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1 ture a conserved DNA-binding domain known as forkhead.
2 recently identified Saccharomyces cerevisiae Forkhead 1 (Fkh1) and Forkhead 2 (Fkh2) as required for
3 ccharomyces cerevisiae Forkhead 1 (Fkh1) and Forkhead 2 (Fkh2) as required for the clustering of a su
4 on in the phosphopeptide-binding site of the forkhead-associated (FHA) domain disrupted normal Mnk lo
5 r (APLF) is a DNA repair factor containing a forkhead-associated (FHA) domain that supports binding t
7 Mutations of the ligand-binding residues of Forkhead-associated (FHA) domains of Rad53, Dun1, Xrs2,
8 It harbors both a plant homeodomain and a forkhead-associated domain implicated in epigenetic reco
11 ecruits BAP1 to the target genes through the forkhead-associated domain, which interacts with Thr(P)-
14 ells were found to coexpress pioneer factors forkhead box (Fox) a1 and Foxa2 before neuroendocrine di
16 ne expression profiling revealed a subset of Forkhead box (Fox) genes that are regulated by Shh signa
18 racetylation and nuclear localization of the forkhead box (Fox) protein FoxO3a, followed by enhanced
25 tion of glucocorticoid receptor signaling or forkhead box (FOXO) 1/3 inhibition abolished the rapamyc
29 g enhancers, which are also dependent on the forkhead box A1/A2 (FOXA1/A2) transcription factors (TFs
31 with NK2 homeobox 1 (Nkx2.1) for binding to forkhead box A2 (Foxa2) to drive hepatic differentiation
32 homeobox 1 (PDX1), NK6 homeobox 1 (NKX6.1), forkhead box A2 (FOXA2), and NK2 homeobox 2 (NKX2.2) - f
33 transcription factors Nkx2.1, Gata6, Foxa2 (forkhead box a2), and Foxf1 mimic the expression pattern
34 n in the developmental transcription factor, forkhead box A2, FOXA2 (c.505T>C, p.S169P) in a child wi
35 ing in vivo microarray analysis, we identify forkhead box C1 (Foxc1) as a transcriptional partner of
36 tionally ablating a key transcription factor Forkhead box C1 (FOXC1) expressed in hair follicle SCs (
39 t the expression of two genes in the region, forkhead box E1 (FOXE1) and PTC susceptibility candidate
43 Lindau tumor suppressor (VHL) protein in the forkhead box FOXD1 cell lineage, from which stromal prog
45 Based on these findings, we discover that forkhead box H1 (FOXH1), a transcription factor required
46 se-pair duplication in the first exon of the forkhead box I3 gene (FOXI3) shared by all three breeds.
47 The mechanistic role of cross talk between Forkhead box M1 (FOXM1) and HGF/Met signaling in promoti
48 st cancer cell lines, we found that oncogene forkhead box M1 (FOXM1) interacts with SMAD3 to sustain
50 ndent expression of the transcription factor forkhead box M1 (FOXM1) is necessary for cell proliferat
51 elated gene-1 (Brg1) chromatin remodeler and forkhead box M1 (FoxM1) transcription factor cooperate w
53 ncubation with thiostrepton (an inhibitor of forkhead box M1 [FOXM1]) or verteporfin (inhibitor of th
54 s, including the GRB2 interactome as well as Forkhead Box M1 and its downstream target, the tryptopha
55 by modulating transcription factors p53 and forkhead box M1, which was not observed with sequential
58 ial cell (TEC)-specific transcription factor Forkhead box N1 (FOXN1) has been implicated as a compone
60 ional regulator of epithelial cell function, Forkhead Box N1 (Foxn1), and its two regulated targets,
61 vation of the downstream signaling molecules forkhead box O (FOXO) and p70 S6 kinase in a tissue and
65 activity of the DAF-16 transcription factor (forkhead box O (FOXO) homologue), whose global targets w
66 -dependent protein kinase (PKG2) to activate forkhead box O (FoxO) in colon cancer cells and in the c
71 photoreceptor differentiation by modulating Forkhead box O (FOXO), target of rapamycin, and Hippo si
72 ectin-5'-AMP-activated protein kinase (AMPK)-forkhead box O (FOXO)-signaling axis stemming from at th
75 The regulation of catabolic signalling via forkhead box O 1 and protein ubiquitination is SIRT1 dep
77 rt that tribbles homologue 2 (TRIB2) ablates forkhead box O activation and disrupts the p53/MDM2 regu
78 ed new PERK substrates transcription factors Forkhead box O protein and diacyglycerol a lipid signali
79 ts of JH on growth rate are dependent on the forkhead box O transcription factor (FOXO), which is neg
80 nscription factor activity by overexpressing forkhead box O transcription factor 1 rescued the abnorm
81 ycin activity by rapamycin or restoration of forkhead box O transcription factor activity by overexpr
82 lian target of rapamycin and inactivation of forkhead box O transcription factor-signaling pathways.
