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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.
22      Here, we report that the proto-oncogene c-maf, a basic region/leucine zipper transcription facto
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
27                                 Furthermore, c-Maf acts in synergy with the nuclear factor of activat
28 cation, there is selective expression of one c-maf allele in 2 informative lines with translocations.
29              Co-transfections using Pax6 and c-Maf alone revealed moderate and strong activations of
30  that bind the oncoproteins c-Jun, c-Fos and c-Maf (also called JUN, FOS and MAF, respectively), were
31                                    Restoring c-Maf and Bmi1 expression in Twist-deficient macrophages
32 vitro translated proteins revealed that both c-Maf and c-Maf bound to NQO1 gene ARE as homodimers and
33                       We have shown that the c-Maf and c-Myb transcription factors physically interac
34 a 10 amino acids at the carboxyl terminus of c-Maf and contains a different 3'-untranslated region co
35 d by DNA-binding transcription factors Pax6, c-Maf and CREB bound to its promoter region.
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
38                                         Both c-Maf and Cryaa regulatory regions contain arrays of AP-
39 s, abolished T-bet expression, and increased c-MAF and GATA-3 protein in vivo.
40 neous induction of the transcription factors c-Maf and Gata-3, mediated by the kinases p38 MAPK and S
41  the expression of the transcription factors c-maf and GATA-3.
42                                         Both c-Maf and IL-10 induction during Th17 polarization depen
43 imulated PDCD4 degradation and expression of c-Maf and IL-10 production.
44 decreased expression of IL-7Ralpha, BATF and c-Maf and increased expression of Bcl11b and Lef1.
45               These results demonstrate that c-maf and its target binding site are not required for I
46 evels of the requisite transcription factors c-Maf and Jun B.
47                          The synergy between c-Maf and JunB can be attributed to cooperative DNA bind
48                                              c-maf and junB mRNA, protein, and activity were signific
49 lation of the Th2-type transcription factors c-Maf and JunB, which consequently enhances IL-4 and IL-
50 ption factors have been described, including c-Maf and JunB.
51                         TBP was also part of c-Maf and MafA (two other large Maf proteins)-containing
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
54 embers of the large Maf family, specifically c-Maf and MafB.
55 hey increased nuclear Nrf2 levels, prevented c-Maf and MafG induction, and prevented the fall in Nrf2
56 ell at 20 hours after LCA treatment, whereas c-Maf and MafG remained persistently induced.
57                            Nuclear levels of c-Maf and MafG, which can negatively regulate ARE, were
58           We identify transcription factors, c-Maf and NFIL3, and negative co-stimulatory molecules,
59 der Tr1-skewing conditions, the AhR bound to c-Maf and promoted transactivation of the Il10 and Il21
60 periments revealed that CBP and p300 bind to c-Maf and Prox-1 but not to Sox-1.
61  expression of the key transcription factors c-Maf and Prox1.
62 ter binding of the proinflammatory inhibitor c-Maf and the transcriptional repressor Bmi1.
63 multiple myeloma SET domain [MMSET]), 16q23 (c-maf), and 20q11 (mafB).
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
67 ociated with sustained expression of GATA-3, c-MAF, and JunB in an IL-4-independent manner.
68 ns of Pax6/Pax6(5a), large Mafs (MafA, MafB, c-Maf, and NRL), Sox1, Sox2, Six3, and RARbeta/RXRbeta.
69 /RXRbeta, and lens fiber-factors Pax6, MafA, c-Maf, and NRL.
70 s of distinct cell types in the gonad: MAFB, C-MAF, and VCAM1.
71 influenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activatin
72                                              c-Maf appears to function primarily in Treg specializati
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
75 transcriptional factor Bcl6 as well as IRF4, c-Maf, Batf, and STAT3/5.
76  5 (CXCR5), musculoaponeurotic fibrosarcoma (c-Maf), Bcl6, basic leucine zipper transcription factor
77          The corresponding cellular protein, c-Maf belongs to a family of related bZip proteins toget
78           Furthermore, mutation of a defined c-maf binding site within the proximal IL-4 promoter, wh
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
82                          We demonstrate that c-maf binds this site in vivo and synergistically augmen
83                                              c-Maf binds to a c-Maf response element (MARE) in the pr
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
86                                We found that c-Maf bound to the Il22 promoter and was both necessary
87                         The co-activation of c-Maf by CBP/p300 requires histone acetyltransferase act
88            As predicted for dysregulation of c-maf by translocation, there is selective expression of
89 examined cytokine production in mice lacking c-Maf (c-maf(-/-)).
