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1 UBF bound with low affinity to nucleosome cores formed w
2 UBF could be stripped from ternary complexes with compet
3 UBF function in enhancement differs from that at the pro
4 UBF is a DNA binding protein with multiple HMG domains t
5 UBF is an HMG box-containing factor that binds to the rD
6 UBF is required for enhancer function.
7 UBF itself does not bind stably to rDNA but rapidly asso
8 UBF mRNA levels began to increase within 3-6 h of the in
9 UBF mutations at K232/254A and K232/254R restored rDNA t
10 UBF proteins (known to interact with both IRS-1 and beta
11 UBF showed marked significant differences (p<0.05) in co
12 UBF trimethylation leads to nucleolar chromatin condensa
13 nt assays show that while the formation of a UBF-SL1 complex can partially relieve the inhibition of
14 ion of transcription, only the assembly of a UBF-SL1-Pol I initiation complex on the rDNA promoter co
15 ardiomyocytes indicated that the accumulated UBF protein was phosphorylated and, thus, in the active
19 nsitive (phosphorylation of eEF2, ERK1/2 and UBF; gene expression of the myostatin target Mighty as w
21 ies demonstrated that a subset of CENP-C and UBF/NOR-90 is colocalized at nucleoli of interphase HeLa
22 pUL31, CMV fails to reorganize nucleolin and UBF and exhibits a replication defect at a low multiplic
23 This increased interaction between Rb and UBF correlated with the reduced rate of rDNA transcripti
25 r binding, RNA polymerase I recruitment, and UBF stabilization and that SL1-promoter complex formatio
27 mmunofluorescence labeling shows treacle and UBF colocalize to specific nucleolar organizer regions a
30 man cells coimmunoprecipitated with the anti-UBF antibody after mixing, indicating that the UBF-SL-1
31 reatment of N1S1 cell extracts with the anti-UBF antibody depleted the extracts of SL-1 activity but
32 tment of UBF-depleted extracts with the anti-UBF antibody depleted the extracts of SL-1 activity only
35 antly, CK2 regulates the interaction between UBF and SL1 by counteracting the inhibitory effect of HM
36 n, we have identified an interaction between UBF and TAF1, a factor involved in the transcription of
37 ot solely mediated by an interaction between UBF and TATA-binding protein, which is also a component
40 ding transcription factor (UBTF, also called UBF) is thought to function exclusively in RNA polymeras
41 revious studies have shown that the cellular UBF content increased in adrenergic- and contraction-ind
43 ecreased ipsilateral, but not contralateral, UBF vasodilatory responses to exogenous E2beta by approx
44 BF, intraarterial L-NAME partially decreased UBF dose dependently (r = 0.73, n = 46, P < 0.001) while
46 moreover, incubation of the dephosphorylated UBF with nuclear extracts from exponentially growing cel
47 pproximately 60 bp of additional linker DNA, UBF bound with high affinity similar to its binding to n
48 is effect could be reversed by knocking down UBF or overexpressing RNASE1, which removes RNA-DNA hybr
49 ICI 182 780 infusion inhibited the elevated UBF seen in follicular phase and late pregnant ewes in a
50 ecombinant phosphorylated UBF and endogenous UBF from exponentially growing NIH 3T3 cells but not by
53 ription requires the upstream binding factor UBF and the selectivity factor SL1 to assemble coordinat
54 ls we identified the upstream binding factor UBF, a DNA-binding protein and component of the RNA poly
55 lymerase I activator upstream binding factor UBF-1 at interphase nucleoli, and this interaction is ep
58 We found that pol I transcription factor UBF interacts with pre-rRNA processing factors as analyz
65 hich interacts with upstream binding factor (UBF) and affects transcription of the ribosomal DNA gene
69 rein, we found that upstream binding factor (UBF) interacts with ESET, a histone H3K9 methyltransfera
71 disruption by anti-upstream binding factor (UBF) microinjection (in the absence of DNA damage) also
73 ctly interacts with upstream binding factor (UBF) through its PHD1 domain and suppresses ribosomal RN
75 GF-2 interacts with upstream binding factor (UBF), an architectural transcription factor essential fo
76 The function of upstream binding factor (UBF), an essential component of the RNA polymerase (pol)
78 ence that contained upstream binding factor (UBF), EPB3 genes, SHCL1, ASB-4-like sequence, and acidic
