ライフサイエンスコーパス: be sufficient to activate

1 ulation of a small region of the core domain is sufficient to activate a large number of p53 cancer m

2 activation distal to PI3K and AKT activation is sufficient to activate a molecular signaling cascade

3 These findings establish that BLC is sufficient to activate a pathway of events leading to

4 Brief activation of BMP signaling is sufficient to activate a posterior HOX code and direc

5 rs commonly during colon cancer progression, is sufficient to activate a PRL-3-mediated cell survival

6 ion of cyd-1 and cdk-4 in transgenic animals is sufficient to activate a S-phase reporter gene.

7 We propose that Cdk1 inactivation is sufficient to activate a signaling pathway leading to

8 rprisingly that agonist binding to NR3 alone is sufficient to activate a significant component of NR1

9 provide direct evidence that SH3 engagement is sufficient to activate a Src family kinase in vivo an

10 hat conditional inactivation of PHD2 in mice is sufficient to activate a subset of HIF target genes,

11 Importantly, BMCs from young mice were sufficient to activate a tumor-supportive microenvi

12 AlF(4)(-) with the nucleotide-free Galpha(s) is sufficient to activate AC.

13 can elicit a proinflammatory cell death that is sufficient to activate adaptive antitumor immune resp

14 N, a negative regulator of PI(3)K signaling, is sufficient to activate Akt, but has only a modest eff

15 with the lipid phosphatase activity of PTEN was sufficient to activate Akt/mTOR/p70S6K signaling.

16 These data demonstrate that HSP60 binding is sufficient to activate alpha 3 beta 1 integrin functi

17 oduces an increase in the AMP/ATP ratio that is sufficient to activate AMP-activated kinase.

18 e provide the first proof that talin binding is sufficient to activate and extend membrane-embedded i

19 transduction of Tax into primary lymphocytes was sufficient to activate and maintain telomerase expre

20 SIRT1 expression induced by ERalpha was sufficient to activate antioxidant and prosurvival g

21 acetate-responsive element (TRE), only Cdc42 was sufficient to activate AP-1/TRE.

22 that this relatively small amount of pCD40L is sufficient to activate APCs, owing to the difficulty

23 tion of only approximately 10-100 receptors, was sufficient to activate approximately 20,000 CD18 and

24 e two kinases together but neither one alone is sufficient to activate ARE-containing promoter.

25 ne production mediated by TDO2 in TNBC cells was sufficient to activate aryl hydrocarbon receptor (Ah

26 ehaviour during early gonad development, and is sufficient to activate aspects of male germ cell beha

27 was found that these linguistic visual cues are sufficient to activate auditory cortex in normal hea

28 the program of autophagy gene expression and is sufficient to activate autophagic protein degradation

29 inding to CD1b-phospholipid complexes, which is sufficient to activate autoreactive responses to CD1b

30 Crp4(20-92) at Ser(43) downward arrowIle(44) is sufficient to activate bactericidal activity, and ami

31 in pre-malignant B cells, Myc overexpression is sufficient to activate BCR and PI3K/Akt signaling pat

32 integrin-binding PTB-like F3 domain of talin is sufficient to activate beta3 integrins.

33 Linear di-ubiquitins were sufficient to activate both the IKK complex in vitr

34 To determine whether membrane association is sufficient to activate Btk, we targeted Btk to the pl

35 eover, a single substrate of MAPK, p90(Rsk), is sufficient to activate Bub1 in vitro and in vivo.

36 utations and deletions within the SH3 domain are sufficient to activate c-ABL transforming ability.

37 To determine whether oligomerization alone is sufficient to activate c-Abl, we have generated and c

38 al and central domain fragments of complexin is sufficient to activate Ca(2+)-triggered release using

39 we show that chemical-induced growth arrest is sufficient to activate caspase-2 and induce apoptosis

40 dimerization nor cleavage of caspase-8 alone is sufficient to activate caspase-8 or induce apoptosis

41 n fact, as low as 2.5 nM of Smac-mimic alone was sufficient to activate caspase-3 and induce apoptosi

42 c with another mitochondrial protein, Smac, was sufficient to activate caspases, however.

43 s Otx binding sites fused to basal promoters are sufficient to activate CAT reporter gene expression

44 exclusively on podocytes of transgenic mice were sufficient to activate CD8+ T cells in vivo.

45 We propose that pre-SMAC signals are sufficient to activate cell adhesion, but not produc

46 ith their appropriate cell surface receptors was sufficient to activate cellular Sp1 and NF-kappaB.