83 ements of insulin signaling pathways such as forkhead box O transcriptional signaling or glucose tran
84 antagonist, which led to p-Tie2 suppression, forkhead box O1 (FOXO1) activation, increased ANG2 expre
90 tivated the phosphoinositol 3-kinase/Akt and forkhead box O1 pathways (showing a dose-dependent effec
92 PAX3-FOXO1 (paired box gene 3 fused with forkhead box O1) fusion RNA, which is considered a hallm
93 f the stress-responsive transcription factor forkhead box O3 (FoxO3) in mediating injury-induced prox
94 y, overexpression of a transcription factor, forkhead box O3 (FoxO3), which is implicated in aging, b
95 l target of rapamycin complex 1 (mTORC1) and forkhead box o3 (Foxo3a) acted downstream of Akt to infl
97 tion 2 homolog 1 (SIRT1), which deacetylates forkhead box o3 (FOXO3a), leading to repression of proap
100 vated Akt1 increased both GSK3alpha/beta and forkhead box of the O class transcription class 3 (FoxO3
102 shown that loss of the transcription factors forkhead box P1 (Foxp1) and Foxp4, which are critical fo
103 iR-150 expressed relatively higher levels of forkhead box P1 (FOXP1) and GRB2-associated binding prot
105 enetic approaches to investigate the role of forkhead box P1 (FOXP1) in transcriptional control of MS
107 errant AKT activity and decreased downstream forkhead box P1 (FOXP1)/FGF and NOTCH1/EPHB2 signaling,
108 n the gene encoding the transcription factor forkhead box P2 (FOXP2) result in brain developmental ab
110 associated with decreased expression of the forkhead box P3 (FoxP3) 44- and 47-kDa splicing forms, o
111 crophages had an enhanced capacity to induce forkhead box P3 (FOXP3) expression in naive CD4(+) T cel
113 ve insights into to the demethylation of the forkhead box P3 (Foxp3) locus during the induced T regul
115 okine production by splenocytes, and splenic forkhead box P3 (FOXP3)(+) regulatory T (Treg) cells wer
117 immunologic conditions, lymphocyte subsets, forkhead box P3 (FOXP3)(+) Treg cell levels, and phenoty
120 ocyte activation gene 3 (LAG3)(+), CD49b(-), forkhead box P3 (Foxp3)(-) regulatory T cells in vitro,
121 X) syndrome, which is caused by mutations in forkhead box P3 (FOXP3), and IPEX-like disorders caused
123 3, interleukin-6, tumor necrosis factor, and forkhead box P3 prominently placed in a regulatory conne
126 etal DCs effectively primed antigen-specific forkhead box P3(+) regulatory T cells after in vitro coi
128 ory circuit encompassing tolerogenic DCs and forkhead box P3(+) Treg cells that could be targeted for
130 antigen-specific regulatory T cells (CD25(+) forkhead box P3(+)) at the expense of effector (IFN-gamm
131 n accumulation of activated CD4(+) Foxp3(-) (forkhead box P3) IFN-gamma(+) T cells in the heart-drain
132 ng, which has the capacity to stimulate CD4+ forkhead box P3+ (Foxp3+) regulatory T cells (Tregs), ac
133 hat its deficiency causes a cell-autonomous, Forkhead box P3-independent failure of peripheral CD4(+)
135 caused a reduction in IL-13(+) CD4 T cells, forkhead box P3-positive regulatory T cells, and IL-5(+)
136 tinaldehyde dehydrogenase and specialized in forkhead box p3-positive regulatory T-cell conversion.
