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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
5 r (APLF) is a DNA repair factor containing a forkhead-associated (FHA) domain that supports binding t
6 ated XRCC1 stimulates PNKP by binding to its forkhead-associated (FHA) domain, whereas nonphosphoryla
9 , and demonstrate that the GGDEF and sensory forkhead-associated (FHA) domains form an asymmetric dim
12 It harbors both a plant homeodomain and a forkhead-associated domain implicated in epigenetic reco
15 tein MxiG (MxiG(C)), which is a noncanonical forkhead-associated domain, and MxiK has an elongated st
17 ule consisting of 2 phosphothreonine-binding Forkhead-associated domains joined by an intrinsically d
18 I109 is a highly conserved residue in the forkhead box (Fox) domain of FOXF2, a member of the Fox
19 ne expression profiling revealed a subset of Forkhead box (Fox) genes that are regulated by Shh signa
25 tion of glucocorticoid receptor signaling or forkhead box (FOXO) 1/3 inhibition abolished the rapamyc
26 letion of another P subfamily members of the forkhead box (Foxp) subfamily member Foxp1 in Treg cells
31 some and the pioneering transcription factor forkhead box A1 (FOXA1), both of which are implicated in
33 essive activity in an enhancer-specific, but forkhead box A1-dependent and active, ER-independent man
38 with NK2 homeobox 1 (Nkx2.1) for binding to forkhead box A2 (Foxa2) to drive hepatic differentiation
39 homeobox 1 (PDX1), NK6 homeobox 1 (NKX6.1), forkhead box A2 (FOXA2), and NK2 homeobox 2 (NKX2.2) - f
40 n in the developmental transcription factor, forkhead box A2, FOXA2 (c.505T>C, p.S169P) in a child wi
41 tionally ablating a key transcription factor Forkhead box C1 (FOXC1) expressed in hair follicle SCs (
45 factors-mesogenin 1 (Msgn1), T-box 6 (Tbx6), forkhead box C1 (Foxc1), paired box 3 (Pax3), Paraxis, m
47 genetic variants in apolipoprotein E (APOE), forkhead box class O3a, clusterin, and phosphatidylinosi
52 ion factor FOXM1 (forkhead box M1) or FOXF1 (forkhead box F1), both downstream targets of VEGF, can i
53 this study, we examined the role of FoxM1, a forkhead box family member transcription factor in tubul
54 Forkhead box N1 (FOXN1) is a member of the forkhead box family of transcription factors and plays a
56 Here we identify FOXB2, an uncharacterized forkhead box family transcription factor, as a potent ac
57 Lindau tumor suppressor (VHL) protein in the forkhead box FOXD1 cell lineage, from which stromal prog
58 erozygous for a loss-of-function mutation in forkhead box I3 (FOXI3), a candidate gene within the com
59 se-pair duplication in the first exon of the forkhead box I3 gene (FOXI3) shared by all three breeds.
60 The mechanistic role of cross talk between Forkhead box M1 (FOXM1) and HGF/Met signaling in promoti
63 elated gene-1 (Brg1) chromatin remodeler and forkhead box M1 (FoxM1) transcription factor cooperate w
67 ncubation with thiostrepton (an inhibitor of forkhead box M1 [FOXM1]) or verteporfin (inhibitor of th
68 s, including the GRB2 interactome as well as Forkhead Box M1 and its downstream target, the tryptopha
69 of proangiogenic transcription factor FOXM1 (forkhead box M1) or FOXF1 (forkhead box F1), both downst
70 by modulating transcription factors p53 and forkhead box M1, which was not observed with sequential
75 ents with compound heterozygous mutations in forkhead box N1 (FOXN1), a transcription factor essentia
76 ional regulator of epithelial cell function, Forkhead Box N1 (Foxn1), and its two regulated targets,
79 activity of the DAF-16 transcription factor (forkhead box O (FOXO) homologue), whose global targets w
80 -dependent protein kinase (PKG2) to activate forkhead box O (FoxO) in colon cancer cells and in the c
82 ification appeared to be abnormally elevated forkhead box O (FOXO) signaling in the ETC-deficient ISC
84 ds are scarce, skeletal progenitors activate forkhead box O (FOXO) transcription factors, which bind
86 nsing pathways, including sirtuin 1 (SIRT1), forkhead box O (FoxO), AMP-activated protein kinase (AMP
