ライフサイエンスコーパス: Et

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-1 is required for KSHV-induced expression of VEGFR3,

10 Ets-1 knockdown does not alter the expression of another

11 Ets-2 acts as an independent preinduction repressor in n

12 Ets-2 binding to ARRE-2 in chromatin is stronger in naiv

13 Ets-2 silences directly constitutive or induced IL-2 exp

14 Ets-2, like its closely related homologue Ets-1, is a me

15 recognized by the previously described AST-1 Ets domain factor, and two distinct types of homeodomain

16 ythroblastosis virus E26 oncogene homolog 1 (Ets-1).

17 E26 transformation-specific sequence 1 (Ets-1), the prototype of the ETS family of transcription

18 enediamines, such as derivatives 1(Me) and 1(Et), in both the solid-state and solution phases.

19 We found that activator protein 1 (AP-1), Ets related gene (Erg) and GR pathways were differential

20 ) ethyl complexes, (PONOP)M(C2H5) (M = Ir (1-Et), Rh (2-Et)) and the iridium(I) propyl complex (PONOP

21 stal structure of a DNA complex of the Ets-2 Ets domain.

22 tivation of the transcription factor Ets1/2 (Ets).

23 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),

24 Therefore, despite high levels of ERK1/2, Ets-1 target genes including DUSP6 and cyclins D1, D3, a

25 on experiments show that Sox9, Pax7, Msx1/2, Ets-1, TFAP2A and FoxD3, all are required for enhancer a

26 -(EtH)(+)), was prepared by protonation of 2-Et at -150 degrees C.

27 plexes, (PONOP)M(C2H5) (M = Ir (1-Et), Rh (2-Et)) and the iridium(I) propyl complex (PONOP)Ir(C3H7) (

28 d through an Ir(V) complex ((carb)PNP)Ir(H)3(Et) which reductively eliminates ethane with a very low

29 B(C6F5)3 and Cp2Zr{N(SiHMe2)2}R (R = Me (3), Et (5), n-C3H7 (7), CH horizontal lineCHSiMe3 (9)) provi

30 can be prepared by treatment of 5 with BF(3).Et(2)O and allyltributylstannane.

31 3) in DMF at 100 degrees C for 18 h or BF(3).Et(2)O at rt.

32 oyed as external nucleophiles in these BF(3).Et(2)O-promoted reactions.

33 ic addition derived products when Cs(2)CO(3)/Et(3)N is used as base.

34 ns of phosphine oxides by HSiCl(3), HSiCl(3)/Et(3)N, and Si(2)Cl(6) and the reductions of phosphine s

35 ain-specific homeobox/POU domain protein 3b, Ets variant gene 1, substance P, somatostatin, vasoactiv

36 Lu](2)(mu-OC identical withCO)[K(18-crown-6)(Et(2)O)(2)](2), 6a.

37 In addition, Ets-1 is located in both the nucleus and cytoplasm of re

38 le for Etv2 that is mediated by two adjacent Ets motifs in the proximal promoter.

39 Although Ets-1 negatively regulates the expression of Blimp1, a k

40 ar import mechanism of NRF-2 is unique among Ets factors.

41 g of c-Jun (an AP-1 factor) and Etv5/ERM (an Ets factor) to these regions in lens chromatin.

42 We sought to define the role of Etv5, an Ets-family transcription factor, in TH17 cell developmen

43 tion site 1 (Fli-1) transcription factor, an Ets family member, is implicated in the pathogenesis of

44 We also implicated an Ets-1 transcription factor-regulated increase in express

45 Ets homologous factor (EHF) is an Ets family transcription factor expressed in many epithe

46 k3/Net/Sap2 (here referred to as Elk3) is an Ets ternary complex transcriptional repressor known for

47 SPIB is an Ets transcription factor that is expressed exclusively i

48 This signature is composed of an Ets domain-binding site, recognized by the previously de

49 riptive embryology, skeletogenesis in Sp and Et has long been known to occur by distinct means.

50 PU.1 and Ets-1 represent archetypes for studying site discriminat

51 wo sequence-divergent ETS homologs, PU.1 and Ets-1, to DNA sites harboring a hemi- and fully methylat

52 egulatory regions contain arrays of AP-1 and Ets-binding sites.

