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PMID |
Sentence |
1 |
9305891
|
Pit-1 and GATA-2 interact and functionally cooperate to activate the thyrotropin beta-subunit promoter.
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2 |
9305891
|
The P1 region of the mouse TSHbeta promoter (-133 to -88) region interacts with Pit-1 and an additional 50-kDa factor at an adjacent site that resembles a consensus GATA binding site.
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3 |
9305891
|
When both Pit-1 and GATA-2 were combined, a slower migrating complex, indicative of a ternary protein-DNA interaction was observed.
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4 |
9305891
|
Cotransfection of both Pit-1 and GATA-2 into CV-1 cells synergistically stimulated mouse TSHbeta promoter activity 8.5-fold, while each factor alone had a minimal effect.
|
5 |
9305891
|
Finally, we show that GATA-2 directly interacts with Pit-1 in solution.
|
6 |
9305891
|
Pit-1 and GATA-2 interact and functionally cooperate to activate the thyrotropin beta-subunit promoter.
|
7 |
9305891
|
The P1 region of the mouse TSHbeta promoter (-133 to -88) region interacts with Pit-1 and an additional 50-kDa factor at an adjacent site that resembles a consensus GATA binding site.
|
8 |
9305891
|
When both Pit-1 and GATA-2 were combined, a slower migrating complex, indicative of a ternary protein-DNA interaction was observed.
|
9 |
9305891
|
Cotransfection of both Pit-1 and GATA-2 into CV-1 cells synergistically stimulated mouse TSHbeta promoter activity 8.5-fold, while each factor alone had a minimal effect.
|
10 |
9305891
|
Finally, we show that GATA-2 directly interacts with Pit-1 in solution.
|
11 |
9305891
|
Pit-1 and GATA-2 interact and functionally cooperate to activate the thyrotropin beta-subunit promoter.
|
12 |
9305891
|
The P1 region of the mouse TSHbeta promoter (-133 to -88) region interacts with Pit-1 and an additional 50-kDa factor at an adjacent site that resembles a consensus GATA binding site.
|
13 |
9305891
|
When both Pit-1 and GATA-2 were combined, a slower migrating complex, indicative of a ternary protein-DNA interaction was observed.
|
14 |
9305891
|
Cotransfection of both Pit-1 and GATA-2 into CV-1 cells synergistically stimulated mouse TSHbeta promoter activity 8.5-fold, while each factor alone had a minimal effect.
|
15 |
9305891
|
Finally, we show that GATA-2 directly interacts with Pit-1 in solution.
|
16 |
9305891
|
Pit-1 and GATA-2 interact and functionally cooperate to activate the thyrotropin beta-subunit promoter.
|
17 |
9305891
|
The P1 region of the mouse TSHbeta promoter (-133 to -88) region interacts with Pit-1 and an additional 50-kDa factor at an adjacent site that resembles a consensus GATA binding site.
|
18 |
9305891
|
When both Pit-1 and GATA-2 were combined, a slower migrating complex, indicative of a ternary protein-DNA interaction was observed.
|
19 |
9305891
|
Cotransfection of both Pit-1 and GATA-2 into CV-1 cells synergistically stimulated mouse TSHbeta promoter activity 8.5-fold, while each factor alone had a minimal effect.
|
20 |
9305891
|
Finally, we show that GATA-2 directly interacts with Pit-1 in solution.
|
21 |
11167015
|
Levels of GATA-1/GATA-2 transcription factors modulate expression of embryonic and fetal hemoglobins.
|
22 |
11167015
|
GATA-1 and GATA-2, coexpressed in erythroid cells, are important for expression of erythroid genes.
|
23 |
11167015
|
Conserved GATA sites were found in each of the hypersensitive sites in both beta-and alpha clusters and in proximal regulatory regions of the zeta-, epsilon- and gamma-globin but not the alpha, delta or beta-globin genes.
|
24 |
11167015
|
We then tested the effect of increasing levels of GATA-1 and GATA-2 on the expression of endogenous globin genes in human erythroid cells.
|
25 |
11167015
|
Increasing GATA-1 levels in K562 cells decreased the levels of epsilon-globin mRNA but had no effect on the levels of expression of gamma, zeta or alpha-globin genes.