90 tion of transcriptional activation domain of c-Maf (c-Maf) led to significant loss of MARE-mediated p
91             Immunoblotting demonstrates that c-Maf can be modified at lysine 33 by SUMO-1 (small ubiq
92                             Thus, transgenic c-Maf can strongly influence autoimmune disease developm
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
95                     It was not known whether c-Maf controlled the transcription of other Th2 cytokine
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
100        In contrast to wild-type protein, the c-Maf D90V mutant protein is not inhibited by protein ki
101                                           In c-Maf-deficient murine macrophages, IL-10 production is
102 ules, and general immune homeostasis are not c-Maf dependent.
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
105         Although it has been postulated that c-maf directs the Th2-specific expression of the IL-4 ge
106 ow in this article that introduction of Maf (c-Maf) does induce the capacity to express IL-21.
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
110                   It also induced GATA-3 and c-maf expression and downregulated IL-12Rbeta2 chain exp
111  T-cell receptor (TCR)/CD28-induced IL-4 and c-Maf expression and, conversely, enhanced interferon ga
112   Here, we show that Pax6 directly regulates c-Maf expression during lens development.
113                                              c-Maf expression in effector cells was regulated by IL-4
114 ed by p53 and negatively regulate Twist2 and c-Maf expression in microglia and the RAW macrophage cel
115                         IL-6 induces similar c-Maf expression in protein kinase Ctheta-deficient CD4(
116              Northern analysis revealed that c-Maf expression increases 2 h after t-BHQ treatment.
117 lecting, at least in part, the dependence of c-Maf expression on Ca2+/NFAT signaling.
118  enhancer (CR1) recapitulated the endogenous c-Maf expression pattern in lens and retinal pigmented e
119                                 IL-27-driven c-Maf expression transactivates IL-21 production, which
120                Co-culture led to upregulated c-Maf expression with no decrease in the proportion of T
121 s, Vav1 is selectively required for IL-4 and c-Maf expression, a requirement reflecting, at least in
122                         IL-4 can up-regulate c-Maf expression, its binding to IL-10 promoter, and dos
123 cus but also for inducing Il4, Il5, Il13 and c-Maf expression.
124 expression, but only partially by retroviral c-Maf expression.
125 macrophages likely via its ability to induce c-Maf expression.
126  Ca(2+) signal pathways, block IL-6-mediated c-Maf expression.
127 inflammatory and tolerogenic signals promote c-Maf expression.
128        IL-10 expression also correlated with c-maf expression.
129                      These data suggest that c-Maf facilitates the initial chondrocyte terminal diffe
130 IL-4-producing mast cells do not express the c-maf factor.
131  the IL-4 gene in vivo, direct evidence that c-maf functions during the differentiation of normal, pr
132                             We conclude that c-Maf has a critical and selective function in IL-4 gene
133                                        Pax6, c-Maf, Hsf4, Prox1, Sox1, and a few additional factors r
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
136                        The overexpression of c-Maf in human hepatoblastoma (Hep-G2) cells led to the
137                                Expression of c-Maf in human immature myeloblastic cells inhibited CD1
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
141                        Ectopic expression of c-maf in mature Th1 cells did not confer on them the abi
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
145          This was in contrast to the role of c-Maf in the activation of Maf recognition element (MARE
146 nd super shift assays showed the presence of c-Maf in the ARE-nuclear protein complex.
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
149                     To elucidate the role of c-Maf in vivo, we examined cytokine production in mice l
150                                        Thus, c-maf increases HIV-1 expression in IL-4-producing CD4 T
151 Here, we provide evidence demonstrating that c-maf, independent of IL-4, is essential for normal indu
152                                              c-Maf induces changes in nuclear DNA-binding activities
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
155                                              c-Maf induction requires both IL-6- and TCR-initiated si
156 ze Th17 immunity by IL-10 production through c-Maf induction.
157  [cyclin D1]; 4p16 [FGFR3 and MMSET]; 16q23 [c-maf]) involved in nearly half of MM tumors.