79 of its coactivator, upstream binding factor (UBF), increased in the atrophied heart whereas protein l
88 the HMG box factor [Upstream binding factor (UBF)] and SL1 at the rRNA gene promoter is necessary to
89 d the upstream binding transcription factor (UBF), which interacts with the upstream control element
90 rRNA transcription (upstream-binding factor [UBF]), processing (nucleolin, fibrillarin, and RNase MRP
91 ion of a ribosomal DNA transcription factor, UBF, correlated with increased rates of ribosome biogene
92 ion domain of the rDNA transcription factor, UBF, which significantly reduced its ability to associat
104 NIH 3T3 cells but not by hypophosphorylated UBF from cells treated with rapamycin or dephosphorylate
106 pleted the extracts of SL-1 activity only if UBF was added to the extract prior to the immunodepletio
107 rexpressed beta-catenin, further implicating UBF as a transcriptional enhancer of the beta-catenin pa
108 kg) caused parallel increases (P < 0.001) in UBF (15+/-3 to 130+/-16 ml/min) and uterine cGMP secreti
115 rial L-NAME partially inhibited increases in UBF dose-dependently (r = 0.66, n = 18, P < 0.003) while
116 e that exogenous E2beta-induced increases in UBF in the Ovx animal and endogenous E2beta-mediated ele
117 cGMP modulate estrogen-induced increases in UBF, and if cyclooxygenase inhibition modifies E2beta re
119 ression and anxiety-associated reductions in UBF may not be a pathway by which risk is conferred duri
124 on to UBF, manifesting by markedly increased UBF binding to the rDNA promoter and to the 5'- external
125 over, we showed that large T antigen-induced UBF phosphorylation promotes the formation of a stable U
126 , overexpression of recombinant Rb inhibited UBF-dependent activation of transcription from a cotrans
129 recipitation of [32P] orthophosphate-labeled UBF from hypertrophying neonatal cardiomyocytes suggeste
130 precipitation of [32P]orthophosphate-labeled UBF from hypertrophying, neonatal cardiomyocytes indicat
131 very strong positive correlation for Mabonde UBF in citric and lactic acid pretreatment (r = 0.999, p
136 t of UBF completely abolished the ability of UBF to interact with SL1; moreover, incubation of the de
137 curate Pol I transcription in the absence of UBF and can interact with the rDNA promoter independentl
138 etention of CHP1 attenuates the abundance of UBF in the nucleolus and inhibits RNA synthesis when qui
139 ne acetylation and/or through acetylation of UBF or one of the other components of rDNA transcription
140 al gene transcription through acetylation of UBF, a ribosomal specific transcription factor, as well
143 pothesis in which the dynamic association of UBF with ribosomal DNA clusters recruits the pol I trans
146 a model wherein regulation of the binding of UBF to Rb and, perhaps the cellular content of PAF53, ar
147 IIB activity, suggesting that the binding of UBF to SL-1 is specific and not solely mediated by an in
150 a combination of the dimerization domain of UBF and HMG boxes 1-3 are sufficient to specify its role
151 hoacceptor sites in the C-terminal domain of UBF is important for promoting multiple rounds of Pol I
153 ndicated that the carboxy-terminal domain of UBF, which is necessary for transcriptional activation,
154 and endogenous E2beta-mediated elevations of UBF during the follicular phase and late pregnancy are p
155 We hypothesized that elevated expression of UBF was part of the mechanism by which these hypertrophi
157 e Rib1 interaction and enhancer functions of UBF and can conclude that direct interaction with Rib1 i
158 We further show that hyperphosphorylation of UBF occurs as a result of up-regulation of both cyclin D
161 UBF/Rb complex does block the interaction of UBF with SL-1, as indicated by using the 48 kDa subunit
165 show that a novel epigenetic modification of UBF is linked to impaired rDNA transcription and nucleol
166 and PMA demonstrates that the modulation of UBF phosphorylation is an additional pathway by which ri
167 hese studies suggest that phosphorylation of UBF and subsequent binding to TBP represent a key regula
168 ce implicating a role for phosphorylation of UBF in the control of growth-induced increases in rRNA t
169 ding assay, we found that phosphorylation of UBF in vivo in response to stimulation with different gr
172 s the physical and antioxidant properties of UBF hitherto absent in composite food formulations.