139 ptor (ER), glucocorticoid receptor (GR), and forkhead box protein 1 (FoxA1) are significant factors i
141 ressor that is transcriptionally silenced by forkhead box protein 1 (FOXP1) in the aggressive, activa
142 ession of the oncogenic transcription factor forkhead box protein 1 (FOXP1) is a common feature of di
143 s of the signature Treg transcription factor Forkhead box protein 3 (Foxp3) and Treg function under v
144 The identification of CD25 and subsequently Forkhead box protein 3 (Foxp3) as markers for regulatory
145 on between the expression of the Treg marker forkhead box protein 3 (FoxP3) in biopsies of PTLDs and
146 eg function and increased methylation in the forkhead box protein 3 (FOXP3) locus (P < 0.05), conditi
149 challenge, symptoms, Treg cell numbers, and forkhead box protein 3 (Foxp3), TH2 and TH17 cytokine, a
150 nterparts (pTregs) are imprinted with unique Forkhead box protein 3 (Foxp3)-dependent and independent
152 y associated with an increased expression of forkhead box protein 3 and a decreased expression of Cep
153 ing on a farm and increased peripheral blood forkhead box protein 3 expression and correlated inverse
154 protein 3-positive Treg cells compared with forkhead box protein 3-negative conventional T cells.
155 , promote the expansion of immunosuppressive forkhead box protein 3-positive CD8+ regulatory T cells,
156 elevance, HuMoSCs induce long-lasting memory forkhead box protein 3-positive CD8+ regulatory T lympho
157 that IVIg significantly increases numbers of forkhead box protein 3-positive regulatory T (Treg) cell
158 tolerance restoration, favoring expansion of forkhead box protein 3-positive regulatory T cells along
159 n IL-10 production, numbers of CD4(+)CD25(+) forkhead box protein 3-positive regulatory T cells, and
160 teins and the cytokine production profile of forkhead box protein 3-positive Treg cells compared with
161 lbumin, suppressing the normal generation of forkhead box protein 3-positive Treg cells while promoti
164 T/enhancer-binding protein beta (C/EBPbeta), forkhead box protein A2 (FOXA2), and retinoid X receptor
166 ly demonstrated that the winged helix factor forkhead box protein A3 (Foxa3) regulates the expansion
167 or 5 (ATF5), early growth response 1 (EGR1), forkhead box protein A3 (FOXA3), JUNB, Kruppel-like fact
168 MAPK signaling, and the transcription factor Forkhead Box Protein C2 (FOXC2) known to promote cancer
169 , including increases in multicilin gene and forkhead box protein J1 expression and inhibition of the
170 ace, (ii) expression of transcription factor forkhead box protein J1, and (iii) presence of multiple
171 e inhibitor BI2536 suppressed binding of the Forkhead box protein K1 (FOXK1) transcriptional represso
172 the converse experiment and lineage-labeled forkhead box protein L1(Foxl1)-positive hepatic progenit
173 eatured upstream binding sites recognized by forkhead box protein M1 (FoxM1), a key transcription fac
177 transcription factors such as T-cell factor, forkhead box protein O, and hypoxia inducible factor 1al
178 effector genes and the transcription factors forkhead box protein O1 (Foxo1) and Klf2 in DP thymocyte
180 PGE2, through PI3K/AKT activation, promoted Forkhead box protein O1 (FOXO1) phosphorylation and FOXO
182 3-kinase (PI3K) signaling involving PTEN and forkhead box protein O1 (Foxo1), supporting autoantibody
186 racterized by expression of the paired box 3-forkhead box protein O1 (PAX3-FOXO1) fusion oncogene.
