ライフサイエンスコーパス: AP-1

1 n via the activation of activator protein-1 (AP-1).

2 ng partner, forming transcriptionally active AP-1.

3 t cells can compensate for long-term loss of AP-1.

4 -3, while dendritic targeting is mediated by AP-1.

5 and MR demonstrated a potential to activate AP-1.

6 rophages partly via the transcription factor AP-1.

7 directly induced inhibitors of NF-kappaB and AP-1.

8 onents of the oncogenic transcription factor AP-1.

9 e transcription factors NF-kappaB, NFAT, and AP-1.

10 binds to AP-3 with higher efficiency than to AP-1.

11 y the sigma1 subunit of the clathrin adaptor AP-1.

12 and the transcription factors NF-kappaB and AP-1.

13 mutations in the sigma1A subunit isoform of AP-1.

14 educed activity of nuclear factor-kappaB and AP-1.

15 tivated signalling pathways, notably JNK and AP-1.

16 Arf1 induced trimerization and activation of AP-1.

17 t sites that do not require cooperation with AP-1.

18 n and nuclear translocation of NF-kappaB and AP-1.

19 s a random coil with diminished affinity for AP-1.

20 used BRET to study the in vivo activation of AP-1.

21 origenic transcription factors MYC, E2F3 and AP-1.

22 onse elements (TREs), even in the absence of AP-1.

23 on nuclear transcript factors NF-kappaB and AP-1.

24 the viral lytic cycle that is homologous to AP-1.

25 Adaptor proteins (AP 1-5) are heterotetrameric complexes that facilitate s

26 ed that residue 172 in Arf1 is necessary for AP-1 activation and is required for the efficient sortin

27 and lipids to regulate TLR2-L-induced NF-kB/AP-1 activation in THP1 cells were analyzed.

28 nd PG vesicles inhibits TLR2-L-induced NF-kB/AP-1 activation in THP1 cells.

29 itin ligase Trim7 as a critical component of AP-1 activation via Ras.

30 nitroxidative stress, IKK/NF-kappaB and JNK/AP-1 activation, inflammatory cytokine, chemokine, and a

31 ino acids to SsaG had no effect on NF-kappaB/AP-1 activation.

32 chanism linking growth factor signalling and AP-1 activation.

33 RNA attenuated pregnenolone sulfate-induced AP-1 activation.

34 hibits MMP-1 expression by suppressing c-Jun/AP-1 activation.

35 ich is necessary for its kinase activity and AP-1 activation.

36 d CD44V6 expression is through EGR1-mediated AP-1 (activator protein-1) activity and that the EGR1- a

37 as mediated through the suppression of c-Fos/AP-1 activity at transcriptional and post transcriptiona

38 stains ERK signaling, which is important for AP-1 activity in lung fibroblasts.

39 egative regulator of the cell cycle, whereas AP-1 activity in myeloid inflammatory responses has larg

40 istant BMI1(+) CSCs, which exhibit increased AP-1 activity that drives invasive growth and metastasis

41 and subsequent effects on cell signaling and AP-1 activity, leading to changes in the expression of i

42 e transcription of CD44V6 via an effect upon AP-1 activity.

43 n, as well as decreased activator protein 1 (AP-1) activity.

44 osphorylation-dependent interaction with the AP-1 adaptor complex.

45 regulates the spatiotemporal recruitment of AP-1 and also drives a conformational change favoring an

46 latory subunit 9b) and the clathrin adaptors AP-1 and AP-2.

47 nt for binding the clathrin adaptor proteins AP-1 and AP-2in vitro Surprisingly, mutating the LL moti

48 AP-1 and Arf1 disruption affects the accumulation of Fz/

49 tituents of super enhancers, are occupied by AP-1 and cohesin complex members, and originate from pri

50 APKs p38 and ERK1/2 suppresses activation of AP-1 and CREB signaling pathways and attenuates LPS-indu

51 capacity for innate immune responses through AP-1 and CREB signaling pathways.

