N terminus of Ets-1 interacts with a part of the ERK2 D-recruitment si
213 n-releasing group (kH/kD = 1.7-2.5; X = OMe, Et), whereas an inverse isotope effect was measured for
214  carried out targeted functional analyses on Et skeletogenesis to identify the presence, or demonstra
215 rol the activity of this subset of oncogenic Ets transcription factors.
216 yridinium salts and either Hantzsch ester or Et(3) N, photoinduced single-electron transfer could be
217 g A) and 13(2) carboalkoxy groups (R = Me or Et) were constructed in 37-61% yield from the hydrobilin
218 ranes, [RR'PBH(2)](n) (R = Ph; R' = H, Ph or Et), or are trapped in the form of CAAC-phosphinoborane
219 polymers, [RR'PBH(2)](n) (R = Ph; R' = Ph or Et).
220 tations in certain E-box, NFkappaB, MEF2, or Ets family binding sites--known to be important for the
221 were obtained with the p-Me, m,p-diMe, and p-Et phenyl derivatives 3c, 3e, and 3f, respectively, and
222 the anionic, trivalent, terbium precursor, [(Et(2)O)K][Tb(NP(1,2-bis-(t)Bu-diamidoethane)(NEt(2)))(4)
223 CH2CH3 insertion products, (C5Me5)2Y[(i)PrNC(Et)N(i)Pr-kappa(2)N,N'], 4, and [(C5Me5)2Y(mu-O2CEt)]2,
224 de ligand (trans-[Ni(F)(2-C5NF4)(PR3)2], R = Et 1a, Cy 1b, trans-[Pd(F)(4-C5NF4)(PCy3)2] 2, trans-[Pt
225  esters [P(3)O(9)R](2-) (3a: R = Me; 3b: R = Et) in greater than 60% isolated yield.
226 ecursor 8 with 1 molar equiv of K[BHR3] (R = Et, sBu) in THF at room temperature.
227             Interestingly, when K[BHR3] (R = Et, sBu) is employed as a hydride source to react with 3
228 aturing a mesityl (R = Mes) or an ethyl (R = Et) substituent initiate the living ring-opening alkyne
229 iCH3(pyridine)] (1a-pyr, R = Me; 1b-pyr, R = Et; 1c-pyr, R = iPr) convert ethylene to hyperbranched l
230  [Ge9R3R'](0), where R = Si(SiMe3)3 and R' = Et (1), Sn(n)Bu3 (2), or Tl (3).
231 the composition Au(32) (R(3) P)(12) Cl(8) (R=Et, (n) Pr, (n) Bu) were synthesized in a straightforwar
232 erizations of rac-8DL(Me) with rac-8DL(R) (R=Et, Bu) have yielded high-molecular-weight, crystalline
233  behavior of the related dimer beta-1a (R1 = Et, R2 = F), which readily dissociates into a pair of ra
234                     Alkyl Grignard reagents (Et, (n)Bu, (i)Pr, cyclohexyl), with the exception of (t)
235 vestigate the specific contribution of renal Ets-1, we transplanted kidneys from ES or SS rats into s
236              Prior binding of the repressive Ets transcription factor Etv6 predicts cohesin binding a
237              Bioinformatic analysis revealed Ets binding sites on the miR-155 promoter, and we found
238  or cooperative binding to closely separated Ets binding sites in a palindromic arrangement.
239    Ethyl-coenzyme M (CH3CH2-S-CH2CH2-SO3(-), Et-S-CoM) serves as a homologous substrate for the enzym
240 ) catalyst and nucleophilic fluoride source (Et(3)N.3HF), allylic trichloroacetimidates undergo rapid
241 unknown motif-pairs with constrained spacing-Ets and Homeobox as well as Ets and E-box.
242             The E26 transformation-specific (Ets-1) transcription factor is autoinhibited by a confor
243                    Cyclosporine A stabilizes Ets-2 mRNA and protein when the cells are activated.
244 attering showed PU.1 to be more dynamic than Ets-1; moreover, dynamic changes are strongly coupled to
245 ce a more stringent sequence preference than Ets-1 and its proximal sequence homologs.
246                          We demonstrate that Et/Lat negatively regulates the JAK/STAT pathway activit
247                   Surprisingly, we find that Et/Lat is able to bind to both JAK and STAT92E but, desp
248                                 We find that Et/Lat is trafficked through the endocytic machinery for
249                              We propose that Ets-2 expression and protein binding to the ARRE-2 of th
250                          Here we report that Ets-1 destruction is regulated by the deubiquitinating e
251                                          The Et groups can be easily replaced with F atoms using BF3.
252  switch from N-methylimidazole (N-MI) to the Et(3)N N-ligand efficiently alters diastereoselectivity
253                                          The Ets domain crystallized with two distinct species in the
254                                          The Ets-Related Gene (ERG) belongs to the Ets family of tran
255 e for Forkhead transcription factors and the Ets transcription factor Etv2, for activity in vivo.