87 ectin-5'-AMP-activated protein kinase (AMPK)-forkhead box O (FOXO)-signaling axis stemming from at th
90 The regulation of catabolic signalling via forkhead box O 1 and protein ubiquitination is SIRT1 dep
93 rt that tribbles homologue 2 (TRIB2) ablates forkhead box O activation and disrupts the p53/MDM2 regu
94 ed new PERK substrates transcription factors Forkhead box O protein and diacyglycerol a lipid signali
95 ements of insulin signaling pathways such as forkhead box O transcriptional signaling or glucose tran
96 antagonist, which led to p-Tie2 suppression, forkhead box O1 (FOXO1) activation, increased ANG2 expre
97 arget insulin-regulated transcription factor forkhead box O1 (FoxO1) and, accordingly, expression of
98 phosphorylation of the transcription factor forkhead box O1 (FOXO1) at Ser-249, leading to transcrip
101 Dhh both opens the BBB via the modulation of forkhead box O1 (FoxO1) transcriptional activity and ind
103 ), Glucagon (GCG)], differentiation markers [Forkhead box O1 (FOXO1), Paired box 6, SRY box 9, NK6 Ho
105 PAX3-FOXO1 (paired box gene 3 fused with forkhead box O1) fusion RNA, which is considered a hallm
107 f the stress-responsive transcription factor forkhead box O3 (FoxO3) in mediating injury-induced prox
108 -223-3p directly repressed the expression of forkhead box O3 (FOXO3), and FOXO3 negatively regulated
109 y, overexpression of a transcription factor, forkhead box O3 (FoxO3), which is implicated in aging, b
112 tion 2 homolog 1 (SIRT1), which deacetylates forkhead box o3 (FOXO3a), leading to repression of proap
114 vated Akt1 increased both GSK3alpha/beta and forkhead box of the O class transcription class 3 (FoxO3
117 shown that loss of the transcription factors forkhead box P1 (Foxp1) and Foxp4, which are critical fo
118 enetic approaches to investigate the role of forkhead box P1 (FOXP1) in transcriptional control of MS
120 errant AKT activity and decreased downstream forkhead box P1 (FOXP1)/FGF and NOTCH1/EPHB2 signaling,
121 n the gene encoding the transcription factor forkhead box P2 (FOXP2) result in brain developmental ab
123 red for differentiation of T(h)17 cells) and forkhead box P3 (Foxp3) (required for the differentiatio
124 allergic responses linked to Smad3-dependent forkhead box P3 (Foxp3) expression and IL-10 production.
125 CD25 regulatory T cells (Treg) and increased forkhead box P3 (Foxp3) expression in tolerant grafts.
126 ve insights into to the demethylation of the forkhead box P3 (Foxp3) locus during the induced T regul
129 , splenocyte cytokine production and splenic forkhead box P3 (FOXP3)(+) regulatory T (Treg) cells wer
130 okine production by splenocytes, and splenic forkhead box P3 (FOXP3)(+) regulatory T (Treg) cells wer
132 immunologic conditions, lymphocyte subsets, forkhead box P3 (FOXP3)(+) Treg cell levels, and phenoty
135 ocyte activation gene 3 (LAG3)(+), CD49b(-), forkhead box P3 (Foxp3)(-) regulatory T cells in vitro,
136 oliferation and increased mRNA expression of forkhead box P3 (FOXP3), a transcription factor which is
137 X) syndrome, which is caused by mutations in forkhead box P3 (FOXP3), and IPEX-like disorders caused
138 reg lineage-determining transcription factor forkhead box P3 (FOXP3), and Treg-specific deletion of m
139 ance through the master transcription factor forkhead box P3 (FOXP3), which is crucial for Treg cell
140 came robust T-regulatory cells (Tregs) in WT forkhead box P3 (Foxp3)-green fluorescent protein mice,
141 3, interleukin-6, tumor necrosis factor, and forkhead box P3 prominently placed in a regulatory conne
144 etal DCs effectively primed antigen-specific forkhead box P3(+) regulatory T cells after in vitro coi
147 ory circuit encompassing tolerogenic DCs and forkhead box P3(+) Treg cells that could be targeted for
149 n accumulation of activated CD4(+) Foxp3(-) (forkhead box P3) IFN-gamma(+) T cells in the heart-drain
150 essed the T(reg) transcription factor FoxP3 (Forkhead Box P3) protein as detected by flow cytometry.