47 truncated pre-TCR or an intact alphabetaTCR was sufficient to activate characteristic TCR signaling

48 and correct juxtaposition of the loxP sites is sufficient to activate Cre in this system.

49 R activation, and nuclear transport of TORC1 was sufficient to activate CRE-dependent transcription.

50 We discover one dominant mutation is sufficient to activate cyclization, and together with

51 response to DNA damage, and DINO expression was sufficient to activate damage signaling and cell cyc

52 localization of active Ace2 to mother nuclei is sufficient to activate daughter-specific genes in mot

53 DR1 and that short-term exposure to collagen is sufficient to activate DDR1 in Hodgkin lymphoma-deriv

54 Furthermore, BZLF1 expression in AGS cells is sufficient to activate DHRS9 gene expression and incr

55 through Piezo2), fire action potentials, and are sufficient to activate downstream sensory neurons.

56 EBV lytic genes; however, TG treatment alone was sufficient to activate EBV lytic replication.

57 n of the wild-type DME polypeptide in pollen is sufficient to activate ectopic paternal MEA and MEA:G

58 a functionally equivalent homologue of En-2 is sufficient to activate ELF-1 expression by itself.

59 ains, as expression of the tandem EH domains was sufficient to activate Elk-1.

60 fused to the bacteriophage MS2 coat protein are sufficient to activate enhancer-dependent splicing i

61 r binding at neutral pH and >or=22 degrees C is sufficient to activate Env for fusion.

62 indicate that receptor binding at neutral pH is sufficient to activate EnvA, such that ASLV-A particl

63 on of ETV6-RUNX1 alone in normal pre-B cells is sufficient to activate EPOR transcription.

64 We conclude that contact with laminin-5 is sufficient to activate ERK and to stimulate osteogeni

65 oximal half of the cytoplasmic domain of Mpl is sufficient to activate ERK in vitro and support base-

66 used to test if either or both of these PKCs are sufficient to activate ERKs, JNKs, and/or p38(MAPK)

67 ed subsets of neuroblasts and show that Runt is sufficient to activate even-skipped expression in the

68 Repeats of this region are sufficient to activate expression of a heterologous

69 from a well characterized GAP gene, GAP-43, is sufficient to activate expression in both developing

70 opic expression of Fgf8 in the mesencephalon is sufficient to activate expression of Engrailed-2 (En-

71 dition of as little as 10 ng of toxin per ml is sufficient to activate expression of genes encoding t

72 Cisplatin (</=50 mumol/L) exposure was sufficient to activate expression of the BRCA1-IRIS-

73 endritic spines in rat CA1 pyramidal neurons was sufficient to activate extracellular signal-regulate

74 A), a universal modulator of motor activity, is sufficient to activate fictive crawling in the medici

75 r binding of the soluble Tva (sTva) receptor was sufficient to activate fully the fusogenic potential

76 nsitive to caffeine, and that either pathway is sufficient to activate G(2) arrest.

77 alf-sites, whereas thyroid hormone receptors are sufficient to activate gene expression maximally fro

78 Approximately 3 kb of 5' flanking sequence is sufficient to activate gene expression in the cardiac

79 hese studies that glycerol kinase expression is sufficient to activate glycerol signaling in beta cel

80 co-stimulation of G(12/13) and G(i) pathways is sufficient to activate GPIIb/IIIa in human platelets

81 erm lineage and, when expressed ectopically, is sufficient to activate gut differentiation in nonendo

82 sion of the transcription factor SPIB or EHF is sufficient to activate HCK-dependent apical-to-basola

83 These Pit-1 elements are sufficient to activate hGH-N expression in the mouse

84 ion of a wild-type regulatory subunit of PKA is sufficient to activate Hh target gene transcription.

85 Ectopic expression of AP2alpha is sufficient to activate high-level expression of NC-sp

86 f cytokines into culture supernatants, which were sufficient to activate HIV-1 replication in latentl

87 excitation of the AFD thermosensory neurons is sufficient to activate HSF1 in another cell, even in

88 However, store depletion by thapsigargin is sufficient to activate hTRPC3 channels when expressed

89 when loaded onto CD1d, directly stained, and was sufficient to activate, human and mouse iNKT cells.

90 ings, a single dose of virosomal HAV vaccine is sufficient to activate immune memory and may provide

91 activation of inflammasomes by influenza and was sufficient to activate inflammasomes in primed macro

92 ructural analyses to show that talin binding is sufficient to activate integrin alphaIIbbeta3.

