ライフサイエンスコーパス: AP-1

1 e and the transcription factors Fos and Jun (AP-1).

2 gh transcription factor activator protein-1 (AP-1).

3 e the LPS-stimulated activation of NF-kappaB/AP-1.

4 upport a functional role for Irc6 binding to AP-1.

5 Laa2 revealed that it binds to both Laa1 and AP-1.

6 ncluding motifs for the GC receptor cofactor AP-1.

7 ar to mutations that remove the gamma-ear of AP-1.

8 ng partner, forming transcriptionally active AP-1.

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

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

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

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

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

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

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

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

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

18 d T cell anergy/exhaustion in the absence of AP-1.

19 (CPs) (1.1 +/- 1.5 mug/L), anabaenopeptins (APs) (1.0 +/- 0.6 mug/L), anatoxin-a (AT-A) (0.03 +/- 0.

20 d with escalating doses of bovine intestinal AP (1, 5, or 25U/kg/hr).

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

22 s to correctly tune the NFAT, NF-kappaB, and AP-1 activation cascades.

23 rowth via inhibition of AKT, NF-kB, CREB and AP-1 activation in DeltaMEGF11 MDA-MB-231 and 468 cells.

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

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

26 ed accessibility were highly associated with AP-1 (activator protein 1) binding sites.

27 upancy of GATA2 (GATA-binding protein 2) and AP-1 (activator protein 1) is significantly lower compar

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

29 und proto-oncogene subunit), a member of the AP-1 (activator protein-1) family of transcription facto

30 that increased SRF phosphorylation activates AP-1 (activator protein-1)-dependent enhancers that dire

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

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

33 Broad inhibition of AP-1 activity prevented chromatin opening at AP-1 sites

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

35 d stilbenoids regulated attenuation of NF-kB/AP-1 activity upstream by inhibiting the phosphorylation

36 Moreover, NF-kB/AP-1 activity was blocked by the inhibition of nSMase2.

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

38 y of tamoxifen to increase proliferation and AP-1 activity.

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

40 gnature in SCCOHT cells that depends upon by AP-1 activity.

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

42 This recycling requires the AP-1 adaptor, suggesting that AP-1 can recycle secretory

43 ite without affecting the binding of NFAT or AP-1 alone to DNA.

44 ion was associated with reduced induction of AP-1 and a failure of proper chromatin remodeling.

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

46 6 and p34 bind to clathrin adaptor complexes AP-1 and AP-2 and are members of a conserved family char

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

48 leucine-zipper) proteins, exemplified by the AP-1 and CEBPbeta recognition of 5mC; and bHLH (basic he

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

50 ges in Kupffer cell enhancers were driven by AP-1 and EGR that reprogrammed LXR functions required fo

51 chment of accessible chromatin in motifs for AP-1 and EGR transcription factors.

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

53 lay between immediate early transcription of AP-1 and Hippo pathway function.

54 substances reduced the activity of NF-kappaB/AP-1 and later attenuated the expression of TNF-alpha.

55 Although both EPSIN1/AP-1 and MTV1/AP-4 pairs reside at the TGN, high-resolut

56 ng events activate the transcription factors AP-1 and NF-kappaB, leading to the down-regulation of LI

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

58 the transcriptional regulators NFkappaB and AP-1 and promote different functional outcomes, such as

59 a2 mediates the interaction between Laa1 and AP-1 and reveal that this interaction promotes the stabl

60 e demonstrate that IL-2 activates binding of AP-1 and STAT5 at sites that can subsequently bind linea

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

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

63 ying cells of the hair follicle matrix, with AP-1 and TGFB cooperativity driving nMRTF activation.

64 Laa2, that mediates the interaction between AP-1 and the yeast HEATR5 protein Laa1.

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

66 ed JNK to RUNX1 through Activator Protein 1 (AP-1) and investigated the JNK-AP-1-RUNX1 regulatory fee

67 ase reporter assays for activator protein 1 (AP-1) and NF-kappaB.

68 onse in the presence of activator protein-1 (AP-1), and T cell anergy/exhaustion in the absence of AP

69 of the DNA-binding activities of NF-kappaB, AP-1, and multiple other transcription factors with know

70 c variants that most frequently mutated ETS, AP-1, and NF-kB binding motifs, implicating these motifs

71 n and the downstream activation of NFkappaB, AP-1, and NFAT transcriptional activity.

72 , NRF2, YAP/TAZ/TEAD, HIF-1alpha, NF-kappaB, AP-1, and others).

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

74 s-Golgi network to the plasma membrane in an AP-1- and Arf1/4-dependent manner.