52 d Cryaa regulatory regions contain arrays of AP-1 and Ets-binding sites.

53 s via interactions with the adaptor proteins AP-1 and GGAs.

54 of transcription factors such as NF-kappaB, AP-1 and HSF1 which mediate changes in gene expression.

55 for the transcription factors NF-kappaB and AP-1 and later at those for the transcription factors IR

56 o immune receptors for the activation of the AP-1 and NF-kappaB master transcriptional programs.

57 teomic approach to screen viral proteins for AP-1 and NF-kappaB promoter activity in AP-1- and NF-kap

58 Although IL-33 induces AP-1 and NF-kappaB, NFAT signaling has not been describe

59 The three Trim12-CypA fusions all activated AP-1 and restricted HIV-1 transduction, whereas the Trim

60 erved engulfment receptor Draper, as well as AP-1 and STAT92E.

61 vity of the transcription factors JUN and/or AP-1 and TEAD.

62 he c-Fos subunit of the transcription factor AP-1 and thereby inhibited TLR4-triggered induction of i

63 To examine genes regulated by AP-1 and to examine how it interacts with other inducibl

64 Here, we study how AP-1 and Zta recognize these methyl groups within their

65 by activating a unique activator protein 1 (AP-1) and runx1 transcription program autonomous to the

66 ription factor complex, activator protein 1 (AP-1), and promoted SIRT1 association with the AP-1 site

67 ctivates IkappaB kinase (IKK)/NF-kappaB, JNK/AP-1, and c/EBPbeta and stimulates the expression of var

68 ption factor complexes, such as NFkappaB and AP-1, and trans-repress the transcription of cytokines,

69 for AP-1 and NF-kappaB promoter activity in AP-1- and NF-kappaB-luciferase reporter assays.

70 binding activity was confirmed using TP53-, AP-1- and NF-kappaB-specific REs or p21, SERPINE1 and IL

71 tial for protein-protein interactions within AP-1- and Sox9-containing complexes.

72 Our bottom-up approach demonstrates that AP-1- and TEAD4-associated cis-regulatory elements form

73 tage TLR5 agonist that activates NF-kappaB-, AP-1-, and STAT3-driven immunomodulatory signaling pathw

74 rogen-independent phenotypes by altering the AP-1/androgen receptor regulatory circuit in PCa cells.

75 actions, previously established for clathrin-AP-1/AP-2 coats, to a non-clathrin coat.

76 Both AP-3 and AP-1 are localized to the Golgi but occupy adjacent doma

77 partments, others find that the two forms of AP-1 are present in the same vesicle but recognize diffe

78 highlighted potential residues mediating the AP-1/Arf1 interaction and the unlocking of the complex.

79 Here we identified Fra-2/AP-1 as a key regulator of terminal epidermal differenti

80 ium subunit (micro1) of the clathrin adaptor AP-1 as a top hit.

81 These findings support the notion of AP-1 as an effector of polarized sorting in neurons and

82 Together, our results uncover AP-1 as an important determinant for inflammation-induce

83 scaffold protein CKA (connector of kinase to AP-1) as essential for autophagosome transport in neuron

84 ear homology, Arf-binding) proteins and the AP-1 (assembly protein-1) complex.

85 indicated that direct co-binding of Sox9 and AP-1 at target motifs promoted gene activity.

86 cellular pool of L-selectin colocalizes with AP-1 at the trans-Golgi network.

87 K pathway activation, suggesting that an ERK-AP-1 axis plays an important role in translating TCR sig

88 ucture that serves as a recognition site for AP-1 binding and governs Golgi export.

89 Because patch formation and AP-1 binding are dependent on proper folding of the cyto

90 er landscape and quantitative acetylation at AP-1 binding sites.

91 Likewise, neither GR nor MR affected AP-1 binding, but repression or activation of AP-1 repor

92 a strong enrichment for activator protein 1 (AP-1)-binding events, suggesting that multi-loop activat

93 expression and bound the Fshb promoter at an AP-1-binding site in a complex with c-JUN.