93 in of RIG-I, as it would be in the filament, is sufficient to activate interferon signaling.

94 increase in animals on a low-iron diet that is sufficient to activate IRP2.

95 iated overexpression of cyclin E is shown to be sufficient to activate islet cell proliferation.

96 VOCs from rhizobacteria for as little as 4 d was sufficient to activate ISR in Arabidopsis seedlings.

97 The recent demonstration that Rh monomer is sufficient to activate its cognate G protein, transdu

98 Induced dimerization of Mps1 is sufficient to activate its kinase activity in cells.

99 ation of 183 amino terminal residues of Vav2 is sufficient to activate its oncogenic potential.

100 rate that the IL-4R alpha cytoplasmic domain is sufficient to activate JAK-1 and STAT6 and to induce

101 ion assays, we show that the E1B 19K protein is sufficient to activate JNK and can strongly induce c-

102 his study, we found that MLK3 overexpression is sufficient to activate JNK potently without affecting

103 F-RII and associates indirectly with TNF-RI, is sufficient to activate JNK upon overexpression; (iii)

104 ivated kinase 1 (PAK1) and PAK2 in 293 cells is sufficient to activate JNK/SAPK and to a lesser exten

105 ells (C10) was inhibited and that H2O2 alone was sufficient to activate JNK and induce cell death.

106 ted by H2O2 and that overexpression of TRAF2 was sufficient to activate JNK provide an explanation fo

107 chondroitin sulfate proteoglycans) promoter is sufficient to activate lacZ reporter gene expression

108 Such Ca(2+) currents passing through SACs are sufficient to activate large-conductance Ca(2+)-acti

109 Conditioned medium from stretched AVICs was sufficient to activate leukocytes.

110 e that CO acts within a genetic pathway that is sufficient to activate LFY and TFL transcription, but

111 ncrease in WC-1 levels after light treatment is sufficient to activate light-regulated gene expressio

112 Direct stimulation with virus was sufficient to activate M2 gene expression in the wil

113 ved in mice with dominant Th2-type responses are sufficient to activate macrophages to destroy amasti

114 mbrane fusion and indicates that cathepsin L is sufficient to activate membrane fusion by SARS-CoV S.

115 In contrast, neither CpG ODN nor LPS alone is sufficient to activate memory B cells in vivo.

116 Bak inhibitors, i.e. Mcl-1 and Bcl-x(L), may be sufficient to activate mitochondrial apoptosis in the

117 MMP-3 alone is sufficient to activate MMP-9 on the ocular surface.

118 Although ectopic expression of PU.1 alone was sufficient to activate modest levels of IL-1beta tra

119 We propose that intermediate Mid levels are sufficient to activate MTD1 transcription and to rep

120 the inflammatory cytokines IL-6 or TNF-alpha was sufficient to activate mTOR, while preventing mTOR a

121 Finally, D1R stimulation alone was sufficient to activate mTORC1 in the NAc to promote

122 postulates, we found the E. coli pathobiont was sufficient to activate Naip5-Nlrc4 and cause disease

123 tion, even very weak TCR-ligand interactions are sufficient to activate naive T cells, induce rapid i

124 Consistent with this finding, XDmrt4 is sufficient to activate neurogenin, Xebf2, and neural

125 stitutively active form (delta Tlr4) of Tlr4 is sufficient to activate NF kappa B and COX-2 expressio

126 Bcl10 overexpression is sufficient to activate NF-kappaB, a process that requ

127 ound that expression of PIV5 L protein alone is sufficient to activate NF-kappaB.

128 pha-EGFP fusion protein showed that IKKalpha was sufficient to activate NF-kappaB activity and induce

129 prolonged nonlethal increase in the UPR that was sufficient to activate NF-kappaB and expression of t

130 on with the bacterium Pseudomonas aeruginosa was sufficient to activate NF-kappaB, and this activatio

131 , thus establishing that the Ly-49D receptor is sufficient to activate NK cells to lyse this target.

132 minimal C-terminal flagellin peptide, which is sufficient to activate NLRC4.

