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1 Pit-1 and Ets-1 binding to a composite element synergist
2 Pit-1 and Pit-1beta constitute such a pair of transcript
3 Pit-1 enhances the Ras signaling pathway to the prolacti
4 Pit-1 interaction with the Pitx2 C terminus masks the in
5 Pit-1 interacts with CCAAT/enhancer-binding protein alph
6 Pit-1 is essential for the establishment of these lineag
7 Pit-1, a member of the POU domain family of transcriptio
8 Pit-1, a pituitary-specific POU homeodomain transcriptio
9 Pit-1/GHF-1 is a pituitary-specific, POU homeodomain tra
10 Pit-1/TR synergy is therefore a consequence of a novel s
11 they express the transcription factor GHF-1 (Pit-1) but not growth hormone (GH) or prolactin (PRL).
13 e gibbon ape leukemia virus receptor Glvr-1 (Pit-1) or the amphotropic retrovirus receptor Ram-1 (Pit
16 g known transcription factors, such as Sp-1, Pit-1, glucocorticoid receptor, and hypoxia-inducible fa
17 action surface in Ets-1, which reduced Ets-1/Pit-1 binding in vitro, did not significantly affect Ets
18 e we show that the organization of the Ets-1/Pit-1 composite element tolerates significant flexibilit
19 olecular features: organization of the Ets-1/Pit-1 composite element, physical interaction of these t
20 he rPRL promoter via the most proximal GHF-1/Pit-1 binding site, footprint I, and synergized with GHF
21 itary-specific, POU-homeodomain factor GHF-1/Pit-1 is necessary, but not sufficient, for cell-specifi
24 ed with bona fide binding sites for either a Pit-1 monomer or dimer, and these sites tolerated a sepa
25 tocyte nuclear factor-1beta (HNF-1beta) is a Pit-1, Oct-1/2, Unc-86 (POU) homeodomain-containing tran
26 tocyte nuclear factor-1beta (HNF-1beta) is a Pit-1, Oct-1/2, UNC-86 (POU)/homeodomain-containing tran
27 omposite Pit-1/ETS protein-binding site or a Pit-1 element with no known affinity for ETS proteins re
31 w that the physical interaction of Ets-1 and Pit-1 is not required for Ras responsiveness or synergy
32 amino acid differences between the Oct-1 and Pit-1 POUs domains is the key determinant for the differ
33 ogated binding of both recombinant Pit-1 and Pit-1-containing nuclear extracts revealed that the two
34 scription factors, including Sp1, Zn-15, and Pit-1, predictable and developmentally appropriate expre
38 ed GH genes, co-expression of C/EBPalpha and Pit-1 synergistically activated the transfected rGH prom
42 ll line, which expresses prolactin (PRL) and Pit-1, but not the T3 receptor (TR) or GH, was used as a
44 ifferential use of distinct TAD subtypes and Pit-1 TAD subregions to mediate either synergy or Ras re
45 fective in DNA binding, transactivation, and Pit-1 synergism activities, did not suppress the wild ty
46 analyses, the NPC in HSMCs was identified as Pit-1 (Glvr-1), a member of the novel type III NPCs.
50 isrupts the cooperative interactions between Pit-1 and ETS-1 and blocks the induction of Pit-1-depend
52 t with gibbon ape leukemia retrovirus (binds Pit-1 receptor), indicating that Pit-2 is the form of Na
55 d transcriptional activation domains of both Pit-1 and TR reduced Pit-1/TR synergy in parallel with t
56 aneous infection with vectors targeting both Pit-1 and Pit-2 yielded transduction efficiencies consis
58 signaling in the anterior pituitary via both Pit-1-dependent and -independent pathways, yielding diff
61 ast, the hGH-N transgene is not activated by Pit-1 sites native to either the hGH-N or rat (r)GH gene
65 NA binding analysis using either a composite Pit-1/ETS protein-binding site or a Pit-1 element with n
67 type III sodium-dependent P(i) cotransporter Pit-1 and certain osteoblast and chondrocyte genes (tiss
68 rix GLA protein, the phosphate cotransporter Pit-1, a calcium-sensing receptor related factor, osteop
74 nal Ets binding sites (EBS): a composite EBS/Pit-1 element located at -212 and an EBS that co-localiz
75 xtracts of TtT-97 thyrotropes, which express Pit-1, footprinted this proximal region with a pattern o
78 eas the pituitary-specific POU domain factor Pit-1 activates growth hormone gene expression in one ce
79 ted by the tissue-specific POU domain factor Pit-1, which is initially expressed on Embryonic Day 13.