94 r protein-1) activity and that the EGR1- and AP-1-binding sites in the CD44v6 promoter account for it

95 e transcription factor, activator protein-1 (AP-1), binds to cognate DNA under redox control; yet, th

96 -1 (but not AP-3 or AP-4) and that Rab11 and AP-1 both colocalize with p14 at the TGN.

97 We found that EBV BGLF2 activated AP-1 but not NF-kappaB reporter activity.

98 vealed that p14 Golgi export is dependent on AP-1 (but not AP-3 or AP-4) and that Rab11 and AP-1 both

99 D14, thereby limiting activation of NFkappaB/AP-1 by lipopolysaccharide.

100 lted in the activation of IKK/NF-kappaB, JNK/AP-1, c/EBPbeta, and p38 MAPK and induction of proinflam

101 dhesion molecule E-cadherin and that loss of AP-1 causes the disappearance of the E-cadherin-containi

102 Moreover, ATF3 expression was AP-1(cFOS/cJUN)-dependent and expression levels were mai

103 suppressed SQSTM1 by binding to a consensus AP-1 cis element located around 2 kb upstream of SQSTM1-

104 over, we have described two novel functional AP-1 cis-elements in BDNF promoter I, responsible for th

105 n of exon I transcripts by binding two novel AP-1 cis-elements in promoter I.

106 c domain structure that serves as an unusual AP-1 clathrin adaptor-dependent Golgi export signal in o

107 upports Th17 cell identity by regulating key AP-1 complex constituents.

108 electin is transported constitutively by the AP-1 complex, leading to the formation of a trans-Golgi

109 ranscription factors bind DNA as part of the AP-1 complex, regulate many cellular processes, and play

110 nding of mu1A of the clathrin-coated vesicle AP-1 complex.

111 report that the clathrin adaptor protein 1 (AP-1) complex, although dispensable for the biogenesis o

112 factors, members of the activator protein 1 (AP-1) complex, form heterodimers and bind to DNA via a b

113 These findings identify the activation of AP-1 complexes of the Jun/ATF-type as an important eleme

114 1 and MMP-3 genes, which in association with AP-1 components (c-Fos or Jun), bind STAT-1 in a homodim

115 BRET) to study the Arf1/AP-1 interaction and AP-1 conformational changes in vivo.

116 re, we report the role of a newly identified AP-1 consensus sequence in the TF gene promoter and its

117 ion of AP-1 reporters occurred in a ligand-, AP-1 consensus sequence-, and AP-1 family member-specifi

118 ed using a variety of ligands, two different AP-1 consensus sequences, GR and MR DNA-binding domain m

119 sly shown to reduce ATP7B incorporation into AP-1-containing clathrin-coated vesicles, caused loss of

120 volved in IE gene expression, including Ets, AP-1, CREB, and C/EBP, which lead to the transient ERK-R

121 l reporters that are dependent on Drosophila AP-1 (dAP-1) and STAT92E.

122 ediate chromatin remodeling of the EDC in an AP-1 dependent manner.

123 ere we show that clathrin/adaptor protein 1 (AP-1)-dependent intestinal apical membrane polarity and

124 onstrate the critical role of beta-arrestin2/AP-1-dependent beta2AR signaling in the regulation of CC

125 hosphorylation of the L-selectin tail blocks AP-1-dependent retrograde transport of L-selectin.

126 e that tracheal invasion is controlled by an AP-1-dependent switch in FGF trafficking.

127 1 gamma subunit, as predicted for the common AP-1-dependent trafficking process.

128 16b directly targets c-Jun, thereby reducing AP-1-dependent transcription and sensitizing cells to ER

129 Waals contact with a conserved di-alanine in AP-1 dimer (Ala265 and Ala266 in Jun), or with the corre

130 We propose that AP-3 and AP-1 directly select transmembrane proteins and target t

131 inding to the MnSOD promoter, which leads to AP-1 dissociation followed by MnSOD transcription.

132 e, autoimmune polyendocrine syndrome type 1 (APS-1), distinguished by multi-organ autoimmunity.