133 tion of the intracellular K(+) concentration was sufficient to activate NLRP3, whereas an increase in

134 Overexpression studies indicated that RBP-J was sufficient to activate Notch signaling and potentiat

135 a molecular explanation for why 1) DAG alone is sufficient to activate nPKCs but not cPKCs and 2) nPK

136 nal truncation that cannot bind microtubules is sufficient to activate organelle transport by kinesin

137 P at the rep promoter so that rep expression is sufficient to activate ori V.

138 ible rpoS strain demonstrate that RpoS alone is sufficient to activate OspC expression, even at 23 de

139 et genes with a single transgene, REST-VP16, is sufficient to activate other terminal neuronal differ

140 tion during treadmill-running, and that AMPK is sufficient to activate p-eNOS S1177 in the presence o

141 monstrating that either Lyn or Syk alone may be sufficient to activate p38 MAPK.

142 This mutant receptor is sufficient to activate p38 and cause NMuMG cells to u

143 ssion of GADD45b in AML12 murine hepatocytes is sufficient to activate p38 and to trigger apoptotic c

144 ing apoptosis, we show that ICP27 expression is sufficient to activate p38 signaling to a level that

145 stabilization, however tetramerization alone is sufficient to activate p53 transcriptional targets.

146 ummary, reducing S100B expression with siRNA was sufficient to activate p53, its transcriptional acti

147 that the signal from Ras through PI 3-kinase is sufficient to activate Pak, additional studies sugges

148 S100A12 expression is sufficient to activate pathogenic pathways through th

149 phorylation by creating a CD16/Jak2-K fusion is sufficient to activate pathways that prevent cell dea

150 ied concentrated HCV-RNA-containing exosomes are sufficient to activate pDCs.

151 C-terminal 69 residues of the J-protein Zuo1 are sufficient to activate Pdr1, a transcription factor

152 nce of LBP, 1/1,000 the concentration of LPS is sufficient to activate peripheral blood monocytes.

153 amate receptor, and bath application of NMDA was sufficient to activate PKA.

154 constitutive activation of PI 3-kinase alone is sufficient to activate PKB/Akt, but not the MAP kinas

155 overexpression of constitutively active AMPK was sufficient to activate PKC-zeta and promote Na,K-ATP

156 a(2+), in the absence of any other stimulus, is sufficient to activate PKD.

157 HeLa cells, intermediate gene transcription was sufficient to activate PKR.

158 f as few as 6 amino acids (pro-sigmaKDelta6) is sufficient to activate pro-sigmaK for DNA binding and

159 ion of such boundaries in nonmalignant cells was sufficient to activate proto-oncogenes.

160 dc28 associated with the mitotic cyclin Clb2 is sufficient to activate purified Cdc5 in vitro.

161 n signalling or overexpression of telomerase is sufficient to activate quiescent epidermal stem cells

162 The levels of adenovirus-expressed ICP0 were sufficient to activate quiescent viral genomes in t

163 s by using butyrate on methylated substrates was sufficient to activate recombination, and dexamethas

164 egions of Fzf1p-dependent genes was found to be sufficient to activate reporter gene activity in an *

165 nd that catalytic concentrations of Archease are sufficient to activate RtcB, and that Archease accel

166 ulture system, these physiologic SCN ligands were sufficient to activate SCN antibacterial activity a

167 nhibition of the ERK MAPK signalling pathway was sufficient to activate Scx in mouse limb mesodermal

168 n, whereas adventitious expression of Notch3 was sufficient to activate senescence and p21 expression

169 We show that recombinant Mup proteins are sufficient to activate sensory neurons and initiate

170 either ERS nor release of Ca(2+) from the ER was sufficient to activate SGK1.

171 Expression of AID is sufficient to activate SHM in hybridomas, non-B cells

172 f receptors, activation of a single receptor is sufficient to activate signaling in planta.

173 antagonist bicuculline, indicating that APs are sufficient to activate signals such as ERK in the nu

174 provide evidence that nicotinamide depletion is sufficient to activate Sir2 and that this is the mech

175 ein and Wnt1 or Wnt3a-expressing fibroblasts is sufficient to activate skeletal muscle-specific gene

176 lls from prefused endocardial cushions, BMP2 is sufficient to activate Smad1/5/8 phosphorylation and

177 ly, the cytosolic carboxyl terminus of STIM1 is sufficient to activate SOC, I(crac) and TRPC1 channel

178 ta indicate that (i) increased PI3K activity is sufficient to activate some but not all metabolic res

179 in the absence of its cognate kinase, SsrA, is sufficient to activate SPI-2 transcription.

180 taining 26 arginine or serine residues, that is sufficient to activate splicing when fused to MS2.