|
26 |
11167015
|
Increasing GATA-2 levels increased epsilon-globin and gamma-globin transcripts.
|
27 |
11167015
|
Increasing levels of GATA-1 also caused a decrease in the expression of endogenous GATA-2, while increased levels of GATA-2 had no effect on GATA-1 mRNA.
|
28 |
11167015
|
Our results indicate a differential role of GATA-1 and -2 transcription factors on globin transcripts and suggest a correlation between the conservation of GATA sites in the regulatory regions and the ability of endogenous globin genes to respond to GATA transcription factors.
|
29 |
11167015
|
They also suggest that quantitative changes in the levels of GATA-1 or GATA-2 can result in alterations of globin target gene expression and may participate in the ontogenic control of the globin genes.
|
30 |
11167015
|
Levels of GATA-1/GATA-2 transcription factors modulate expression of embryonic and fetal hemoglobins.
|
31 |
11167015
|
GATA-1 and GATA-2, coexpressed in erythroid cells, are important for expression of erythroid genes.
|
32 |
11167015
|
Conserved GATA sites were found in each of the hypersensitive sites in both beta-and alpha clusters and in proximal regulatory regions of the zeta-, epsilon- and gamma-globin but not the alpha, delta or beta-globin genes.
|
33 |
11167015
|
We then tested the effect of increasing levels of GATA-1 and GATA-2 on the expression of endogenous globin genes in human erythroid cells.
|
34 |
11167015
|
Increasing GATA-1 levels in K562 cells decreased the levels of epsilon-globin mRNA but had no effect on the levels of expression of gamma, zeta or alpha-globin genes.
|
35 |
11167015
|
Increasing GATA-2 levels increased epsilon-globin and gamma-globin transcripts.
|
36 |
11167015
|
Increasing levels of GATA-1 also caused a decrease in the expression of endogenous GATA-2, while increased levels of GATA-2 had no effect on GATA-1 mRNA.
|
37 |
11167015
|
Our results indicate a differential role of GATA-1 and -2 transcription factors on globin transcripts and suggest a correlation between the conservation of GATA sites in the regulatory regions and the ability of endogenous globin genes to respond to GATA transcription factors.
|
38 |
11167015
|
They also suggest that quantitative changes in the levels of GATA-1 or GATA-2 can result in alterations of globin target gene expression and may participate in the ontogenic control of the globin genes.
|
39 |
11167015
|
Levels of GATA-1/GATA-2 transcription factors modulate expression of embryonic and fetal hemoglobins.
|
40 |
11167015
|
GATA-1 and GATA-2, coexpressed in erythroid cells, are important for expression of erythroid genes.
|
41 |
11167015
|
Conserved GATA sites were found in each of the hypersensitive sites in both beta-and alpha clusters and in proximal regulatory regions of the zeta-, epsilon- and gamma-globin but not the alpha, delta or beta-globin genes.
|
42 |
11167015
|
We then tested the effect of increasing levels of GATA-1 and GATA-2 on the expression of endogenous globin genes in human erythroid cells.
|
43 |
11167015
|
Increasing GATA-1 levels in K562 cells decreased the levels of epsilon-globin mRNA but had no effect on the levels of expression of gamma, zeta or alpha-globin genes.
|
44 |
11167015
|
Increasing GATA-2 levels increased epsilon-globin and gamma-globin transcripts.
|
45 |
11167015
|
Increasing levels of GATA-1 also caused a decrease in the expression of endogenous GATA-2, while increased levels of GATA-2 had no effect on GATA-1 mRNA.
|
46 |
11167015
|
Our results indicate a differential role of GATA-1 and -2 transcription factors on globin transcripts and suggest a correlation between the conservation of GATA sites in the regulatory regions and the ability of endogenous globin genes to respond to GATA transcription factors.
|
47 |
11167015
|
They also suggest that quantitative changes in the levels of GATA-1 or GATA-2 can result in alterations of globin target gene expression and may participate in the ontogenic control of the globin genes.
|
48 |
11167015
|
Levels of GATA-1/GATA-2 transcription factors modulate expression of embryonic and fetal hemoglobins.