133 e also studied the conformational changes in AP-1 driven by Arf1 in live cells and found that opening

134 Here, inflammation generates a cFOS AP-1 early response that indirectly affects MMP13 gene e

135 g was consistent with a trans-mechanism, and AP-1 effects were confirmed for specific gene targets in

136 ifiers, such as histone deacetylase 3, in an AP-1 element dependent manner.

137 inner thymine residues corresponding to the AP-1 element, resulting in the four spatially equivalent

138 JUN, which in turn governs transcription of AP-1-element containing G1-phase cell cycle regulators s

139 ive effects through the suppression of c-Fos/AP-1 expression and activity in OA chondrocytes under pa

140 AP-1 expression correlated with increased MK DNA synthes

141 The AP-1 factor basic leucine zipper transcription factor, A

142 hIP) assays established binding of c-Jun (an AP-1 factor) and Etv5/ERM (an Ets factor) to these regio

143 Here we show the activator protein-1 (AP-1) factor JunB is an essential regulator of Th17 cell

144 the EP4 receptor and repressed Fosb and Fos AP-1 factors in a beta-catenin-independent manner.

145 AP-1 factors respond to MAP kinase signalling and compri

146 in a ligand-, AP-1 consensus sequence-, and AP-1 family member-specific manner.

147 (ERK5) phosphorylation and the expression of AP-1 family members (c-Fos/c-Jun).

148 hich formed heterodimeric complexes with the AP-1 family members activating transcription factor (ATF

149 LBCL cell lines expressed high levels of the AP-1 family members c-Jun, JunB, and JunD, which formed

150 Together, the data support a model in which AP-1 family members contribute to Sox9 action in the tra

151 Among AP-1 family members, Jun and Fosl2 were highly expressed

152 moters, leading to enhanced loading of other AP-1 family members, thereby leading to cellular growth.

153 nd siRNA knockdown or overexpression of core AP-1 family members.

154 restrict alternative CD4(+) T-cell potential.AP-1 family transcription factors regulate CD4(+) T help

155 r (TCF) Elk-1 attenuated the upregulation of AP-1 following stimulation of TRPM3 channels.

156 the mechanism underlying redox-regulation of AP-1 Fos/Jun transcription factors and provide structura

157 A series of crystal structures of the AP-1 FosB/JunD bZIP domains reveal ordered DNA-binding r

158 Reduced AP-1 function increased the Atp7a presence in early/recy

159 blocked upon siRNA-mediated knockdown of the AP-1 gamma subunit, as predicted for the common AP-1-dep

160 tion and reciprocally activate NF-kappaB and AP-1 gene programs implicated in malignancy.

161 ity for all four sequences examined, whereas AP-1 has considerably reduced affinity for the asymmetri

162 kly repress NFkappaB, its role in modulating AP-1 has not been established.

163 n of TP63 and NF-kappaB complexes through an AP-1 hub, further supporting our findings.

164 lls (NF-kappaB), STAT3, activator protein-1 (AP-1), hypoxia-inducible factor-1 (HIF-1), and tumor pro

165 ed the functional interplay between Sox9 and AP-1 in mammalian chondrocyte development.

166 between c-Jun and Nrf2 supporting a role for AP-1 in regulating 4-HNE-induced GSTA4 expression.

167 HUVECs, and have established a new role for AP-1 in the basolateral constitutive secretion of VWF.

168 he transcription factor activator protein-1 (AP-1) in ABC DLBCL.

169 tion, MKK4 (but not MKK7) activation and JNK/AP-1 induction, leading to a Bak- and Bax-dependent mito

170 te a specific set of vascular genes and that AP-1 inhibition shifts the balance between smooth muscle

171 AP-1 inhibitors and gene-specific small interfering RNAs

172 Furthermore, a druggable AP-1 inhibitory small molecule suppresses skin phenotype

173 nce energy transfer (BRET) to study the Arf1/AP-1 interaction and AP-1 conformational changes in vivo

174 wide redistribution of the cREL/p63/p73, and AP-1 interactome, to diminish TAp73 tumor suppressor fun

175 AP-1 is a clathrin adaptor recruited to the trans-Golgi

176 Furthermore, AP-1 is required for de novo binding of TEAD4, a transcr

177 T: Activator protein 1 (AP-1) is a transcription factor that recognizes two vers

178 erently, whereas the corresponding Ala266 of AP-1 Jun protein lacks such flexibility.