53 acute myeloid leukemia 1 protein (AML1)- and Ets family transcription factor PU.1-dependent transcrip

54 s revealed increased phospho-MEK, G-CSF, and Ets expression and enhanced neutrophil recruitment compa

55 ibility to dimethyl sulfate for PU.1/DNA and Ets-1/DNA complexes, indicating that the dynamics of PU.

56 ducible transcription factors, NF-kappaB and Ets-1, to the locus.

57 2 mRNA expression, Ets-2 protein levels, and Ets-2 binding to ARRE-2 decrease upon cell activation fo

58 eceptor important for lymphangiogenesis, and Ets-1 activates the promoter of VEGFR3.

59 y demonstrated important roles for Mesp1 and Ets variant 2 (Etv2) during lineage specification, but t

60 s-1 precedes rapid nuclear entry of NFAT and Ets-1 deficiency results in impaired nuclear entry, but

61 Usp9x and Ets-1 levels are coincidently elevated in melanoma with

62 Both Ets1, another Ets family member, and Fli-1 drive transcription from th

63 detected during bulk electrolysis of aqueous Et-Fl(+) solutions at several potentials above +1.9 V ve

64 strained spacing-Ets and Homeobox as well as Ets and E-box.

65 of Etv2 at midgestation, binding of Etv2 at Ets-binding sites in the Fli1 promoter is replaced by Fl

66 tions of E4 cardiomyocytes prove optimal at ~Et,E4 both in vivo and in vitro.

67 e N-heterocyclic amines and ligand backbone (Et vs Pr) are found to modulate structural and reactivit

68 dentity and pointing to interactions between Ets and KLF factors in promoting epithelial fate.

69 osome 11p13, is an intergenic region between Ets homologous factor (EHF) and Apaf-1 interacting prote

70 Delivery of miR-199a-5p blocked Ets-1 expression in HMECs, whereas knockdown endogenous

71 Both Ets and Gata factors have been shown to have important r

72 Both GABP and PU.1 bound Ets sites in the Lbr promoter in vitro, and in vivo with

73 1/p-X-C6H4OH (rho = -3.3 for X = OMe, t-Bu, Et, and Me; rho = +1.5 for X = F, Cl, and CF3).

74 ich is then reduced to the tertiary amine by Et(2)SiH(2).

75 Cycloadditions are facilitated by Et(2)AlCl, presumably via chelation between the two carb

76 1) does not rescue the expression of IL-2 by Ets-1-deficient Th cells.

77 unique bipartite mode of ERK2 engagement by Ets-1 and involves two suboptimal noncanonical docking i

78 e the highly specific recognition of ERK2 by Ets-1, and enable the optimal localization of its dynami

79 In naive Th cells, Ets-2 mRNA expression, Ets-2 protein levels, and Ets-2 b

80 Versus a CGC(Et)Ti + SNSCr tandem catalyst, Ti-C0-Cr(SNS) yields poly

81 y titanium olefin polymerization center (CGC(Et)Ti) covalently linked to a chromium bis(thioether)ami

82 ly, those achieved by tandem mononuclear CGC(Et)Ti and SNSCr catalysts under identical reaction condi

83 In contrast, the tandem CGC(Et)Ti + SNSCr system yields 91.0% n-propyl branches unde

84 The R groups were CF3, CHO, COMe/Et, CO2Me, CONMe2/Et2, H, and 1-propynyl.

85 scription factors, which share the conserved Ets DNA-binding domain, number nearly 30 members in huma

86 , we report that Fli1 binds to the conserved Ets-binding sites within promoter and enhancer regions o

87 We demonstrate that Etv2 binds to conserved Ets-binding sites within the promoter region of the Fli1

88 oter region of SAM-pointed domain-containing Ets-like factor (SPDEF), a driver of mucous differentiat

89 he promoter of SAM-pointed domain-containing Ets-like factor (SPDEF), a known factor for goblet cell

90 Conversely, Ets-2 silencing allows for constitutive IL-2 expression

91 ation by creating signaling-incompetent Dome:Et/Lat heterodimers.

92 oliferation and survival (Ret/Gdnf and EdnrB/Et-3 pathways, Sox10 and Phox2b transcription factors),

93 Tissue elasticity, Et, increases daily for heart to 1-2 kPa by embryonic da

94 manner that recapitulates that of endogenous Ets-1 expression in the neural crest.