151 ssion of the immunoregulatory markers IL-10, forkhead box P3, and cytotoxic T lymphocyte-associated p
153 response and accumulation of IL-10-producing forkhead box P3-negative effector CD4(+) T cells in the
155 lung injury is mediated by a novel subset of forkhead box P3-positive AMs that limits inflammation, f
156 er of differentiation 25-positive (CD25(+) ) forkhead box P3-positive CD4(+) regulatory T-cell freque
157 of effector CD4(+) T cells and inhibition of forkhead box P3-positive regulatory T (Treg) cells, but
158 ficacy were evaluated alongside PNA-specific forkhead box P3-positive regulatory T cells and IL-10(+)
159 caused a reduction in IL-13(+) CD4 T cells, forkhead box P3-positive regulatory T cells, and IL-5(+)
160 tinaldehyde dehydrogenase and specialized in forkhead box p3-positive regulatory T-cell conversion.
163 ptor (ER), glucocorticoid receptor (GR), and forkhead box protein 1 (FoxA1) are significant factors i
165 ressor that is transcriptionally silenced by forkhead box protein 1 (FOXP1) in the aggressive, activa
166 ession of the oncogenic transcription factor forkhead box protein 1 (FOXP1) is a common feature of di
168 challenge, symptoms, Treg cell numbers, and forkhead box protein 3 (Foxp3), TH2 and TH17 cytokine, a
169 ing on a farm and increased peripheral blood forkhead box protein 3 expression and correlated inverse
170 ere are 2 main subsets of Treg cells: FOXP3 (forkhead box protein 3)-positive Treg cells, which do no
172 , promote the expansion of immunosuppressive forkhead box protein 3-positive CD8+ regulatory T cells,
173 elevance, HuMoSCs induce long-lasting memory forkhead box protein 3-positive CD8+ regulatory T lympho
174 tolerance restoration, favoring expansion of forkhead box protein 3-positive regulatory T cells along
175 lbumin, suppressing the normal generation of forkhead box protein 3-positive Treg cells while promoti
176 ermining transcription factors including ER, forkhead box protein A1 (FOXA1) and GATA-binding factor
180 tion of invasion genes through inhibition of Forkhead box protein A1 (FOXA1), an invasion suppressor
183 MAPK signaling, and the transcription factor Forkhead Box Protein C2 (FOXC2) known to promote cancer
184 the converse experiment and lineage-labeled forkhead box protein L1(Foxl1)-positive hepatic progenit
185 eatured upstream binding sites recognized by forkhead box protein M1 (FoxM1), a key transcription fac
186 was associated with inhibited expression of forkhead box protein M1 (Foxm1), a reparative transcript
188 hat insulin-like peptide receptor (INSR) and forkhead box protein O (FoxO) are important genetic driv
189 transcription factors such as T-cell factor, forkhead box protein O, and hypoxia inducible factor 1al
190 effector genes and the transcription factors forkhead box protein O1 (Foxo1) and Klf2 in DP thymocyte
191 rtant role of the antioxidant defense factor forkhead box protein O1 (FoxO1) in the KSHV life cycle.