179 pectedly intricate organization of the inner AP-1 layer of the clathrin coat.

180 d PAM-1 accumulated on the cell surface when AP-1 levels were reduced.

181 Here, we show that AP-1, like NF-kappaB, was controlled by constitutive act

182 nidulans and mediated by NapA, a homolog of AP-1-like bZIP transcription factor, which is essential

183 ndrocytes identified marked enrichment of an AP-1-like motif.

184 The AP-1-like transcription factor Yap8 is critical for arse

185 Aldosterone activation of AP-1 may contribute to its proinflammatory effects in th

186 are un/misfolded to cause EKV likely via an AP-1-mediated mechanism and identifies a small molecule

187 Chs3 is maintained not only by its efficient AP-1-mediated recycling, but also by recycling through t

188 RK phosphorylation as well as NF-kappaB- and AP-1-mediated transcription.

189 we find that the adaptor protein complex-1 (AP-1) mediates trafficking of Ca(V)2.2 from the trans-Go

190 show that FOSL1 is the main immediate early AP-1 member induced by melanoma oncogenes.

191 Here the authors show that the AP-1 member JunB is a nonredundant regulator of transcri

192 Consistent with the binding of TAp73 and AP-1 members on the target promoters in a c-Jun-dependen

193 Furthermore, ATF3 bound the proximal MMP13 AP-1 motif in stimulated chondrocytes at time points tha

194 co-activated a Col10a1 enhancer in Sox9 and AP-1 motif-dependent manners consistent with their combi

195 actor 4 (TCF4) at CTTTG motifs as well as at AP-1 motifs (TGAXTCA).

196 Consistent with this, the frequency of AP-1 motifs was elevated in regions upstream of PN-KC-de

197 ting activation of itself and its downstream AP-1/NF-AT1 axis, which in turn elicits EGFR expression.

198 ranscription factors including NF-kappaB and AP-1, Nrf2 targets, cytokines, chemokines and other infl

199 Inhibiting AP-1 or BMI1 sensitized tumors to cisplatin-based chemot

200 the onset of virus infection, activates the AP-1 pathway and enhances EBV reactivation and virus pro

201 -TLR4 signaling in hepatocytes via NF-kB and AP-1 pathways.

202 PMECs through the IKKbeta/NF-kappaB and MAPK/AP-1 pathways.

203 eractions with the Wnt/beta-catenin/TCF4 and AP-1 pathways.

204 emness through activation of SDF-1/CXCR4 and AP-1 pathways.

205 ressed, growth-factor-inducible TFs FOS/JUN (AP-1) play a central role in enhancer selection.

206 ramming by EGR and NFAT with reduced EBF and AP-1 programming imbalances the normal B cell epigenetic

207 complexes of transcription factors NFAT and AP-1 promote effector T cell differentiation.

208 tant-TREM1 plasmid carrying mutations in the AP-1 promoter binding site.

209 nd in vitro and ex vivo analyses showed that AP-1 promotes chondrocyte hypertrophy.

210 OS, andJUND) were up-regulated at d9 and two AP-1 proteins (JunD and c-Fos) were up-regulated both at

211 ation of chaperones Bip and Hsp70 as well as AP-1 proteins c-Fos and JunB, in addition to molecular s

212 oreover, our results show that the effect of AP-1 proteins on the activity of rat BDNF promoters III

213 NF promoters III and VI is indirect, because AP-1 proteins were not detected to bind the respective p

214 ight for therapeutic interventions targeting AP-1 proteins.