181 neutralizes general splicing inhibitors, and is sufficient to activate splicing when recruited to pre

182 for the first time that S727 phosphorylation is sufficient to activate Stat3, thereby driving prostat

183 , directly interfering with axonal transport is sufficient to activate stress kinase pathways initiat

184 de in hair follicles, and ODC overexpression is sufficient to activate such cells to expand clonally

185 Expression of p40(phox) was sufficient to activate superoxide production in COS(

186 support a model where adding AMPA receptors is sufficient to activate synapses that had few receptor

187 for CD4, CD26, CD28, CD44, CD45RA, or CD45RO were sufficient to activate T cells when co-immobilized

188 Thus suppression of PKA activity is sufficient to activate targets of the Shh signaling p

189 lf-major histocompatibility complex class II is sufficient to activate TCR Tg T cells and serve as a

190 f activate development, that A beta proteins are sufficient to activate the A developmental pathway i

191 rs in the biochemical milieu of these wounds are sufficient to activate the inflammasome, as wound-co

192 haIIb/beta3 transmembrane domain heterodimer are sufficient to activate the integrin.

193 of the cytoplasmic domain of the betaL chain are sufficient to activate the Jak-Stat pathway and trig

194 concentrations of butyrate in colonic lumen are sufficient to activate the receptor maximally, there

195 ichoic acid as would be expected if alarmins are sufficient to activate the TLRs.

196 " particles as would be expected if alarmins are sufficient to activate the TLRs.

197 duction of RpoS expression did not appear to be sufficient to activate the acid tolerance response.

198 the activation loop at Thr(410) is known to be sufficient to activate the kinase function of full-le

199 results demonstrate that dimerization alone is sufficient to activate the Abl kinase and provide a m

200 The caspase-2-released Cyt c is sufficient to activate the Apaf-caspase-9 apoptosome

201 ough calmodulin-dependent kinase II (CaMKII) is sufficient to activate the APC/C and terminate CSF ar

202 wding of checkpoint mediator proteins on DNA is sufficient to activate the ATR kinase.

203 trating that colocalization of these sensors is sufficient to activate the checkpoint in the absence

204 The presence of a single, lagging chromosome is sufficient to activate the checkpoint, producing a de

205 g P-selectin, we found that P-selectin alone is sufficient to activate the complement system, marked

206 ce is limited to approximately 120 pN, which is sufficient to activate the conformational change of t

207 The base is sufficient to activate the CP for degradation of pept

208 donuclease-induced double-strand break (DSB) is sufficient to activate the DNA damage checkpoint and

209 Ectopic expression of ast-1 is sufficient to activate the dopamine pathway in some c

210 We now show that RUNX1 is sufficient to activate the endogenous mouse Ebeta ele

211 core enhancer fragment of the 1.4-kb E alpha is sufficient to activate the enhancer-dependent step of

212 HOTAIR overexpression is sufficient to activate the ER transcriptional program

213 The C-terminal domain of FtsK is sufficient to activate the exchange of the second pai

214 We conclude that DA is sufficient to activate the full crawl motor program a

215 that expression of a set of defined factors is sufficient to activate the gene networks governing HS

216 I interferon receptor (IFN-R) in mouse cells is sufficient to activate the Jak-Stat pathway and to el

217 acidification of the membrane/boundary layer is sufficient to activate the light-sensitive channels.

218 re treated with NaB or TSA, neither of which is sufficient to activate the lytic cycle, an increase o

219 a single phosphorylation of Tyr-542 of SHP-2 is sufficient to activate the MAP kinase pathway in livi

220 w that binding of JIP1 and FEZ1 to Kinesin-1 is sufficient to activate the motor for MT binding and m

221 in the context of a different kinase domain, is sufficient to activate the multiple pathways leading

222 e find that a few seconds of exposure to TNF is sufficient to activate the NF-kappaB pathway in HeLa

223 dria outer membranes, and we found that this is sufficient to activate the NLRP3 inflammasome.

224 Here we demonstrate that R alone is sufficient to activate the pol promoter in EBV-negati

225 ian meal moth (Plodia interpunctella), which is sufficient to activate the prophenoloxidase (proPO) p

226 y activity coupled to serotonergic signaling is sufficient to activate the protective HSR prior to fr

227 6 in the extracellular half of the membrane is sufficient to activate the receptor and that TM segme

228 ulate that a force of 10 pN generated in 1 s is sufficient to activate the rigidity response.

229 elle to the plasma membrane by myristylation is sufficient to activate the signal transduction pathwa

230 in macromeres (the progenitors of NSM cells) is sufficient to activate the skeletogenic GRN.

