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1 clin D3), 4p16 (FGFR3 and MMSET), and 16q23 (c-maf).
2 ic, osteopontin-positive chondrocytes in the c-maf-/-.
3 iched for the transcription factors IRF4 and c-Maf.
4 igher expression of the transcription factor c-Maf.
5 X6(5a) variants and other factors, e.g. MafA/c-Maf.
6 egulated by AP-1 and may also be a target of c-Maf.
7 fferent 3'-untranslated region compared with c-Maf.
8 ssion of the Th2-specific factors GATA-3 and c-Maf.
9 interleukin-4-specific transcription factor c-Maf.
10 ted with a decreased induction of GATA-3 and c-maf.
11 uired expression of the transcription factor c-Maf.
12 anoma cells resulted in the up-regulation of c-maf.
13 other cells is dependent on the presence of c-maf.
14 oncogenes: bcl-9, bcl-10, PAX-5, MMSET, and c-maf.
15 directly and indirectly via up-regulation of c-Maf.
16 MiR-155 is a microRNA that targets 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.
22 IL-10 and had increased mRNA expression for c-Maf, a transcription factor that upregulates IL-10 gen
23 butes to immune deviation in T1D by reducing c-Maf access to and transactivation of the IL-4 gene.
24 on of both cytokines, other factors, such as c-Maf act specifically on IL-22 and enable the separate
25 Thus, cartilage is a novel system in which c-Maf acts during development, where c-Maf is required f
28 that bind the oncoproteins c-Jun, c-Fos and c-Maf (also called JUN, FOS and MAF, respectively), were
29 tinct gene programs, and validated roles for c-MAF and BCL6 as regulators affecting type 1 and type 3
31 vitro translated proteins revealed that both c-Maf and c-Maf bound to NQO1 gene ARE as homodimers and
33 a 10 amino acids at the carboxyl terminus of c-Maf and contains a different 3'-untranslated region co
35 data demonstrate a novel mechanism of Pax6, c-Maf and CREB function, through regulation of chromatin
36 pression correlate with increased binding of c-Maf and CREB to the promoter and of CREB to DCR3, a br
39 neous induction of the transcription factors c-Maf and Gata-3, mediated by the kinases p38 MAPK and S
48 lation of the Th2-type transcription factors c-Maf and JunB, which consequently enhances IL-4 and IL-
51 gism promotes activation of transcription by c-Maf and MafA on the alphaB-crystallin promoter, and is
52 gene signatures were observed in cases with c-MAF and MAFB activation and CCND1 and CCND3 activation
53 of genes encoding the transcription factors c-Maf and Mafb and directly promoted expression of trans
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
66 volved in Th2 development (IL-4, GATA-3, and c-maf), and decreased mRNA for genes involved in Th1 dev
67 sion of the transcriptional repressor factor c-Maf, and a decreased binding of GAP-12 to the gene pro
68 ta was also synergistic with IL-27 to induce c-Maf, and it induced Stat1-independent IL-10 expression
70 ns of Pax6/Pax6(5a), large Mafs (MafA, MafB, c-Maf, and NRL), Sox1, Sox2, Six3, and RARbeta/RXRbeta.
73 influenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activatin
76 l hydrocarbon receptor, along with STAT3 and c-Maf, are recruited to promoter elements on Entpd1 and
77 and enhanced by IL-21 expression through the c-Maf/aryl hydrocarbon receptor pathway, independent of
80 3 development and ILC1 conversion solidified c-Maf as a gatekeeper of type 1 regulatory transformatio
81 tudy, we identified the transcription factor c-Maf as a universal regulator of Tgammadelta17 cell dif
84 5 (CXCR5), musculoaponeurotic fibrosarcoma (c-Maf), Bcl6, basic leucine zipper transcription factor
87 sion of 22 genes whose promoters contained a c-Maf binding site, including hyaluronan synthase 1 (HAS
88 driven luciferase reporter activity, reduces c-Maf binding to the IL-4p in chromatin immunoprecipitat
89 demonstrate that despite normal expression, c-Maf binds poorly to the IL-4 promoter (IL-4p) in NOD C
91 ssion of the transcription factors Bcl-6 and c-Maf, both of which are needed for development of folli
92 slated proteins revealed that both c-Maf and c-Maf bound to NQO1 gene ARE as homodimers and heterodim
95 tion of transcriptional activation domain of c-Maf (c-Maf) led to significant loss of MARE-mediated p
98 eloid cell lines, we inducibly expressed the c-Maf cDNA in 2 bipotent human myeloid progenitor cells.