158                In this article, we show that c-Maf is a critical transcription factor regulating this
159                                   Therefore, c-Maf is a novel regulator of Treg specialization, which
160                                              c-maf is a T helper (Th)2 cell-specific transcription fa
161  Taken together, these data demonstrate that c-Maf is an indispensable yet constitutive transcription
162                                     Although c-Maf is crucial for Th2 differentiation and production
163                     The transcription factor c-Maf is essential for the induction of IL-10 by Tr1 cel
164                                 Furthermore, c-Maf is expressed constitutively in resting monocytes/m
165                                              c-maf is expressed in hypertrophic chondrocytes during f
166                                              c-Maf is expressed in Th2 but not Th1 clones and is indu
167                               Sumoylation of c-Maf is increased in NOD CD4 cells as compared with CD4
168                         As in other T cells, c-Maf is induced in Tregs by IL-6 and TGF-beta, suggesti
169                          We demonstrate that c-Maf is one of the physiological mediators of IL-10's i
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
172                                        Thus, c-Maf is required for the differentiation of the vertebr
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.
175 more, Twist2, a transcriptional activator of c-Maf, is increased in p53-deficient microglia.
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
179 ivity and prevented the increase in MafG and c-Maf levels.
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
182 of Pax6 and c-Maf to multiple regions of the c-Maf locus in lens chromatin.
183 elopment and function including Pax-6, Six3, c-Maf, Maf1, Sox-4, Foxc1, Rx, and Ldb2 were present amo
184  multiple myelomas harboring cyclin D1/D3 or c-MAF/MAFB translocations.
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.
188             CD4+ T cells and NK T cells from c-maf(-/-) mice were markedly deficient in IL-4 producti
189                                        While c-Maf mRNA and protein levels remain constant during mye
190 cers and nonproducers have similar Gata3 and c-maf mRNA expression.
191 nding to the c-Maf promoter and induction of c-Maf mRNA.
192               Only these 6 lines overexpress c-maf mRNA.
193              We report a semi-dominant mouse c-Maf mutation recovered after ENU mutatgenesis which re
194             Unlike null and loss-of-function c-Maf mutations, which cause severe runting and renal ab
195  results together led to the conclusion that c-Maf negatively regulates ARE-mediated detoxifying enzy
196                                      Neither c-Maf nor JunB induced Th2 development in Stat6-deficien
197                                              c-Maf-null macrophages exhibit strongly impaired IL-10 p
198 d to enhance LPS-induced IL-10 production in c-Maf-null macrophages.
199                                           In c-maf-null mice, fetal bone length is decreased approxim
200 mature hypertrophic chondrocytes at E15.5 in c-maf-null tibiae, with decreased expression domains of
201 rmal proliferation rate and apoptosis in the c-maf-null.
202 ecrease in MMP-13 expression at E15.5 in the c-maf-null.
203 revious novel finding that the protooncogene c-Maf of the basic leucine zipper family of transcriptio
204 pers with c-Jun, JunB or c-Fos, but not with c-Maf or MafB.
205                                 Knockdown of c-Maf or MafG individually blunted the LCA-induced decre
206                                 Knockdown of c-Maf or MafG individually increased the expression of G
207  the expression of Pax-6, alphaA-crystallin, c-maf, or PDGF-R alpha.
208 xpression and could be rescued completely by c-Maf overexpression in T cells.
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
212                     The transcription factor c-Maf plays a critical and selective role in IL-4 gene t
213                   It remains unclear whether c-maf possesses any IL-4-independent function in regulat
214 erized a novel FGF2-responsive region in the c-Maf promoter (-272/-70, FRE).
215  and thereby decreased Twist2 binding to the c-Maf promoter and induction of c-Maf mRNA.
216                 We show that Stat3 binds the c-maf promoter in CD4 T cells after IL-6 stimulation, an
217 L-6 stimulation, and also transactivates the c-maf promoter in reporter gene assays.
218                                     A 1.3-kb c-Maf promoter with a 1.6-kb upstream enhancer (CR1) rec
219 d the complex allowing Twist2 to bind to the c-Maf promoter.
220               These studies demonstrate that c-maf promotes Th2 differentiation by IL-4-dependent mec
221                           Elevated levels of c-Maf protein led to marked increases in Myb:Maf complex
222 of MafA and MafB along with two forms of the c-Maf protein.
223 proximately 500-kb region centromeric to the c-maf proto-oncogene at 16q23.
