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1 d cytokine production in mice lacking c-Maf (c-maf(-/-)).
2 clin D3), 4p16 (FGFR3 and MMSET), and 16q23 (c-maf).
3 ic, osteopontin-positive chondrocytes in the c-maf-/-.
4 igher expression of the transcription factor c-Maf.
5 directly and indirectly via up-regulation of c-Maf.
6 X6(5a) variants and other factors, e.g. MafA/c-Maf.
7 egulated by AP-1 and may also be a target of c-Maf.
8 fferent 3'-untranslated region compared with c-Maf.
9 MiR-155 is a microRNA that targets c-Maf.
10 ssion of the Th2-specific factors GATA-3 and c-Maf.
11 interleukin-4-specific transcription factor c-Maf.
12 ted with a decreased induction of GATA-3 and c-maf.
13 anoma cells resulted in the up-regulation of c-maf.
14 other cells is dependent on the presence of c-maf.
15 oncogenes: bcl-9, bcl-10, PAX-5, MMSET, and c-maf.
16 ocation breakpoints in these 6 lines bracket c-maf.
17 R, releasing Twist2, which induces IL-10 via c-Maf.
18 Th2-inducing transcription factors GATA3 or c-Maf.
19 f the anti-inflammatory transcription factor c-Maf.
20 ific molecular target of p53 in microglia is c-Maf.
21 s in vivo required coexpression of Bcl-6 and c-Maf.
23 IL-10 and had increased mRNA expression for c-Maf, a transcription factor that upregulates IL-10 gen
24 butes to immune deviation in T1D by reducing c-Maf access to and transactivation of the IL-4 gene.
25 on of both cytokines, other factors, such as c-Maf act specifically on IL-22 and enable the separate
26 Thus, cartilage is a novel system in which c-Maf acts during development, where c-Maf is required f
28 cation, there is selective expression of one c-maf allele in 2 informative lines with translocations.
30 that bind the oncoproteins c-Jun, c-Fos and c-Maf (also called JUN, FOS and MAF, respectively), were
32 vitro translated proteins revealed that both c-Maf and c-Maf bound to NQO1 gene ARE as homodimers and
34 a 10 amino acids at the carboxyl terminus of c-Maf and contains a different 3'-untranslated region co
36 data demonstrate a novel mechanism of Pax6, c-Maf and CREB function, through regulation of chromatin
37 pression correlate with increased binding of c-Maf and CREB to the promoter and of CREB to DCR3, a br
40 neous induction of the transcription factors c-Maf and Gata-3, mediated by the kinases p38 MAPK and S
49 lation of the Th2-type transcription factors c-Maf and JunB, which consequently enhances IL-4 and IL-
52 gism promotes activation of transcription by c-Maf and MafA on the alphaB-crystallin promoter, and is
53 gene signatures were observed in cases with c-MAF and MAFB activation and CCND1 and CCND3 activation
55 hey increased nuclear Nrf2 levels, prevented c-Maf and MafG induction, and prevented the fall in Nrf2
59 der Tr1-skewing conditions, the AhR bound to c-Maf and promoted transactivation of the Il10 and Il21
64 volved in Th2 development (IL-4, GATA-3, and c-maf), and decreased mRNA for genes involved in Th1 dev
65 sion of the transcriptional repressor factor c-Maf, and a decreased binding of GAP-12 to the gene pro
66 ta was also synergistic with IL-27 to induce c-Maf, and it induced Stat1-independent IL-10 expression
68 ns of Pax6/Pax6(5a), large Mafs (MafA, MafB, c-Maf, and NRL), Sox1, Sox2, Six3, and RARbeta/RXRbeta.
71 influenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activatin
73 w that mice lacking the transcription factor c-Maf are microphthalmic secondary to defective lens for
74 and enhanced by IL-21 expression through the c-Maf/aryl hydrocarbon receptor pathway, independent of
76 5 (CXCR5), musculoaponeurotic fibrosarcoma (c-Maf), Bcl6, basic leucine zipper transcription factor
79 sion of 22 genes whose promoters contained a c-Maf binding site, including hyaluronan synthase 1 (HAS
80 driven luciferase reporter activity, reduces c-Maf binding to the IL-4p in chromatin immunoprecipitat
81 demonstrate that despite normal expression, c-Maf binds poorly to the IL-4 promoter (IL-4p) in NOD C
84 ssion of the transcription factors Bcl-6 and c-Maf, both of which are needed for development of folli
85 slated proteins revealed that both c-Maf and c-Maf bound to NQO1 gene ARE as homodimers and heterodim
90 tion of transcriptional activation domain of c-Maf (c-Maf) led to significant loss of MARE-mediated p
93 eloid cell lines, we inducibly expressed the c-Maf cDNA in 2 bipotent human myeloid progenitor cells.