231 absence of tension at the yeast kinetochore is sufficient to activate the spindle checkpoint in mito

232 Each of these highly conserved sequences is sufficient to activate the splicing of a heterologous

233 ization of the extracellular domains of PpkA is sufficient to activate the T6SS.

234 more, we show that Kin2 kinase domain itself is sufficient to activate the UPR, suggesting that Kin2

235 these channels induces a depolarization that is sufficient to activate the voltage-dependent calcium

236 , we show that a monoallelic mutation of p53 was sufficient to activate the Aha1/Hsp90 ATPase axis le

237 the ER stress response, human IRE1 (hIRE1), was sufficient to activate the ATF6 reporter gene, while

238 Adding the ROS hydrogen peroxide was sufficient to activate the Ca(2+) channels and trigg

239 of blood alcohol to approximately 120 mg/dL was sufficient to activate the cell death program in vis

240 otransfection with a SOX9 expression plasmid was sufficient to activate the enhancer, and mutation of

241 rated that removal of 20 C-terminal residues was sufficient to activate the enzyme fully.

242 Episomal expression of HPV-16 oncoproteins was sufficient to activate the FA pathway.

243 Tax was sufficient to activate the phosphoinositide-3 kinase

244 In reporter gene assays, XBP-1 alone was sufficient to activate the R promoter, whereas the c

245 the amino and the carboxyl terminus domains was sufficient to activate the transforming potential of

246 Overexpression of ATF4 was sufficient to activate the VEGF promoter, and arseni

247 and constitutively active alleles of p70S6k were sufficient to activate the cyclin E promoter.

248 r T cells nor a global inflammatory stimulus were sufficient to activate the low-avidity CD8(+) T cel

249 ia inhibitory factor (LIF), only OSM and LIF were sufficient to activate the STAT reporter in myotube

250 stripped glucocorticoid receptors and alone are sufficient to activate them to bind steroids.

251 exposure to a combination of IL-12 and IL-18 is sufficient to activate them.

252 However, it is unknown which nAChR subtypes are sufficient to activate these neurons.

253 hat small changes in peptidoglycan structure are sufficient to activate these stress responses, sugge

254 Here we report that SIPK alone is sufficient to activate these defense responses.

255 in the absence of Tor, overexpression of leo is sufficient to activate tll expression.

256 enome and that differentiation signals alone are sufficient to activate transcription from the late p

257 rid to an hsp70 promoter in Drosophila cells is sufficient to activate transcription in the absence o

258 Using this assay, we showed that Mga is sufficient to activate transcription in vitro for Mga

259 d a 5.5-kb enhancer in the Wnt-1 locus which is sufficient to activate transcription of a reporter ge

260 n the Xenopus embryo, we show that myocardin is sufficient to activate transcription of a wide range

261 ichostatin A induces histone acetylation and is sufficient to activate transcription repressed by G9a

262 the DNA-binding domain (residues 264 to 420) is sufficient to activate transcription when it is local

263 dicarboxylic acid transport protein D (DctD) is sufficient to activate transcription.

264 ing of the Lsk1 kinase at the ste11 promoter is sufficient to activate transcription.

265 Spermine was sufficient to activate transcription of these IS ele

266 upstream of the translation initiation site, was sufficient to activate transcription.

267 Extracellular TG2 was sufficient to activate transforming growth factor-be

268 However, diacylglycerols were sufficient to activate TRPC3 in a protein kinase C-

269 human luminal cancer cells, BRCA1 silencing was sufficient to activate TWIST and EMT and increase tu

270 BzpF is sufficient to activate two of these genes.

271 ullin/CDC53-F box protein ubiquitin ligases, was sufficient to activate UBCH5c to synthesize polyubiq

272 that production of superoxide in the matrix was sufficient to activate UCP2.

273 we tested whether this fragment of E(delta) is sufficient to activate VDJ recombination in vivo.

274 th a model in which talin or activated talin is sufficient to activate vinculin.

275 hesis that nAChRs containing alpha6 subunits are sufficient to activate VTA DA neurons, we studied mi

276 pression of LRP6 in mammary epithelial cells is sufficient to activate Wnt signaling and promote cell

277 hich is required for signal transduction and is sufficient to activate Wnt signaling when overexpress

278 Moreover, we show that MIB1 is sufficient to activate Wnt/beta-catenin (CTNNB1) sign

279 ings demonstrate that IRE1alpha dimerization is sufficient to activate XBP1 mRNA splicing in the abse

280 ression of SSP protein in the leaf epidermis is sufficient to activate YDA-dependent signaling.