95 Fli-1 binds to endogenous Ets binding sites in the distal region of the CCL5 promo

96 We have identified regions flanking the ERG Ets domain responsible for autoinhibition of DNA binding

97 increases membrane permeability to ethidium (Etd(+)) and Ca(2+) by activating P2X7 receptors (P2X7Rs)

98 L alone or in combination with ethionamide (Et), amikacin (A), and Z given for 2 or 7 months.

99 , five compounds [R = butyl (Bu), R = ethyl (Et), R = methoxymethyl (MeOMe), R = methyl (Me), and R =

100 Ewing Sarcoma pathogenesis is driven by EWS/Ets fusion oncoproteins, of which EWS/Fli1 is the most c

101 Driven by EWS/Ets, or rarely variant, oncogenic fusions, Ewing Sarcoma

102 Erf is a gene for a ubiquitously expressed Ets DNA-binding domain-containing transcriptional repres

103 In naive Th cells, Ets-2 mRNA expression, Ets-2 protein levels, and Ets-2 binding to ARRE-2 decrea

104 kinase substrates, the transcription factor Ets-1 has no canonical docking motifs, yet it is efficie

105 We found that the transcription factor Ets-1 is highly expressed in KS spindle cells and is upr

106 Interestingly, the transcription factor Ets-1 is uniquely expressed in cranial but not trunk neu

107 cific expression of the transcription factor Ets-1, located within one of these loci on chromosome 8,

108 memory, Th cells by the transcription factor Ets-2 that binds to the antigen receptor response elemen

109 the E-twenty-six (ETS) transcription factors Ets related gene (Erg) and Ets1 were the most common sit

110 fs for E-twenty six/ternary complex factors (Ets/TCF), affected 65.4% of the tumors, with even distri

111 lete set of primary genes upregulated by FGF/Ets shortly after heart progenitor emergence.

112 nderlying the conserved, primary role of FGF/Ets in chordate heart lineage specification.

113 ecific Ets-1-independent regulatory role for Ets-2 in early thymocyte development and survival.

114 S rats and SS rats with only one functioning Ets-1 gene (ES rats) demonstrated similar increases in B

115 h reported data for other ETS domains (e.g., Ets-1, TEL) for which high-affinity binding is driven by

116 nature of the remote substituent along Me > Et > iPr and oligomer molecular weights increase.

117 s the alkyl hydrides, (PONOP)Ir(H)(R) (1-(H)(Et)(+) and 1-(H)(Pr)(+)), respectively.

118 Dynamic (1)H NMR characterization of 1-(H)(Et)(+) establishes site exchange between the Ir-H and Ir

119 hylene through formation of ((carb)PNP)Ir(H)(Et)(C2H4) and by H2 through formation of ((carb)PNP)Ir(H

120 ethane from Ir(III) complex ((carb)PNP)Ir(H)(Et)(H2) is calculated to proceed through an Ir(V) comple

121 by H2 through formation of ((carb)PNP)Ir(H)(Et)(H2).

122 f putative binding sites for SoxE, homeobox, Ets, TFAP2 or Fox proteins results in loss or reduction

123 Ets-2, like its closely related homologue Ets-1, is a member of the Ets family of DNA binding tran

124 HTy and HTy-Et also altered the transcription of specific genes invo

125 Results showed that both HTy and HTy-Et inhibited cell proliferation and arrested the cell cy

126 ts highlight that HTy and its derivative HTy-Et modulate molecular mechanisms involved in colon cance

127 activity of hydroxytyrosyl ethyl ether (HTy-Et) compared to its precursor hydroxytyrosol (HTy) has b

128 ressed in Caco-2 cells exposed to HTy or HTy-Et for 24h, respectively, compared with untreated cells

129 echanisms involved in colon cancer, with HTy-Et being more effective than HTy.

130 Facile Pt(II)-Et functionalization was determined to occur via a low e

131 l linePPh(3))(NR(2))(3) (R = SiMe(3)) (1) in Et(2)O results in generation of the terminal chalcogenid

132 are either missing or operate differently in Et.

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 endritic current injection was also lower in Et animals.

137 xidation of 1 with GaCl(3) in a 1:2 ratio in Et(2)O yields the monocationic diarsenic radical complex

138 croglia are not required for the increase in Etd(+) uptake by astrocytes induced by FGF-1, although t

139 1 and carbenoxolone) prevent the increase in Etd(+) uptake by astrocytes, whereas Gap19, a selective

140 ear evidence for the allosteric mechanism in Ets-2.