94 e of alternative mediators in the absence of c-Maf, consistent with the observation that a functional
96 equent stages of lens morphogenesis, whereas c-Maf controls terminal differentiation of lens fibers,
97 h2-specific transcription factors GATA-3 and c-maf correlated with the increased production of Th2 cy
98 ing lens development, link together the Pax6/c-Maf/crystallin regulatory network, and suggest a novel
99 al co-activator p300 and we demonstrate that c-Maf D90V enhances p300 recruitment in a cell-type depe
103 usive evidence that the transcription factor c-Maf directed the tissue-specific expression of IL-4.
104 in Stat6-deficient CD4 and CD8 T cells, and c-Maf directly transactivated IL-10 gene expression thro
107 errant or reduced expression of Prox1, Pax6, c-Maf, E-cadherin and alpha-, beta- and gamma-crystallin
108 that IL-6 plays a unique role in initiating c-Maf expression after TCR engagement, and may subsequen
109 e defect was associated with a deficiency in c-Maf expression and could be rescued completely by c-Ma
111 T-cell receptor (TCR)/CD28-induced IL-4 and c-Maf expression and, conversely, enhanced interferon ga
114 ed by p53 and negatively regulate Twist2 and c-Maf expression in microglia and the RAW macrophage cel
118 enhancer (CR1) recapitulated the endogenous c-Maf expression pattern in lens and retinal pigmented e
121 s, Vav1 is selectively required for IL-4 and c-Maf expression, a requirement reflecting, at least in
131 the IL-4 gene in vivo, direct evidence that c-maf functions during the differentiation of normal, pr
134 xhibit T(FH) features (including Batf, Bcl6, c-Maf, ICOS, and IL-21 expression) and are able to migra
135 those elements is essential, because loss of c-Maf, IL-21-signaling, or ICOS decreases the frequency
138 in Th2 cells can provide the specificity for c-Maf in IL-4 expression during T cell development and d
139 he role of posttranslational modification of c-Maf in IL-4 production and Th cell-mediated autoimmune
140 y uncovers a novel and important function of c-Maf in macrophages and elucidates its transcriptional
142 ls can be recapitulated by overexpression of c-Maf in myeloid cell lines, we inducibly expressed the
143 -4-independent and CD25-mediated function of c-maf in promoting the production of Th2 cytokines.
144 together, these data reveal a novel role for c-Maf in regulating T effector development, and they sug
147 and macrophages, we investigate the role of c-Maf in the transcriptional regulation of IL-10 and the
148 We now demonstrate that overexpression of c-maf in vivo skews the Th immune response along a Th2 p
151 Here, we provide evidence demonstrating that c-maf, independent of IL-4, is essential for normal indu
153 two genes in the SLI1 region: that encoding c-maf-inducing protein (CMIP, minP = 5.5 x 10(-7) at rs6
154 -stimulated production of IL-4/IL-21 through c-Maf induction is responsible for impaired Th1 differen
161 Taken together, these data demonstrate that c-Maf is an indispensable yet constitutive transcription
170 udy, we report that the transcription factor c-Maf is required for normal chondrocyte differentiation
171 n which c-Maf acts during development, where c-Maf is required for normal chondrocyte differentiation
173 r knowledge, we show for the first time that c-Maf is subjective to tyrosine phosphorylation in Th ce
174 pper transcription factor Maf (also known as c-Maf) is central to osteoblast lineage commitment.
176 his report, we have investigated the role of c-Maf (large Maf) containing the transcriptional activat
177 ore ARE sequence is essential for binding of c-Maf leading to repression of NQO1 gene expression.
178 transcriptional activation domain of c-Maf (c-Maf) led to significant loss of MARE-mediated p53 gene
180 iate these phenotypic changes indicated that c-Maf likely plays a key role in myeloid cell developmen
181 tin immunoprecipitation assays, and enhances c-Maf localization into promyelocytic leukemia nuclear b
183 elopment and function including Pax-6, Six3, c-Maf, Maf1, Sox-4, Foxc1, Rx, and Ldb2 were present amo
185 oxic bile acid induces a switch from Nrf2 to c-Maf/MafG ARE nuclear binding, which leads to decreased
186 ell development; therefore, abnormalities in c-Maf may contribute to reduced IL-4 production by CD4 c