224  site represents the 3' coding region of the c-maf proto-oncogene at 67.0 centimorgans (cM) on chromo
225                                          The c-maf proto-oncogene encodes a basic leucine zipper prot
226                                          The c-maf protooncogene is a T helper cell type 2 (Th2)-spec
227 oth CD4 and CD8 T-cells; here too transgenic c-Maf provided significant protection.
228 ding protein (CBP) and/or p300 interact with c-Maf, Prox-1, or Sox-1 to enhance transcription of crys
229 s fiber cell differentiation is regulated by c-Maf, Prox1 and Sox1.
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
232                     Our results suggest that c-Maf recruits CBP and/or p300 to crystallin promoters l
233 versely, small interfering RNA inhibition of c-maf reduces HIV-1 transcription in IL-4-producing T ce
234                                     Pax6 and c-Maf regulate multiple stages of mammalian lens develop
235 , we have shown that the bZIP proto-oncogene c-Maf regulates expression of alphaA-crystallin (Cryaa)
236      Thus our data suggest that ICOS-induced c-Maf regulates IL-21 production that in turn regulates
237 tle is known about the mechanism that guides c-Maf regulation during early T cell activation.
238 -Maf, we examined the impact of p53 on known c-Maf regulators.
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
242                             c-Maf binds to a c-Maf response element (MARE) in the proximal IL-4 promo
243  in vitro and in vivo experiments identify a c-Maf response element localized to nucleotides -196/-18
244                   Nonetheless, the essential c-Maf-responsive element appears to be located elsewhere
245                              Genetic loss of c-Maf resulted in a defect in IL-21 production and fewer
246 l lamina-specific transcription factors such c-Maf, Rora, and Satb1 are identified for the first time
247                                              c-Maf's inhibition of CD13/APN expression correlates wit
248                          When overexpressed, c-Maf selectively inhibits transcriptional activation of
249 d activators of transcription 4), T-bet, and c-maf showed reduced expression in UCB compared with AB
250                         In addition, Batf-to-c-Maf signalling is an important determinant of IL-4 exp
251                                              c-Maf siRNA inhibited HAS1 expression in M. tuberculosis
252 tes IL-4 promoter, and ectopic expression of c-Maf skews primary T cell response toward the Th2 pathw
253                                              c-Maf small interfering RNA (siRNA) inhibited IL-10 prod
254 )(q23;q11), with the breakpoint telomeric to c-maf, so that the translocation breakpoints in these 6
255                        Ectopic expression of c-Maf stimulates not only exogenously transfected IL-10
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/
259                      Moreover, CS1 increased c-maf-targeted cyclin D2-dependent proliferation, -integ
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
263  directly to the P1 site and synergizes with c-Maf to activate an IL-4 luciferase reporter gene.
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.
267  that Stat6 functions upstream of GATA-3 and c-Maf to induce Th2 development.
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
270 to IL-4 promoter regions and synergizes with c-Maf to positively regulate IL-4 expression.
271  was induced by IL-27, acted in synergy with c-Maf to promote the development of Tr1 cells.
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
274                                Expression of c-Maf transactivated each of these promoters.
275                            In immune system, c-Maf transactivates IL-4 promoter, and ectopic expressi
276                                              c-Maf transactivates the IL-4 gene promoting Th2 cell de
277                        Ectopic expression of c-Maf transactivates the IL-4 promoter in Th1 cells, B c
278  In transfected cells, sumoylation decreases c-Maf transactivation of IL-4p-driven luciferase reporte
279                       A new long form of the c-Maf transcription factor (Lc-Maf) was identified and s
280              We found impaired expression of c-Maf transcription factor functionally associated with
281                                          The c-maf transcription factor is selectively expressed in I
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
285                       Surprisingly, when the c-Maf transgene was backcrossed with the NOD model of sp
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
290                                              c-Maf undergoes tyrosine phosphorylation at Tyr(21), Tyr
291  to c-avian musculoaponeurotic fibrosarcoma (c-Maf)/V-maf musculoaponeurotic fibrosarcoma oncogene ho
292                   Retroviral transduction of c-Maf was able to induce IL-10 expression in Stat6-defic
293                             Up-regulation of c-Maf was dependent on Ca2+/nuclear factor of activated
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
296                      Because MafA, MafB, and c-Maf were each capable of specifically binding to and a
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
299                         The co-expression of c-Maf with MafG rescued the MafG repression of MARE but
300 established in vivo interactions of Pax6 and c-Maf with the alphaA-crystallin promoter in lens cells.

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