141 esence of an autoinhibitory module, which in Ets-1 allosterically inhibits the DNA binding activity.

142 by preventing Akt activity and inactivating Ets-1 function in NSCLC cells.

143 rs involved in IE gene expression, including Ets, AP-1, CREB, and C/EBP, which lead to the transient

144 HV latent vFLIP gene is sufficient to induce Ets-1 expression in an NF-kappaB-dependent fashion.

145 ET-1 induced Ets-like kinase-1 (Elk-1), signal transducer and activat

146 eas knockdown endogenous miR-199a-5p induced Ets-1 expression.

147 Instead, Ets-1 physically and functionally interacts with the nuc

148 ether, these results uncover new inputs into Ets-1, revealing critical links in the cranial neural cr

149 ganic compound, the N(5)-ethylflavinium ion, Et-Fl(+).

150 : NRF-2alpha, which binds to DNA through its Ets domain, and NRF-2beta, which contains the transcript

151 Up to 2.5 mug/L Et-Ph3P(+) was quantified in a small stream from the Hes

152 n the back reaction rapidly leads to labeled Et-S-CoM, which enables intermediate formation to be det

153 ely acting receptor, Eye Transformer/Latran (Et/Lat).

154 activated or memory Th cells; in the latter, Ets-2 participates in a change of the IL-2 promoter arch

155 en-alkylidene [CF(3)-ONO]W horizontal lineCH(Et)(O(t)Bu) (2) and -alkylidyne {MePPh(3)}{[CF(3)-ONO]W

156 lsion to form [CF(3)-ONO]W horizontal lineCH(Et)(OSiMe(3)) (5).

157 tituents slow the reaction in the order Me < Et < (i)Pr < (t)Bu.

158 t also Akt activity is essential to maintain Ets-1 in an active state.

159 f to yield [CF(3)-ONO]W horizontal lineC(Me)(Et)(O(t)Bu) (4), but the bulkier Me(3)SiOTf silylates th

160 dT lesions, with the alkyl group being a Me, Et, nPr, iPr, nBu, iBu or sBu, at a defined site and exa

161 dT lesions, with the alkyl group being a Me, Et, nPr, iPr, nBu, iBu, (R)-sBu and (S)-sBu, are recogni

162 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

163 f the form WN(NR2)3 [R = combinations of Me, Et, (i)Pr, (n)Pr] have been synthesized as precursors fo

164 es the conversion of N2 to N(SiR3)3 (R = Me, Et) at room temperature, representing the highest turnov

165 nzene; 1-ethynyl-2,4,6-R(3)-benzene (R = Me, Et, i-Pr)) and Me(3)SiCCH with seven aryl bromides (thre

166 and three 2,4,6-R(3)-bromobenzenes (R = Me, Et, i-Pr)) with four different phosphines (P-t-Bu(3), t-

167 l bromides (three 2-R-bromobenzenes (R = Me, Et, i-Pr); 2,6-Me(2)-bromobenzene and three 2,4,6-R(3)-b

168 plexes (DNICs) [((R)DDB)Fe(NO)2](+) (R = Me, Et, Iso; (R)DDB = N,N'-bis(2,6-dialkylphenyl)-1,4-diaza-

169 The size (Me, Et, iPr, and tBu) and position (meta and para) of the al

170 of spiroindolenines from 2-substituted (Me, Et) indoles and 2-(pyrrolidin-1-yl)benzaldehydes has bee

171 strocytes that show enhanced Px1 HC-mediated Etd(+) uptake.

172 Within a minimal Ets-1 enhancer region, mutation of putative binding site

173 expression was easily rescued under modelled Ets-factor gain of function, as occurs in TERT promoter

174 leads to the intermediate, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]Mo(Cl)(NHSiMe3) (V), and XOSiMe3 as a co-p

175 IV) terminal imido complex, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]Mo(NSiMe3) (3), with a 1:2 mixture of iPrO

176 n of the Mo(IV) dichloride, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]MoCl2 (1), and the generation of 1 equiv e

177 the intermediate, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]Mo(Cl)(NHSiMe3) (V), and XOSiMe3 as a co-product.