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

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

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

78 Our findings define AP-1 as the key link between T cell activation and chrom

79 Herein, we identify AP-1 as the transcription factor that directs most of th

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

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

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

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

84 horylate c-Jun (as one of the core member of AP-1) at Ser63 and Ser73 after SSL exposure in a JNKs-in

85 inding sites of transcription factors in the AP-1/ATF family; they are also enriched for common diffe

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

87 In affected keratinocytes the AP-1 beta subunit is lost, and the gamma subunit is grea

88 nal two amino acids of Irc6 are required for AP-1 binding and transport function.

89 P-1 motif, and indeed, ChIP-seq demonstrated AP-1 binding at >70% of them.

90 h a virus in which we disrupted the proximal AP-1 binding site in the major immediate early (MIE) enh

91 We identified a consensus AP-1 binding site located in the 2(nd) intron of wg, and

92 Collectively, our data demonstrate AP-1 binding to and activation of the MIE enhancer is a

93 S28Delta infection results in an increase in AP-1 binding to the MIEP, compared with WT latent infect

94 , at least in part, by repressing functional AP-1 binding to the MIEP.

95 ng cryoinjury, and that activator protein-1 (AP-1) binding sites are the most highly enriched motifs

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

97 functionally essential activator protein 1 (AP-1)-binding motifs, and responds to injury, but it can

98 l, EZH1 and EZH2 restricted accessibility to AP-1-binding motifs, and their absence promoted a regula

99 rized gamma-ear-binding sites found in other AP-1-binding proteins.

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

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

102 AP-1 binds to the MIEP and promotes lytic replication, a

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

104 The first structural studies of AP-1 bound to model proteins reveal that platinum(II) bi

105 in or the gamma1 subunit of clathrin adaptor AP-1 by RNA interference in MDCK cells disrupted apical

106 g requires the AP-1 adaptor, suggesting that AP-1 can recycle secretory cargo proteins as well as res

107 Using a dominant-negative AP-1 cell line, we found that both AP-1 DNA-binding acti

108 In transfected Chinese hamster ovary AP-1 cells, the Leu515Phe mutant protein was correctly t

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

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

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

112 MA showed reduced formation of the Nef:MHC-I:AP-1 complex required for MHC-I down-regulation.

113 Here we used the AP-1 complex to study how c-Fos turnover is controlled b

114 Immediate early genes, represented by AP-1 complex, are rapidly induced and control later-phas

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

116 also contributes to the stabilization of the AP-1 complex, removal of which decreases c-Fos half-life

117 P1B1, encoding the large beta subunit of the AP-1 complex.

118 1S1, encoding the small sigma subunit of the AP-1 complex.

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

120 HCMV infection similarly interferes with the AP-1 complex.

121 educed, demonstrating destabilization of the AP-1 complex.

122 al program regulated by activator protein-1 (AP-1) complex, formed by c-Fos and c-Jun that is selecti

123 DD, to interfere with the adaptor protein-1 (AP-1) complex, implicated in intracellular protein sorti

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

125 bunit of heterotetrameric adaptor protein 1 (AP-1) complexes, which mediate endomembrane polarization

126 1 and MMP-3 genes, which in association with AP-1 components (c-Fos or Jun), bind STAT-1 in a homodim

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

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

129 ur experiments demonstrate that clathrin and AP-1 control the sorting of an apical transmembrane prot

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

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

132 as highlighted by the substantial overlap of AP-1-dependent elements with risk loci for multiple immu

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

134 Irc6 is required for AP-1-dependent transport between the TGN and endosomes i

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

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

137 -negative AP-1 cell line, we found that both AP-1 DNA-binding activity and BRG1 reexpression are nece

138 c-Jun, enhanced phosphorylation (Ser73), and AP-1/DNA-binding in response to S. mansoni infection.

139 to identify compounds that disrupt the NFAT:AP-1:DNA complex.

140 These findings establish AP-1 driven aberrant enhancer regulation as an important

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

142 nalling, suggesting contextual regulation of AP-1 driven gene expression by BACH2.

143 F2-driven homeostatic lineage-specific to an AP-1-driven injury-induced gene expression program.

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

145 Jun, a component of the activator protein 1 (AP-1) early response transcription factor, resulting in

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

147 ELF in macrophages enhanced transcription of AP-1-encoding Fos and Jun and, consequently, AP-1 target

148 This work suggests that changes in AP-1-enriched RREs are likely a crucial source of loss o

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

150 d with their reduced ability to induce c-Jun/AP-1 expression on T cell receptor restimulation, a mech

151 ells engineered to overexpress the canonical AP-1 factor c-Jun have enhanced expansion potential, inc

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

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

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

155 ry network mediated by STAT3, NF-kappaB, and AP-1 factors on a genomic scale.