256 ne transcription, which responds to both the Ets domain-containing protein Elk1 (Elk1) and the glucoc
257 on between Etv2 and Gata2 is mediated by the Ets and Gata domains.
258                           In Drosophila, the Ets protein Pointed P1 (PntP1) is required to generate I
259                        Among these genes the Ets-related gene (ERG) is the most frequently overexpres
260                                 However, the Ets motif mutation abrogated stem/progenitor cell regene
261                    Thus, Usp9x modulates the Ets-1/NRAS regulatory network and may have biologic and
262 sic nuclear localization signals (NLSs): the Ets domain within NRF-2alpha and the NLS within NRF-2bet
263  related homologue Ets-1, is a member of the Ets family of DNA binding transcription factors.
264           Here we show that depletion of the Ets family transcription factor GA-binding protein (GABP
265 ow that mice with homozygous deletion of the Ets transcription factor Erg die between embryonic day 1
266 on crystal structure of a DNA complex of the Ets-2 Ets domain.
267  and neither mutant was able to regulate the Ets/IRF composite element or interferon-stimulated respo
268    The Ets-Related Gene (ERG) belongs to the Ets family of transcription factors and is critically im
269 nd form a long-lived complex relative to the Ets-1 counterpart.
270 ding of c-Myc and ETS family proteins to the Ets/E-box motifs derepresses the hTERT promoter by induc
271 y for astrocyte differentiation in which the Ets protein Pointed and the Notch signaling pathway are
272 ow that Btd functions cooperatively with the Ets transcription factor Pointed P1 to promote the gener
273 rcular dichroism (XMCD) spectroscopy of the (Et(4) N)[(Tp)MoFe(3) S(4) Cl(3) ] cubane and Fe L(2,3) -
274                                        Thus, Ets transcription factors specify non-vascular, amniotic
275                                        Thus, Ets-1 is a novel regulator of VEGFR3 and is involved in
276                                        Thus, Ets-1 promotes the expression of IL-2 by modulating the
277 th the transcription factors PU.1 or BATF to Ets or AP-1 composite motifs, associated with genes invo
278                               In contrast to Ets-1, in which the autoinhibition is caused by a combin
279 ty and that the increase in INPP4B is due to Ets-1-mediated transcriptional upregulation in colon can
280 Sp), vs. the cidaroid Eucidaris tribuloides (Et).
281  treated in the same pot with triethylamine (Et(3)N), leading to the selective formation of C3-substi
282 estigate the molecular mechanisms underlying Et/Lat activity.
283 ort a palladium-catalyzed C-N coupling using Et(3)N as a weak, soluble base, which allows a broad sub
284 e components: transpiration from vegetation (Et), direct evaporation from the soil (Es) and vaporizat
285 g proliferation and an OPC-like identity via Ets overactivity.
286 heir MI block index strategy: adjunctive VOM-Et and RFCA alone.
287 (63.8+/-9.4 years) undergoing adjunctive VOM-Et for MI block.
288 ght to evaluate the impact of adjunctive VOM-Et on MI block achievement and durability compared with
289      Beyond facilitating acute MI block, VOM-Et is associated with greater lesion durability as evide
290 vein of Marshall (VOM) ethanol infusion (VOM-Et) can facilitate acute MI block.
291 tients exhibited durable MI block in the VOM-Et group (62.9% [22/35] versus 32.6% [15/46], respective
292 lock was more frequently achieved in the VOM-Et group (98.7% [150/152] versus 63.6% [70/110]; P<0.001
293                                      The VOM-Et group consisted of 152 patients (63.8+/-9.4 years) un
294 ent a repeat procedure during follow-up (VOM-Et group: 23.3% [35/150] versus RFCA group: 65.7% [46/70
295 eric demand of the polymer end-group (Mes vs Et) transferred during the initiation step determines th
296 bis-(t)Bu-diamidoethane)(NEt(2)))(4)] (where Et is ethyl and (t)Bu is tert-butyl).
297 data suggest two distinct mechanisms wherein Ets-1 follows a "dry" mechanism that rapidly parses site
298 used in catalytic amounts when combined with Et(3)N.HBr/TMSBr, which acts as a regenerating system.
299 es of cooperative binding to substrates with Ets binding motifs separated by four and six base pairs
300 -diethyl-2,2-dimethyl-pyrrolidin-5-ylidene ((Et)CAAC) were discovered to afford three different types

 
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