187 y preventing nuclear translocation of FoxO1 (Forkhead box protein O1) and beta-catenin, which contrib
188 am through protein kinase B (AKT) and FOXO1 (forkhead box protein O1) to drive synergistic expression
189 n sequencing screens led to the discovery of forkhead box protein O4 and signal transducer and activa
191 the upregulation of the transcription factor Forkhead box protein P1 (Foxp1), which prevents CD8(+) T
192 sion in cardiomyocytes and overexpression of Forkhead box protein P1 attenuated miR-206-induced cardi
195 ac hypertrophy and survival, suggesting that Forkhead box protein P1 is a functional target of miR-20
199 enotype in Vdelta2 T cells, characterized by forkhead box protein P3 (FoxP3) expression and suppressi
202 eport that nuclear AURKA can be recruited by Forkhead box subclass M1 (FOXM1) as a co-factor to trans
203 y decreasing ROS through increased levels of forkhead box transcription factor 3a (FOXO3a) and a down
207 found that heightened expression of FoxM1, a Forkhead box transcription factor, is regulated during d
208 e present study was to determine the role of forkhead box transcription factors in modulating lipid m
209 (HCV) infection modulates the expression of forkhead box transcription factors, including FoxO1 and
210 nce class switching in a manner dependent on forkhead box, subgroup O (FoxO) transcription factors.
214 pression of Foxp1/2/4 proteins, comprised of Forkhead-box (Fox) transcription factors of the Foxp sub
220 hragm through the use of a dominant-negative forkhead boxO adeno-associated virus vector delivered di
222 s determined by inhibiting the activation of forkhead boxO in the rat diaphragm through the use of a
224 lated animals treated with dominant-negative forkhead boxO showed a significant attenuation of both d
226 tively, these results suggest that targeting forkhead boxO transcription could be a key therapeutic t
227 diaphragm during mechanical ventilation, and forkhead boxO-specific transcription can lead to enhance
231 librium folding and binding mechanism of the forkhead domain of wild-type FoxP1, and of two mutants t
232 ity, and the Myb TF acts in concert with two forkhead domain TFs and Polo kinase to regulate cardiac
240 We have characterized a mouse mutant for the Forkhead family transcription factor Foxi3, which is exp
241 ent signaling results in upregulation of the forkhead family transcription factor, FoxM1, and its tra
245 ave examined the binding properties of three Forkhead (FOX) transcription factors, FOXK2, FOXO3 and F
247 rm (CM) as eliminating the functions of both Forkhead genes in the same Drosophila embryo results in
252 y transactivate the FOXM1 promoter through a Forkhead response element, whereas FOXM1 can activate AU
253 nd antagonizing Foxo1 binding to a consensus forkhead site in this cis-regulatory element that we sho
263 A), independent of p53, but dependent on the forkhead transcription factor class-O family member, FOX
266 regeneration phenotypes and that RNAi of the forkhead transcription factor FoxA, which is expressed i
268 nic stem to epiblast cells and uncovered the forkhead transcription factor FOXD3 as a major regulator
276 nstrate that the expression of the oncogenic forkhead transcription factor FOXM1 is upregulated by GO
277 rongly correlated with the expression of the forkhead transcription factor FoxM1, which binds to the
278 the key nodes in the metabolic network, the forkhead transcription factor FOXO has been shown to int
280 ce, but Akt-dependent phosphorylation of the forkhead transcription factor FoxO1 at serine 256, which
281 D31 signals prevents the localization of the forkhead transcription factor FoxO3 to the nucleus, thus
286 mitotic genes in close proximity to Fkh2, a forkhead transcription factor previously implicated in r
287 on and represses the expression of FOXP2, a forkhead transcription factor tightly associated with sp
290 osphorylation of FOXO3a, a tumor suppressive forkhead transcription factor, leading to its cytoplasmi
291 FOX:ETS motif, a composite binding site for Forkhead transcription factors and the Ets transcription
294 fibroblast growth factor signaling and four Forkhead transcription factors consist the central part
297 d Hi-C experiments on cells depleted for the Forkhead transcription factors, Fkh1 and Fkh2, previousl
299 aracterised genome-wide binding sites of the forkhead/winged helix transcription factor Foxa1, which
300 tions, SRL, however, significantly increased forkhead/winged helix transcription factor P3 (FOXP3) Tr
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