178 al imido complex, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]Mo(NSiMe3) (3), with a 1:2 mixture of iPrOH and Me3S

179 o(IV) dichloride, (eta(5)-C5Me5)[N(Et)C(Ph)N(Et)]MoCl2 (1), and the generation of 1 equiv each of HN(

180 rical tetraalkylammonium cations, Me(4)N(+), Et(4)N(+), (n-Pr)(4)N(+), (n-Bu)(4)N(+), (n-Hex)(4)N(+),

181 x 1 ([Mn2 (O2 CCH3 )(N-Et-HPTB)](ClO4 )2 , N-Et-HPTB=N,N,N',N'-tetrakis(2-(1-ethylbenzimidazolyl))-2-

182 Complex 1 ([Mn2 (O2 CCH3 )(N-Et-HPTB)](ClO4 )2 , N-Et-HPTB=N,N,N',N'-tetrakis(2-(1-et

183 Reaction of [Fe2(N-Et-HPTB)(CH3COS)](BF4)2 (1) with (NO)(BF4) produces a no

184 -Et-HPTB)(O2CPh)(NO)2](BF4)2 (1a) and [Fe2(N-Et-HPTB)(DMF)2(NO)(OH)](BF4)3 (2a), are characterized by

185 heme mononitrosyl diiron(II) complex, [Fe2(N-Et-HPTB)(NO)(DMF)3](BF4)3 (2).

186 Two non-heme iron-nitrosyl species, [Fe2(N-Et-HPTB)(O2CPh)(NO)2](BF4)2 (1a) and [Fe2(N-Et-HPTB)(DMF

187 c (MAZ) compounds of the type EtZn-(R''-Zn)n-Et (R'' = ethyl and propyl branched alkylene groups) wer

188 2-2,6)NCMe}2CH](-); R = Pr(i) ((Dip)Nacnac), Et ((Dep)Nacnac)) using 1,3-cyclohexadiene.

189 elevant to an emerging role of PU.1, but not Ets-1, as a pioneer transcription factor in vivo.

190 robustly bound fully methylated DNA, but not Ets-1, which was substantially inhibited.

191 pled to site discrimination by PU.1, but not Ets-1.

192 Notably, Ets-1 is induced by BRAF or MEK kinase inhibition, resul

193 Nuclear Ets-1 quickly exits the nucleus in response to calcium-d

194 ASO designs comprised of short S-cEt (S-2'-O-Et-2',4'-bridged nucleic acid) gapmer ASOs, approximatel

195 synthesized in the presence of N-Fmoc and O-Et protected phosphoserine and phosphotyrosine to prepar

196 (2)H- and (13)C-labeled isotopologues of Et-S-CoM were used as the substrates, and the time cours

197 ith 2 months of EtZA followed by 5 months of Et or EtZ.

198 )IrHCl with tert-butoxide in the presence of Et(2)SiH(2) under H(2).

199 to the molecular mechanism and regulation of Et/Lat in Drosophila that may inform our understanding o

200 ed by autocrine IL-6 and inhibits accrual of Ets-1, Set1 methyltransferase and trimethylation of hist

201 cognition sequence and the mode of action of Ets post-translational modifications.

202 ely blocks the transcriptional activation of Ets-1, which inhibits its target gene, dual specificity

203 inatorial transcription factor collective of Ets/Dlx/Pbx factors, suggesting deep phylogenetic conser

204 ization did not occur with the ETS domain of Ets-1, a close structural homolog of PU.1, 2:1 complex f

205 f DNA site recognition by the ETS domains of Ets-1 and PU.1, which represent the extremes in amino ac

206 This nuclear exit of Ets-1 precedes rapid nuclear entry of NFAT and Ets-1 def

207 ogram, including the sustained expression of Ets transcription factors such as ETV1 Together, our dat

208 oapoptotic genes and decreased expression of Ets-1 and other hematopoietic genes.

209 ble the autoinhibited and DNA bound forms of Ets-1.

210 Knockdown of Ets-1 affects the ability of KSHV-infected cells to disp

211 Overexpression of Ets-1 not only rescued miR-199a-5p-dependent anti-angiog

212 In contrast, the C-terminal region of Ets-1, including its Pointed (PNT) domain, engages in a

213 mediated predominantly by the regulation of Ets-domain dynamics with only modest structural changes.