81 teins, such as the pituitary-specific factor Pit-1, are members of the homeodomain family of proteins
85 the pituitary-specific transcription factor Pit-1 to the hGH-N promoter and a selective decrease in
87 he co-expression of the transcription factor Pit-1, which removes C/EBPalpha from the heterochromatic
95 P interacts with Pit-1 and is a cofactor for Pit-1-dependent activation of the human GH promoter.
96 e functions of CBP or p/CAF are required for Pit-1 function that is stimulated by cyclic AMP or growt
97 phobic beta-domain residues are required for Pit-1 isoform-specific repression of Ras signaling, and
98 hese findings are consistent with a role for Pit-1 as an initiating factor in hGH locus activation du
100 from -53 to -19, whose pattern differed from Pit-1 in thyrotrope extracts, showed protection patterns
102 ce between the promoter-proximal and the HSI Pit-1 binding sites can be attributed in part to a singl
104 ecular basis of disease-causing mutations in Pit-1 and provide potential basis for the flexible allos
106 o show that two different point mutations in Pit-1, which disrupted distinct activities, affected the
107 vesicles, inhibition of phosphate uptake in Pit-1 knockdown cells blocked the induction of the osteo
110 heir effects on the much weaker, independent Pit-1 and TR activations of the rat growth hormone promo
111 ary cells that do not normally express Lhx3 (Pit-1/0 cells) were treated with 5-aza-2'-deoxycytidine,
116 only a co-repressor complex, the activity of Pit-1 is determined by a regulated balance between a co-
119 POU-S domain is critical for the assembly of Pit-1 with C/EBPalpha, and they showed that DNA-binding
121 lusters containing different combinations of Pit-1-dependent cell types suggests that the Pit-1+ prec
124 Pit-1 and ETS-1 and blocks the induction of Pit-1-dependent prolactin promoter activity by cAMP.
125 t the functional and physical interaction of Pit-1 and Ets-1 is mediated via the POU homeodomain, whi
129 us, the unique transcriptional properties of Pit-1 and Pit-1beta on the rPRL promoter may be due to t
134 the divergent bases between the two sets of Pit-1 elements results in a partial reversal of their tr
139 activity was attributed primarily to POU1F1 (Pit-1) elements at HSI, as linkage to HSI was sufficient
140 ribe the endogenous TRbeta2 locus or produce Pit-1 protein, could be reconstituted to a level approac
141 inhibiting Lef-1 expression and may promote Pit-1 lineage differentiation during pituitary developme
142 en the pituitary-specific POU domain protein Pit-1 and members of the ETS transcription factor family
144 actions of the pituitary-specific HD protein Pit-1 control the development of anterior pituitary cell
147 on of Pitx2 and another homeodomain protein, Pit-1, yielded a synergistic 55-fold activation of the p
151 s that abrogated binding of both recombinant Pit-1 and Pit-1-containing nuclear extracts revealed tha
153 ained sites that interacted with recombinant Pit-1; however, extracts of TtT-97 thyrotropes, which ex
154 ivation domains of both Pit-1 and TR reduced Pit-1/TR synergy in parallel with their effects on the m
155 itary development and that miR-26b regulates Pit-1 expression by inhibiting Lef-1 expression and may
157 hat the Oct-1 POU domain but not the related Pit-1 POU domain can facilitate the binding of SNAPc to
158 ctivation by Pit-1 was dependent on the same Pit-1 sites shown to be important for basal TRbeta2 prom
160 ired for maintenance of expression) and that Pit-1-dependent activation of the distal enhancer can be
168 ealed that removal of regions containing the Pit-1 sites at -456 to -432, -149 to -127, and -124 to -
171 nting identified protected G residues in the Pit-1, Sp1, and Zn-15 binding sites of the GH gene in GC
174 findings suggest that the structures of the Pit-1 binding sites at HSI specify distinct chromatin-de
175 ss or synergy because block mutations of the Pit-1 interaction surface in Ets-1, which reduced Ets-1/
176 rent failure of initial determination of the Pit-1 lineage required for production of growth hormone,
178 port a high resolution X-ray analysis of the Pit-1 POU domain bound to a DNA element as a homodimer.
180 This base affects the conformation of the Pit-1/DNA complex, and reciprocal exchange of the diverg
182 genetic background, we demonstrate that the Pit-1 gene utilizes distinct enhancers for initial gene
183 e two transcriptional responses and that the Pit-1 R2 subregion represents a novel, tissue-specific R
184 Pit-1-dependent cell types suggests that the Pit-1+ precursor cells choose from multiple developmenta
187 cal interaction of these two factors via the Pit-1 homeodomain (amino acids 199-291) and the Ets-1 re
188 These data support a model in which the Pit-1 binding sites in the hGH LCR allosterically progra
192 present report we demonstrate that all three Pit-1 sites in the HSI array contribute to LCR activity
194 sults indicate that phosphate uptake through Pit-1 is essential for SMC calcification and phenotypic
196 o determine which type of Na/Pi transporter (Pit-1 or Pit-2) is regulated by PKC and which PKC isotyp
200 ining nuclear extracts revealed that the two Pit-1 sites between -149 and -102 were important for TRb
202 NA methylation levels, treated and untreated Pit-1/0 genomic DNAs were subjected to bisulfite convers
204 hypothesis directly and to determine whether Pit-1 expression is sufficient to confer hGH locus histo
205 n the HS-I region suggested a model in which Pit-1 binding at HS-I initiates the chromatin modificati
209 promoter (-133 to -88) region interacts with Pit-1 and an additional 50-kDa factor at an adjacent sit
216 ity that appears to function in synergy with Pit-1, activators of A and C protein kinases and possibl
217 alian growth hormone promoter in tandem with Pit-1, was determined in order to elucidate the exon-int
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