100 e of alternative mediators in the absence of c-Maf, consistent with the observation that a functional
103 equent stages of lens morphogenesis, whereas c-Maf controls terminal differentiation of lens fibers,
104 h2-specific transcription factors GATA-3 and c-maf correlated with the increased production of Th2 cy
105 ing lens development, link together the Pax6/c-Maf/crystallin regulatory network, and suggest a novel
106 al co-activator p300 and we demonstrate that c-Maf D90V enhances p300 recruitment in a cell-type depe
109 Phenotypic and transcriptomic profiling of c-Maf-deficient CCR6(-) ILC3s revealed a hyper type 1 di
113 usive evidence that the transcription factor c-Maf directed the tissue-specific expression of IL-4.
115 in Stat6-deficient CD4 and CD8 T cells, and c-Maf directly transactivated IL-10 gene expression thro
117 errant or reduced expression of Prox1, Pax6, c-Maf, E-cadherin and alpha-, beta- and gamma-crystallin
120 that IL-6 plays a unique role in initiating c-Maf expression after TCR engagement, and may subsequen
121 e defect was associated with a deficiency in c-Maf expression and could be rescued completely by c-Ma
123 T-cell receptor (TCR)/CD28-induced IL-4 and c-Maf expression and, conversely, enhanced interferon ga
126 Importantly, beta-glucan treatment reduced c-MAF expression in macrophages and monocytes from patie
127 ed by p53 and negatively regulate Twist2 and c-Maf expression in microglia and the RAW macrophage cel
131 enhancer (CR1) recapitulated the endogenous c-Maf expression pattern in lens and retinal pigmented e
135 s, Vav1 is selectively required for IL-4 and c-Maf expression, a requirement reflecting, at least in
137 ceptor (gammadeltaTCR) signal strength tuned c-Maf expression, which indicates that c-Maf is a core n
148 xhibit T(FH) features (including Batf, Bcl6, c-Maf, ICOS, and IL-21 expression) and are able to migra
149 those elements is essential, because loss of c-Maf, IL-21-signaling, or ICOS decreases the frequency
151 in Th2 cells can provide the specificity for c-Maf in IL-4 expression during T cell development and d
152 he role of posttranslational modification of c-Maf in IL-4 production and Th cell-mediated autoimmune
153 y uncovers a novel and important function of c-Maf in macrophages and elucidates its transcriptional
154 ls can be recapitulated by overexpression of c-Maf in myeloid cell lines, we inducibly expressed the
156 -4-independent and CD25-mediated function of c-maf in promoting the production of Th2 cytokines.
157 together, these data reveal a novel role for c-Maf in regulating T effector development, and they sug
160 and macrophages, we investigate the role of c-Maf in the transcriptional regulation of IL-10 and the
162 Here, we provide evidence demonstrating that c-maf, independent of IL-4, is essential for normal indu
164 two genes in the SLI1 region: that encoding c-maf-inducing protein (CMIP, minP = 5.5 x 10(-7) at rs6
165 -stimulated production of IL-4/IL-21 through c-Maf induction is responsible for impaired Th1 differen
169 tuned c-Maf expression, which indicates that c-Maf is a core node that connects gammadeltaTCR signals
173 Taken together, these data demonstrate that c-Maf is an indispensable yet constitutive transcription
182 udy, we report that the transcription factor c-Maf is required for normal chondrocyte differentiation
183 n which c-Maf acts during development, where c-Maf is required for normal chondrocyte differentiation
185 r knowledge, we show for the first time that c-Maf is subjective to tyrosine phosphorylation in Th ce
186 pper transcription factor Maf (also known as c-Maf) is central to osteoblast lineage commitment.
188 ranscriptional regulator of IL10 in T cells, c-Maf, is significantly decreased by physiological level
189 his report, we have investigated the role of c-Maf (large Maf) containing the transcriptional activat
190 ore ARE sequence is essential for binding of c-Maf leading to repression of NQO1 gene expression.