214 However, the role of Ets-2, a transcription factor that is phosphorylated on

215 After IFN-gamma stimulation of Ets-1(-/-) B cells, activated Stat1, which forms a compl

216 The N terminus of Ets-1 interacts with a part of the ERK2 D-recruitment si

217 The determined structures of [(Et(2)O)Li(C(4)H(3)S)](4) (1), [(THF)(2)Li(C(4)H(3)S)](2)

218 n-releasing group (kH/kD = 1.7-2.5; X = OMe, Et), whereas an inverse isotope effect was measured for

219 carried out targeted functional analyses on Et skeletogenesis to identify the presence, or demonstra

220 d defects in these mice are not dependent on Ets-1 expression.

221 rol the activity of this subset of oncogenic Ets transcription factors.

222 We now report that the oncogenic Ets variant 4 (Etv4) promotes prostate cancer metastasis

223 g A) and 13(2) carboalkoxy groups (R = Me or Et) were constructed in 37-61% yield from the hydrobilin

224 tations in certain E-box, NFkappaB, MEF2, or Ets family binding sites--known to be important for the

225 were obtained with the p-Me, m,p-diMe, and p-Et phenyl derivatives 3c, 3e, and 3f, respectively, and

226 CH2CH3 insertion products, (C5Me5)2Y[(i)PrNC(Et)N(i)Pr-kappa(2)N,N'], 4, and [(C5Me5)2Y(mu-O2CEt)]2,

227 de ligand (trans-[Ni(F)(2-C5NF4)(PR3)2], R = Et 1a, Cy 1b, trans-[Pd(F)(4-C5NF4)(PCy3)2] 2, trans-[Pt

228 la [(eta(6)-p-cymene)RuCl(2){P(OR)(3)}] (R = Et, (i)Pr, Ph) with two easily exchangable chloride liga

229 e)Ru(beta-diketonate){P(OR)(3)}][BF(4)] (R = Et, (i)Pr, Ph) with comparable in vitro toxicity (50% PG

230 ecursor 8 with 1 molar equiv of K[BHR3] (R = Et, sBu) in THF at room temperature.

231 Interestingly, when K[BHR3] (R = Et, sBu) is employed as a hydride source to react with 3

232 aturing a mesityl (R = Mes) or an ethyl (R = Et) substituent initiate the living ring-opening alkyne

233 iCH3(pyridine)] (1a-pyr, R = Me; 1b-pyr, R = Et; 1c-pyr, R = iPr) convert ethylene to hyperbranched l

234 [Ge9R3R'](0), where R = Si(SiMe3)3 and R' = Et (1), Sn(n)Bu3 (2), or Tl (3).

235 behavior of the related dimer beta-1a (R1 = Et, R2 = F), which readily dissociates into a pair of ra

236 Alkyl Grignard reagents (Et, (n)Bu, (i)Pr, cyclohexyl), with the exception of (t)

237 vestigate the specific contribution of renal Ets-1, we transplanted kidneys from ES or SS rats into s

238 Bioinformatic analysis revealed Ets binding sites on the miR-155 promoter, and we found

239 or cooperative binding to closely separated Ets binding sites in a palindromic arrangement.

240 Similarly, Ets-1 knockdown blunted angiogenic response and inductio

241 Ethyl-coenzyme M (CH3CH2-S-CH2CH2-SO3(-), Et-S-CoM) serves as a homologous substrate for the enzym

242 unknown motif-pairs with constrained spacing-Ets and Homeobox as well as Ets and E-box.

243 s is enigmatic given the absence of specific Ets partners.

244 mplicate for the first time a stage-specific Ets-1-independent regulatory role for Ets-2 in early thy

245 The E26 transformation-specific (Ets-1) transcription factor is autoinhibited by a confor

246 Cyclosporine A stabilizes Ets-2 mRNA and protein when the cells are activated.

247 attering showed PU.1 to be more dynamic than Ets-1; moreover, dynamic changes are strongly coupled to

248 ce a more stringent sequence preference than Ets-1 and its proximal sequence homologs.