195 we show that the antioxidant defense factor forkhead box protein O1 (FoxO1) maintains KSHV latency b
197 PGE2, through PI3K/AKT activation, promoted Forkhead box protein O1 (FOXO1) phosphorylation and FOXO
199 3-kinase (PI3K) signaling involving PTEN and forkhead box protein O1 (Foxo1), supporting autoantibody
203 ficiency resulted in nuclear accumulation of Forkhead box protein O1 and subsequently promoted hepati
204 ivation and enhanced nuclear localization of forkhead box protein O1 transcription factors and glycog
205 y preventing nuclear translocation of FoxO1 (Forkhead box protein O1) and beta-catenin, which contrib
206 etic mice with cardiomyocyte-specific FOXO1 (Forkhead box protein O1) deletion showed that FOXO1 boun
207 e B) signaling and phosphorylation of FOXO1 (forkhead box protein O1) suppressing its transcriptional
208 am through protein kinase B (AKT) and FOXO1 (forkhead box protein O1) to drive synergistic expression
209 n sequencing screens led to the discovery of forkhead box protein O4 and signal transducer and activa
214 enotype in Vdelta2 T cells, characterized by forkhead box protein P3 (FoxP3) expression and suppressi
215 14; sparse mast cell degranulation; numerous forkhead box protein P3 (FoxP3)+ regulatory T cells and
217 ory response and enhanced the recruitment of forkhead box protein P3-positive immunosuppressive regul
219 eport that nuclear AURKA can be recruited by Forkhead box subclass M1 (FOXM1) as a co-factor to trans
220 monstrate that pharmacological inhibition of Forkhead box subclass O (FoxO) transcription factors usi
221 y decreasing ROS through increased levels of forkhead box transcription factor 3a (FOXO3a) and a down
225 found that heightened expression of FoxM1, a Forkhead box transcription factor, is regulated during d
226 of AMPKalpha and down-stream targets 4E-BP, Forkhead box transcription factors O (Foxo) and Peroxiso
229 asis.SIGNIFICANCE STATEMENT Mutations of the Forkhead-box protein 2 (FOXP2) gene in humans are the fi
231 k the esophageal gland due to knockdown of a forkhead-box transcription factor, Sm-foxA, which blocks
236 ound that leptin inhibited the expression of forkhead-boxP3 (FoxP3) and its splicing variants contain
240 librium folding and binding mechanism of the forkhead domain of wild-type FoxP1, and of two mutants t
242 within the wing-2 region of the DNA-binding forkhead domain, enable enhanced chromatin mobility and
244 state cancers, we define two hotspots in the forkhead domain: Wing2 (around 50% of all mutations) and
251 ough most forkhead TFs recognize a canonical forkhead (FKH) motif, RYAAAYA, some forkheads recognize
252 is different from the more widely recognized forkhead (FKH) sequence RYAAAYA (where R is purine, and
254 ave examined the binding properties of three Forkhead (FOX) transcription factors, FOXK2, FOXO3 and F
255 rm (CM) as eliminating the functions of both Forkhead genes in the same Drosophila embryo results in
257 he FOX family that recognizes an alternative forkhead-like (FHL) consensus sequence (GACGC) that is d
259 2) one type-restricted transcription factor (Forkhead) only regulates receptor expression, and (3) an
260 distinct roles for SMAD2 and SMAD3 with the forkhead pioneer factor FOXH1 as a partner in the regula
262 anonical forkhead (FKH) motif, RYAAAYA, some forkheads recognize a completely different (FHL) motif,
264 y transactivate the FOXM1 promoter through a Forkhead response element, whereas FOXM1 can activate AU
265 nd antagonizing Foxo1 binding to a consensus forkhead site in this cis-regulatory element that we sho
276 nic stem to epiblast cells and uncovered the forkhead transcription factor FOXD3 as a major regulator
282 nstrate that the expression of the oncogenic forkhead transcription factor FOXM1 is upregulated by GO
283 the key nodes in the metabolic network, the forkhead transcription factor FOXO has been shown to int
284 ce, but Akt-dependent phosphorylation of the forkhead transcription factor FoxO1 at serine 256, which
286 ating both AKT and MAPK signaling to inhibit forkhead transcription factor O3a (FOXO3a) function and
287 mitotic genes in close proximity to Fkh2, a forkhead transcription factor previously implicated in r
288 Here, we study the function of the Tc-foxQ2 forkhead transcription factor, a key regulator of the an
289 osphorylation of FOXO3a, a tumor suppressive forkhead transcription factor, leading to its cytoplasmi
295 e closely related fasting/starvation-induced forkhead transcription factors FOXK1 and FOXK2 induce ae
296 J1, which encodes a well-known member of the forkhead transcription factors important for ciliogenesi
297 d Hi-C experiments on cells depleted for the Forkhead transcription factors, Fkh1 and Fkh2, previousl
298 t of insulin signaling is the FoxO family of Forkhead transcription factors, which translocate from t
300 The Forkhead Box C1 (FOXC1) gene encodes a forkhead/winged helix transcription factor involved in e