175 ort of the hypothesis that the regulation of UBF is a key component of the increased ribosome biogene
180 depended on the C-terminal 'acidic tail' of UBF that was hyperphosphorylated at multiple serine site
181 so demonstrate that the acidic C-terminus of UBF is primarilyresponsible for its observed interaction
186 short hairpin RNA reduced trimethylation of UBF and resulted in the restoration of rDNA transcriptio
189 amined directly the effect of overexpressing UBF on rDNA transcription in neonatal cardiomyocytes in
191 scued by purified recombinant phosphorylated UBF and endogenous UBF from exponentially growing NIH 3T
192 ile the levels of UBF, Ser388 phosphorylated UBF, and other Pol I-related components (POLR1E, TAF1A,
194 ct by recruiting UBF to the promoter, rather UBF performs its own distinct role at the enhancers.
197 We demonstrate that authentic or recombinant UBF and Rb interact directly and this requires a functio
198 rate that enhancers do not act by recruiting UBF to the promoter, rather UBF performs its own distinc
199 le inverse correlation was recorded in M-red UBF for ascorbic and lactic acid pretreatment (r = -0.03
200 zyl (DPPH) differed significantly with M-red UBF recording high TPC (1130.39 +/- 27.26 mg GAE/100g d.
201 use of bupropion was associated with reduced UBF, even after controlling for pregnancy complications.
202 examined the mechanism by which Rb represses UBF-dependent rDNA transcription and determined if other
208 rRNA genes organized in chromatin, we tested UBF's ability to bind rRNA gene enhancers assembled into
211 rther biochemical analysis demonstrated that UBF is phosphorylated by a kinase activity that is stron
213 and treated cardiomyocytes demonstrated that UBF was phosphorylated exclusively on serine residues.
217 e-treated UBF provided further evidence that UBF phosphorylation plays a critical role in the regulat
218 ults are consistent with the hypothesis that UBF is an important factor in the regulation of rDNA tra
219 These results support the hypothesis that UBF is an important regulatory factor during the initiat
225 cores, rather than free DNA, suggesting that UBF binding to nucleosome cores does not displace the co
226 d exonuclease III footprinting suggests that UBF and histone H1 interact with DNA on both sides flank
228 g deletions of the 5'-flanking region of the UBF gene revealed the presence of contraction response e
232 sion and anxiety (acute: coincident with the UBF scan; proximal: within 2 weeks of the scan; chronic:
234 noprecipitation studies using an antibody to UBF demonstrated that TATA-binding protein, a subunit of
236 l, the variant conferred gain of function to UBF, manifesting by markedly increased UBF binding to th
237 The key activator of Pol I transcription, UBF, has been proposed to act by facilitating recruitmen
238 he inability of alkaline phosphatase treated UBF to efficiently activate transcription can be rescued
239 ranscription assays with phosphatase-treated UBF provided further evidence that UBF phosphorylation p
241 o transduce signals into the nucleoplasm via UBF hyperphosphorylation leading to rRNA transcription a
242 structure, we used an in vivo assay in which UBF is targeted via a lac repressor fusion protein to a
244 microscopy showed that TAF1 colocalizes with UBF in Hela cells, and cell fractionation experiments pr
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