249 We demonstrate that Et/Lat negatively regulates the JAK/STAT pathway activit

250 Surprisingly, we find that Et/Lat is able to bind to both JAK and STAT92E but, desp

251 We find that Et/Lat is trafficked through the endocytic machinery for

252 rough PFKm's 3' untranslated region and that Ets proteins are involved in the regulation of PFKm via

253 ected lymphatic endothelium, indicating that Ets-1 is a novel cellular regulator of VEGFR3 expression

254 splay angiogenic phenotypes, indicating that Ets-1 plays a role in KSHV activation of endothelial cel

255 We propose that Ets-2 expression and protein binding to the ARRE-2 of th

256 Here we report that Ets-1 destruction is regulated by the deubiquitinating e

257 Here we show that Ets-1 is also essential for optimal production of IL-2 b

258 The Et groups can be easily replaced with F atoms using BF3.

259 The Ets domain crystallized with two distinct species in the

260 The Ets-Related Gene (ERG) belongs to the Ets family of tran

261 e for Forkhead transcription factors and the Ets transcription factor Etv2, for activity in vivo.

262 ne transcription, which responds to both the Ets domain-containing protein Elk1 (Elk1) and the glucoc

263 on between Etv2 and Gata2 is mediated by the Ets and Gata domains.

264 In Drosophila, the Ets protein Pointed P1 (PntP1) is required to generate I

265 During murine embryogenesis, the Ets factor Erg is highly expressed in endothelial cells

266 Among these genes the Ets-related gene (ERG) is the most frequently overexpres

267 Mice carrying homozygous deletions in the Ets-1 gene exhibited blunted wound blood flow and reduce

268 Thus, Usp9x modulates the Ets-1/NRAS regulatory network and may have biologic and

269 sic nuclear localization signals (NLSs): the Ets domain within NRF-2alpha and the NLS within NRF-2bet

270 c potential is impacted by the status of the Ets domain and the configuration of the 5' UTR region.

271 related homologue Ets-1, is a member of the Ets family of DNA binding transcription factors.

272 Here we show that depletion of the Ets family transcription factor GA-binding protein (GABP

273 ow that mice with homozygous deletion of the Ets transcription factor Erg die between embryonic day 1

274 nduced genes, including three members of the Ets-1 family of transcription factors (TFs).

275 sent study, we show that inactivation of the Ets-1 transcription factor results in a severe decrease

276 on crystal structure of a DNA complex of the Ets-2 Ets domain.

277 and neither mutant was able to regulate the Ets/IRF composite element or interferon-stimulated respo

278 ction studies and ChIP-seq, we show that the Ets transcription factor EHF promotes cornea epithelial

279 thway regulates G-CSF expression through the Ets transcription factor.

280 The Ets-Related Gene (ERG) belongs to the Ets family of transcription factors and is critically im

281 nd form a long-lived complex relative to the Ets-1 counterpart.

282 y for astrocyte differentiation in which the Ets protein Pointed and the Notch signaling pathway are

283 ow that Btd functions cooperatively with the Ets transcription factor Pointed P1 to promote the gener

284 Thus, Ets transcription factors specify non-vascular, amniotic

285 Thus, Ets-1 is a novel regulator of VEGFR3 and is involved in

286 Thus, Ets-1 promotes the expression of IL-2 by modulating the

287 After acid digestion, Pb was ethylated to Et(4)Pb, separated from the digested solution (black sha

288 th the transcription factors PU.1 or BATF to Ets or AP-1 composite motifs, associated with genes invo

289 In contrast to Ets-1, in which the autoinhibition is caused by a combin

290 ty and that the increase in INPP4B is due to Ets-1-mediated transcriptional upregulation in colon can

291 rites, layer 5 neurons from ethanol-treated (Et) animals displayed a lower number and a shorter durat

292 Sp), vs. the cidaroid Eucidaris tribuloides (Et).

293 estigate the molecular mechanisms underlying Et/Lat activity.

294 e components: transpiration from vegetation (Et), direct evaporation from the soil (Es) and vaporizat

295 eric demand of the polymer end-group (Mes vs Et) transferred during the initiation step determines th

296 data suggest two distinct mechanisms wherein Ets-1 follows a "dry" mechanism that rapidly parses site

297 Removal of the silyl groups with Et(3)N.3HF followed by deallylation with PhSO(2)Na/Pd(PP

298 activated Stat1, which forms a complex with Ets-1 in wild-type cells, no longer binds to the T-bet e

299 es of cooperative binding to substrates with Ets binding motifs separated by four and six base pairs

300 dyne {MePPh(3)}{[CF(3)-ONO]W identical withC(Et)(O(t)Bu)} (3) complexes.