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

157 We show that the AP-1 family member FRA2 is aberrantly overexpressed in S

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

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

160 non-redundant genomic locations of different AP-1 family members in macrophages largely result from c

161 ions and genome-wide DNA binding patterns of AP-1 family members in primary and immortalized mouse ma

162 We further show that overexpression of the AP-1 family members Junb and Fosl1 can promote changes i

163 d for transcription-factor-binding motifs of AP-1 family members.

164 Mechanisms by which members of the AP-1 family of transcription factors play non-redundant

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

166 f JunB, a member of the activator protein 1 (AP-1) family of transcription factors (TFs).

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

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

169 We find that AP-1 function is required for the antidepressant effect

170 ant negative approach, we show that blocking AP-1 function leads to defects in cardiomyocyte prolifer

171 Normal AP-1 function requires proteins of the HEAT repeat-conta

172 h the MAPK, PI3K, and JNK cascades, regulate AP-1 function to mediate the beneficial effects of the a

173 esses effector-gene expression by inhibiting AP-1 function.

174 ranscriptional activity and enriching for an AP-1 gene signature.

175 e expanding vascular front, thus creating an AP-1 gradient and enabling organotypic endothelial cell

176 contrast, silencing of the gamma2 subunit of AP-1 had no effect on megalin polarity.

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

178 sults uncover previously overlooked roles of AP-1 in polarized distribution of apical and basolateral

179 with blocked c-Fos expression or lacking its AP-1-independent activity fail to initiate cortical deve

180 ecruitment, while iP1-driven transcripts are AP-1-independent.

181 f wg, and confirmed that it is essential for AP-1 induced wg transcription both in vitro and in vivo.

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

183 Furthermore, AP-1 inhibition almost completely abrogates the hepatome

184 Importantly, small molecule AP-1 inhibitors selectively target LYPD3+/TACSTD2+/LY6D+

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

186 amide (Compound 10), which disrupts the NFAT:AP-1 interaction at the composite antigen-receptor respo

187 This motif in Laa2 is essential for the Laa1-AP-1 interaction.

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

189 We now show AP-1 is a critical component for HCMV reactivation.

190 hat the transcriptional activation of WNT by AP-1 is conserved in human cancer cells.

191 Furthermore, AP-1 is critical for derepression of MIE-driven transcri

192 down regulation of the transcription factor AP-1 is highly prevalent in leiomyomas, the functional c

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

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

195 d by the clathrin adaptor protein complex-1 (AP-1) is important for the proper composition and functi

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

197 Moreover, mutation of this motif disrupted AP-1 localization and function and caused effects simila

198 in leiomyomas, the functional consequence of AP-1 loss on gene transcription in uterine fibroids rema

199 pathogenesis of MEDNIK syndrome is abnormal AP-1-mediated trafficking of copper transporters; this a

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

201 domain when overexpressed partially restores AP-1-mediated transport in cells lacking full-length Irc

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

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

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

205 pened regions were strongly enriched for the AP-1 motif, and indeed, ChIP-seq demonstrated AP-1 bindi

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

207 Furthermore, AP-1 motifs were enriched at the promoters of highly upr

208 ndent pathways: While EPSIN1 associates with AP-1, MTV1 interacts with AP-4, whose function is requir

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

210 enhanced inflammatory signatures (including AP-1/NR4A expression), observed previously in the elderl

211 bile acids, which was highly correlated with AP-1/NR4A signaling and inflammasome activation.

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

213 architecture are driven by the depletion of AP-1 occupancy on chromatin.

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

215 the activation of NF-kappaB (P < 0.001) and AP-1 (P < 0.01, P < 0.05) in ASM cells from asthmatics a

216 ive sites is important for the regulation of AP-1 pathway genes and for osteogenic differentiation an

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

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

219 We demonstrate that activator protein 1 (AP-1) 'pioneers' the senescence enhancer landscape and d

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

221 nhibition of both CDC42:ERK1/2 and NF-kappaB:AP-1 pro-oncogenic signaling pathways in nonmalignant ve

222 orine, but it does not activate Nf-kappaB or AP-1 promoters, unlike the primate TRIMCyps.

223 the mechanism of DNA recognition by a viral AP-1 protein.

224 ight for therapeutic interventions targeting AP-1 proteins.