187 Pax6 and c-Maf, Pax6 has a neutral effect on c-Maf-mediated alphaA-crystallin promoter activation.
195 results together led to the conclusion that c-Maf negatively regulates ARE-mediated detoxifying enzy
200 mature hypertrophic chondrocytes at E15.5 in c-maf-null tibiae, with decreased expression domains of
203 revious novel finding that the protooncogene c-Maf of the basic leucine zipper family of transcriptio
209 The attenuation of Th1 differentiation by c-maf overexpression occurred by a mechanism that was in
210 the transcription factors NFATc2, NF-kB p65, c-Maf, p300, Brg1, STAT6, and GATA-3 assemble at the Il4
211 activation of alphaB-crystallin by Pax6 and c-Maf, Pax6 has a neutral effect on c-Maf-mediated alpha
224 site represents the 3' coding region of the c-maf proto-oncogene at 67.0 centimorgans (cM) on chromo
228 ding protein (CBP) and/or p300 interact with c-Maf, Prox-1, or Sox-1 to enhance transcription of crys
230 y and distinct markers including N-cadherin, c-Maf, Prox1, and alphaA-, alphaB-, and beta-crystallins
231 and differentiation associated with altered c-Maf, Prox1, and p57 expression pattern in the anterior
233 versely, small interfering RNA inhibition of c-maf reduces HIV-1 transcription in IL-4-producing T ce
235 , we have shown that the bZIP proto-oncogene c-Maf regulates expression of alphaA-crystallin (Cryaa)
239 in mice, the transcription factors MafB and c-Maf repress a macrophage-specific enhancer repertoire
240 anscriptional mechanism, we identify a novel c-maf (required for IL-4 expression) transcription facto
241 Inhibition of IL-12 p40 gene expression by c-Maf requires the N-terminal transactivation domain, su
243 in vitro and in vivo experiments identify a c-Maf response element localized to nucleotides -196/-18
246 l lamina-specific transcription factors such c-Maf, Rora, and Satb1 are identified for the first time
249 d activators of transcription 4), T-bet, and c-maf showed reduced expression in UCB compared with AB
252 tes IL-4 promoter, and ectopic expression of c-Maf skews primary T cell response toward the Th2 pathw
254 )(q23;q11), with the breakpoint telomeric to c-maf, so that the translocation breakpoints in these 6
256 stant B10.D2 mice, suggesting that increased c-Maf sumoylation contributes to immune deviation in T1D
257 rentiated in the presence of exogenous IL-4, c-maf(-/-) T cells produced approximately normal levels
258 rmore, we have examined the levels of GATA3, c-Maf, T-bet, and Ets-related molecule during human Th1/
260 ompletely restored Th2 development, inducing c-Maf, Th2-specific DNase I hypersensitive sites in the
261 the T(H)2-specific factors GATA3, STAT6 and c-Maf, the chromatin-remodeling enzyme Brg1 and RNA poly
262 three key elements: the transcription factor c-Maf, the cytokine IL-21, and the costimulatory recepto
264 ells identified the Th2 transcription factor c-Maf to be synergistically up-regulated by IL-6 plus TG
265 l type 2 (Th2)-specific transcription factor c-Maf to cells normally refractory to IL-4 production, s
266 residues is critical for the recruitment of c-Maf to IL-4 promoter and IL-4 production in Th cells.
268 s in myeloid cells, we tested the ability of c-Maf to influence Ets-1- and c-Myb-dependent CD13/APN t
269 ChIP assays revealed binding of Pax6 and c-Maf to multiple regions of the c-Maf locus in lens chr
272 served is likely explained by the ability of c-Maf to transactivate the crystallin gene promoter.
273 and the IL-4-inducing transcription factor, c-maf, to augment IL-4 promoter activity as well as to e
278 In transfected cells, sumoylation decreases c-Maf transactivation of IL-4p-driven luciferase reporte
282 first human tumor in which the basic zipper c-maf transcription factor is shown to function as an on
283 L-4 or other cytokines, rapidly up-regulates c-Maf transcription, as early as 3 h after TCR activatio
284 t beta-cell expression of hemagglutinin, the c-Maf transgene provided significant protection from spo
286 L-4 dependent since this was not observed in c-maf transgenic mice bred onto an IL-4-deficient backgr
287 oduction of IgGl and IgE in the CD4 promoter/c-maf transgenic mice was IL-4 dependent since this was
288 rmore, by expressing GATA-3 in wild-type and c-maf transgenic Th1 cells, we demonstrate that the expr
289 llin is regulated by recruitment of Pax6 and c-Maf, two proteins regulating multiple processes of len
291 to c-avian musculoaponeurotic fibrosarcoma (c-Maf)/V-maf musculoaponeurotic fibrosarcoma oncogene ho
294 interest, co-expression of CBP or p300 with c-Maf was found to synergistically co-activate each prom
295 To determine how p53 negatively regulates c-Maf, we examined the impact of p53 on known c-Maf regu
297 CD14(hi) cells have increased expression of c-Maf, which increases production of two key factors (hy
298 Here we identify the transcription factor c-Maf, which is induced by TGF-beta, as a downstream rep
300 established in vivo interactions of Pax6 and c-Maf with the alphaA-crystallin promoter in lens cells.
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