215 1 also silences Foxa1 promoter by inhibiting AP-1 recruitment.

216 In particular, we identified an AP-1 regulated transcriptional network in dlPFC neurons

217 ntified as a novel c-Fos/activator protein-1(AP-1)-regulated gene.

218 We show that AP-1 regulates the localization of the intercellular adh

219 sential autoantigens, as described for other APS-1-related autoimmune diseases.

220 n of miR-196b inhibited the FOS promoter and AP-1 reporter activity.

221 P-1 binding, but repression or activation of AP-1 reporters occurred in a ligand-, AP-1 consensus seq

222 eq data have consistently shown GR to occupy AP-1 response elements (TREs), even in the absence of AP

223 Thus, the ETS/AP-1 sequence defines a unique gene expression program r

224 he proteasome, autophagy, and TAK1-dependent AP-1 signaling have been suggested to contribute to rest

225 s found to down-regulate peroxisomes via the AP-1 signaling pathway.

226 ociated with inhibition of the NF-kappaB and AP-1 signaling pathways.

227 Importantly, MR modulation of NFkappaB and AP-1 signaling was consistent with a trans-mechanism, an

228 re, the effects of GR and MR on NFkappaB and AP-1 signaling were directly compared using a variety of

229 ion (Stat92E), c-Jun N-terminal kinase (JNK)/AP-1 signaling, and expression of matrix metalloproteina

230 inhibition of the MAPK-activator protein-1 (AP-1) signaling pathway.

231 ation, deletion, and mutation of this distal AP-1 site all significantly suppressed TF promoter activ

232 bioinformatics tools, we found that a novel AP-1 site at -1363 bp of the human TF promoter region is

233 IL1R2 complexes with c-Fos and binds to the AP-1 site at the IL-6 and VEGF-A promoters.

234 promoter activity, indicating a role for the AP-1 site in SIRT1 inhibition.

235 ion factor complex, which bound the proximal AP-1 site in the TF gene promoter and activated TF expre

236 The AP-1 site of the Mmp13 promoter is required for PTH stim

237 -1), and promoted SIRT1 association with the AP-1 site of the Mmp13 promoter.

238 iated by SIRT1 association with c-Jun at the AP-1 site of the Mmp13 promoter.

239 When the AP-1 site was mutated, EX527 was unable to increase PTH-

240 but not the typical c-Fos, bound to the new AP-1 site.

241 n which TAp73 was found to be bound near the AP-1 site.

242 ated the cyclin D1 promoter via NFkappaB and AP-1 sites and sensitized cells to TRAIL-induced apoptos

243 RHS7 of the locus control region relative to AP-1 sites surrounding type-2 cytokine loci in Th2 cells

244 any of these elements contain composite NFAT/AP-1 sites, which typically support cooperative binding,

245 including human-specific activity-responsive AP-1 sites.

246 ing the availability of activator protein-1 (AP-1) sites to Jun family signal-dependent TFs.

247 n of TAp73 from TP53 to activator protein-1 (AP-1) sites.

248 and oligomerization on NF-kappaB-, TP53- or AP-1-specific sequences were independently validated by

249 ntiate transactivation of activator protein (AP)-1 target genes such as cyclin D1.

250 at TAp73 plays a vital role in activation of AP-1 target genes via direct binding to c-Jun at the tar

251 lation by c-JUN and JUND defines a subset of AP-1 target genes with cell migration roles.

252 cruitment of these Fos family members to the AP-1 target promoters on which TAp73 was found to be bou

253 in a c-Jun-dependent manner to transactivate AP-1 target promoters.

254 ion of matrix metalloproteinase 7 (MMP7), an AP-1 target, was also significantly decreased.

255 ry transcription factor activator protein-1 (AP-1) through protein-protein interactions.

256 accumulation of PtdIns4P and recruitment of AP-1 to the TGN.

257 kappaB (NF-kappaB), and activator protein 1 (AP-1) to induce type 2 cytokines.