191 transcriptional activation domain of c-Maf (c-Maf) led to significant loss of MARE-mediated p53 gene
193 iate these phenotypic changes indicated that c-Maf likely plays a key role in myeloid cell developmen
194 tin immunoprecipitation assays, and enhances c-Maf localization into promyelocytic leukemia nuclear b
196 elopment and function including Pax-6, Six3, c-Maf, Maf1, Sox-4, Foxc1, Rx, and Ldb2 were present amo
198 oxic bile acid induces a switch from Nrf2 to c-Maf/MafG ARE nuclear binding, which leads to decreased
199 ell development; therefore, abnormalities in c-Maf may contribute to reduced IL-4 production by CD4 c
200 Pax6 and c-Maf, Pax6 has a neutral effect on c-Maf-mediated alphaA-crystallin promoter activation.
206 results together led to the conclusion that c-Maf negatively regulates ARE-mediated detoxifying enzy
211 mature hypertrophic chondrocytes at E15.5 in c-maf-null tibiae, with decreased expression domains of
214 revious novel finding that the protooncogene c-Maf of the basic leucine zipper family of transcriptio
220 the transcription factors NFATc2, NF-kB p65, c-Maf, p300, Brg1, STAT6, and GATA-3 assemble at the Il4
221 activation of alphaB-crystallin by Pax6 and c-Maf, Pax6 has a neutral effect on c-Maf-mediated alpha
233 site represents the 3' coding region of the c-maf proto-oncogene at 67.0 centimorgans (cM) on chromo
236 ding protein (CBP) and/or p300 interact with c-Maf, Prox-1, or Sox-1 to enhance transcription of crys
238 y and distinct markers including N-cadherin, c-Maf, Prox1, and alphaA-, alphaB-, and beta-crystallins
239 and differentiation associated with altered c-Maf, Prox1, and p57 expression pattern in the anterior
241 versely, small interfering RNA inhibition of c-maf reduces HIV-1 transcription in IL-4-producing T ce
243 , we have shown that the bZIP proto-oncogene c-Maf regulates expression of alphaA-crystallin (Cryaa)
247 in mice, the transcription factors MafB and c-Maf repress a macrophage-specific enhancer repertoire
248 anscriptional mechanism, we identify a novel c-maf (required for IL-4 expression) transcription facto
249 Inhibition of IL-12 p40 gene expression by c-Maf requires the N-terminal transactivation domain, su
250 in vitro and in vivo experiments identify a c-Maf response element localized to nucleotides -196/-18
253 l lamina-specific transcription factors such c-Maf, Rora, and Satb1 are identified for the first time
255 d activators of transcription 4), T-bet, and c-maf showed reduced expression in UCB compared with AB
258 tes IL-4 promoter, and ectopic expression of c-Maf skews primary T cell response toward the Th2 pathw
261 stant B10.D2 mice, suggesting that increased c-Maf sumoylation contributes to immune deviation in T1D
262 rentiated in the presence of exogenous IL-4, c-maf(-/-) T cells produced approximately normal levels
263 rmore, we have examined the levels of GATA3, c-Maf, T-bet, and Ets-related molecule during human Th1/
265 ompletely restored Th2 development, inducing c-Maf, Th2-specific DNase I hypersensitive sites in the
266 the T(H)2-specific factors GATA3, STAT6 and c-Maf, the chromatin-remodeling enzyme Brg1 and RNA poly
267 three key elements: the transcription factor c-Maf, the cytokine IL-21, and the costimulatory recepto
268 ells identified the Th2 transcription factor c-Maf to be synergistically up-regulated by IL-6 plus TG
269 l type 2 (Th2)-specific transcription factor c-Maf to cells normally refractory to IL-4 production, s
270 residues is critical for the recruitment of c-Maf to IL-4 promoter and IL-4 production in Th cells.
272 ChIP assays revealed binding of Pax6 and c-Maf to multiple regions of the c-Maf locus in lens chr
275 served is likely explained by the ability of c-Maf to transactivate the crystallin gene promoter.
276 and the IL-4-inducing transcription factor, c-maf, to augment IL-4 promoter activity as well as to e
280 In transfected cells, sumoylation decreases c-Maf transactivation of IL-4p-driven luciferase reporte
282 f the JCI, Liu and colleagues identified the c-Maf transcription factor as a master regulator of prot
285 L-4 or other cytokines, rapidly up-regulates c-Maf transcription, as early as 3 h after TCR activatio
286 t beta-cell expression of hemagglutinin, the c-Maf transgene provided significant protection from spo
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.