225 tumor cell lines reveal that arsenoplatin-1 (AP-1), [Pt(mu-NHC(CH(3))O)(2)ClAs(OH)(2)], the first rep

226 We find that AP-1 readily enters cells and binds to DNA with an intac

227 Concomitantly, AP-1 recruitment to the MIE enhancer is significantly de

228 e internal promoter, iP2, are dependent upon AP-1 recruitment, while iP1-driven transcripts are AP-1-

229 1 also silences Foxa1 promoter by inhibiting AP-1 recruitment.

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

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

232 d gene expression analyses, we find that the AP-1 response in regenerating adult zebrafish cardiomyoc

233 ntiated cJUN transcriptional activity of the AP-1-responsive MMP9-luciferase reporter, which was abol

234 or Protein 1 (AP-1) and investigated the JNK-AP-1-RUNX1 regulatory feedback loop, which can be modula

235 ct at multiple levels of NF-kappaB, STAT and AP-1 signaling cascades.

236 JNK/AP-1 signaling commissions chromatin accessibility and S

237 Particularly, ERK3 is critical for AP-1 signaling through its interaction and regulation of

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

239 plicated HDAC8 in the regulation of MAPK and AP-1 signaling.

240 his activity was abolished at high levels of AP-1 signalling, suggesting contextual regulation of AP-

241 retained chimera, revealed that clathrin and AP-1 silencing disrupted apical sorting of megalin in bo

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

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

244 AP-1 activity prevented chromatin opening at AP-1 sites and reduced the expression of nearby genes.

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

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

247 As a consequence of the perturbed AP-1 sorting, m154 promotes lysosomal degradation of sev

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

249 Silencing of AP-1 subunits in primary myometrium cells leads to trans

250 Genetic deletion or chemical inhibition of AP-1 suppresses growth of YAP-driven cancer cells, such

251 on of a luciferase reporter containing BACH2/AP-1 target sequences from the mouse Ifng + 18k enhancer

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

253 AP-1-encoding Fos and Jun and, consequently, AP-1 targets including Il10.

254 JUN) and potentiating the transactivation of AP-1 targets such as osteocalcin (Bglap) and matrix meta

255 ) signaling to activate activator protein-1 (AP-1) that in turn transcriptionally enhances the expres

256 fied based on their ability to interact with AP-1, the functional significance of this interaction wa

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

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

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

260 rthermore, HI-TOPK-032 decreased SSL-induced AP-1 transactivation activity.

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

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

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

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

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

266 ng with increased chromatin accessibility of AP-1 transcription factor motifs and overexpression of t

267 /3)-dependent manner, and Jun proto-oncogene AP-1 transcription factor subunit (AP-1) was required fo

268 t in part, by binding to Jun proto-oncogene, AP-1 transcription factor subunit (cJUN) and potentiatin

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

270 on of the mRNAs of JUND (JunD proto-oncogene AP-1 transcription factor subunit) and HIV-1 genes, and

271 phosphorylation of cellular fos (c-fos), an AP-1 transcription factor subunit, to repress MIEP-drive

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

273 onstrating the benefits of the method on the AP-1 transcription factor, the dimerization and DNA bind

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

275 AP-1 transcription factors directly upregulate the expre

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

277 AP-1 transcription factors play an essential role in the

278 rward loop mediated by the MEK/ERK-activated AP-1 transcription factors, JUNB and FOSB, which is resp

279 mediated through inhibition of cEBPbeta-NFkB-AP-1 transcription machinery.

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

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

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

283 tion by attenuating the activator protein-1 (AP-1) transcription factor subunit, c-fos, expression an

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

285 nriched for binding motifs for NF-kappaB and AP-1, transcription factors involved in activation of T

286 to stimulate downstream NFkappaB, NFAT, and AP-1 transcriptional activity.

287 The AP-1 transcriptional program modulates the expression of

288 otably, BPQD-RMNV-mediated PTT combined with aPD-1 treatment significantly delayed residual and metas

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

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

291 -oncogene AP-1 transcription factor subunit (AP-1) was required for constitutive miR-144-3p expressio

292 rammed cell death protein 1 (PD-1) antibody (aPD-1) was employed to prevent the CD8(+) T cells from e

293 Nuclear c-Jun, a component of AP-1, was observed specifically in border zone cardiomyo

294 to binding sites of the transcription factor AP-1, where it represses effector-gene expression by inh

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

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

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

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

299 teraction promotes the stable association of AP-1 with membranes in yeast.

300 hese compounds, we evaluated interactions of AP-1 with the two important classes of biomolecules-prot