258 like kinase 3 (Plk3) signaling and the c-Jun.AP-1 transcription complex, resulting in apoptosis of co

259 intergenic regions were heavily enriched for AP-1 transcription factor binding sites and were frequen

260 allele-specific differences at rs7132434 for AP-1 transcription factor binding.

261 ingly, little is known about the role of the AP-1 transcription factor c-Jun in macrophage activation

262 eq, we demonstrate that the cistrome for the AP-1 transcription factor c-Jun is comprised of 13,800 b

263 erated with MAPK signaling through the c-Jun/AP-1 transcription factor complex to activate CD73 trans

264 er protein c-Jun, a major constituent of the AP-1 transcription factor complex, or expression of a c-

265 FOS-like antigen 1 (FOSL1), a component of AP-1 transcription factor complexes, contributes to the

266 Here, we studied the regulatory role of the AP-1 transcription factor family in blood development us

267 nscription of several genes belonging to the AP-1 transcription factor family.

268 nscription factors such as NF-kappaB and the AP-1 transcription factor member c-Fos.

269 splicing, NF-kappaB signaling pathways, the AP-1 transcription factor network, chromatin remodeling,

270 T cells 3 (NFATc3) and FosB proto-oncogene, AP-1 transcription factor subunit (FosB) are involved in

271 ta (Fshb) transcription via induction of the AP-1 transcription factor, a heterodimer of c-FOS and c-

272 Here, we demonstrate that the AP-1 transcription factor, Fos-like antigen 2 (Fosl2), p

273 lammation, express c-Fos, a component of the AP-1 transcription factor.

274 neered form of NFAT1 unable to interact with AP-1 transcription factors diminished T cell receptor (T

275 AP-1 transcription factors directly upregulate the expre

276 The role of AP-1 transcription factors in early B cell development a

277 ated in response to TrkB signaling, and that AP-1 transcription factors participate in the induction

278 ms behind this autoregulation, we found that AP-1 transcription factors, comprising Jun and Fos famil

279 onal activity while increasing TLR5-mediated AP-1 transcription.

280 r FOS forms part of the activator protein 1 (AP-1) transcription factor complex, which plays a pivota

281 which forms part of the activator protein 1 (AP-1) transcription factor complex.

282 c-Jun is a component of activator protein-1 (AP-1) transcription factor complexes that regulates proc

283 as a potentiator of the Activator Protein-1 (AP-1) transcription factor.

284 hear-flow exposure, six activator protein 1 (AP-1) transcripts (ATF4,JUNB,JUN,FOSB,FOS, andJUND) were

285 oscopy structures of the Nef- and Arf1-bound AP-1 trimer in the active and inactive states.

286 e to shear forces results in JNK activation, AP-1 up-regulation, and downstream transcriptional chang

287 linked to both the shear stress response and AP-1 up-regulation.

288 he transcription factor activator protein-1 (AP-1) via stimulation of transient receptor potential me

289 Furthermore, transcription factor AP-1 was a main factor in IL-5-induced HSP70-1 in respon

290 The upregulation of AP-1 was attenuated in cells that overexpressed mitogen

291 The expression of the activator protein 1 (AP-1) was increased in lung tissues from mouse after BLM

292 Additionally, activator protein 1 (AP-1) was shown to be essential in mediating CCR2 expres

293 matrix, using the adaptor protein complex 1 (AP-1), where it may provide the bulk of collagen-bound s

294 y compact conformational ensemble that binds AP-1, whereas CLK2-PAGE4 is more expanded and resembles

295 n induced the transcription factors NFAT and AP-1 which created thousands of new DNase I-hypersensiti

296 The adaptor protein-1 complex (AP-1), which transports cargo between the trans-Golgi ne

297 g and subsequent activation of NF-kappaB and AP-1, which are transcriptional activators of innate imm

298 Yeast have two forms of AP-1, which differ only in the mu chain.

299 lation, stimulating the transcription factor AP-1, which in turn enhances transcription of amyloid-be

300 lternate mu chains creates distinct forms of AP-1 with altered cargo sorting, but how these subunits