|
49 |
11167015
|
GATA-1 and GATA-2, coexpressed in erythroid cells, are important for expression of erythroid genes.
|
50 |
11167015
|
Conserved GATA sites were found in each of the hypersensitive sites in both beta-and alpha clusters and in proximal regulatory regions of the zeta-, epsilon- and gamma-globin but not the alpha, delta or beta-globin genes.
|
51 |
11167015
|
We then tested the effect of increasing levels of GATA-1 and GATA-2 on the expression of endogenous globin genes in human erythroid cells.
|
52 |
11167015
|
Increasing GATA-1 levels in K562 cells decreased the levels of epsilon-globin mRNA but had no effect on the levels of expression of gamma, zeta or alpha-globin genes.
|
53 |
11167015
|
Increasing GATA-2 levels increased epsilon-globin and gamma-globin transcripts.
|
54 |
11167015
|
Increasing levels of GATA-1 also caused a decrease in the expression of endogenous GATA-2, while increased levels of GATA-2 had no effect on GATA-1 mRNA.
|
55 |
11167015
|
Our results indicate a differential role of GATA-1 and -2 transcription factors on globin transcripts and suggest a correlation between the conservation of GATA sites in the regulatory regions and the ability of endogenous globin genes to respond to GATA transcription factors.
|
56 |
11167015
|
They also suggest that quantitative changes in the levels of GATA-1 or GATA-2 can result in alterations of globin target gene expression and may participate in the ontogenic control of the globin genes.
|
57 |
11167015
|
Levels of GATA-1/GATA-2 transcription factors modulate expression of embryonic and fetal hemoglobins.
|
58 |
11167015
|
GATA-1 and GATA-2, coexpressed in erythroid cells, are important for expression of erythroid genes.
|
59 |
11167015
|
Conserved GATA sites were found in each of the hypersensitive sites in both beta-and alpha clusters and in proximal regulatory regions of the zeta-, epsilon- and gamma-globin but not the alpha, delta or beta-globin genes.
|
60 |
11167015
|
We then tested the effect of increasing levels of GATA-1 and GATA-2 on the expression of endogenous globin genes in human erythroid cells.
|
61 |
11167015
|
Increasing GATA-1 levels in K562 cells decreased the levels of epsilon-globin mRNA but had no effect on the levels of expression of gamma, zeta or alpha-globin genes.
|
62 |
11167015
|
Increasing GATA-2 levels increased epsilon-globin and gamma-globin transcripts.
|
63 |
11167015
|
Increasing levels of GATA-1 also caused a decrease in the expression of endogenous GATA-2, while increased levels of GATA-2 had no effect on GATA-1 mRNA.
|
64 |
11167015
|
Our results indicate a differential role of GATA-1 and -2 transcription factors on globin transcripts and suggest a correlation between the conservation of GATA sites in the regulatory regions and the ability of endogenous globin genes to respond to GATA transcription factors.
|
65 |
11167015
|
They also suggest that quantitative changes in the levels of GATA-1 or GATA-2 can result in alterations of globin target gene expression and may participate in the ontogenic control of the globin genes.
|
66 |
11167015
|
Levels of GATA-1/GATA-2 transcription factors modulate expression of embryonic and fetal hemoglobins.
|
67 |
11167015
|
GATA-1 and GATA-2, coexpressed in erythroid cells, are important for expression of erythroid genes.
|
68 |
11167015
|
Conserved GATA sites were found in each of the hypersensitive sites in both beta-and alpha clusters and in proximal regulatory regions of the zeta-, epsilon- and gamma-globin but not the alpha, delta or beta-globin genes.
|
69 |
11167015
|
We then tested the effect of increasing levels of GATA-1 and GATA-2 on the expression of endogenous globin genes in human erythroid cells.
|
70 |
11167015
|
Increasing GATA-1 levels in K562 cells decreased the levels of epsilon-globin mRNA but had no effect on the levels of expression of gamma, zeta or alpha-globin genes.
|
71 |
11167015
|
Increasing GATA-2 levels increased epsilon-globin and gamma-globin transcripts.
|
72 |
11167015
|
Increasing levels of GATA-1 also caused a decrease in the expression of endogenous GATA-2, while increased levels of GATA-2 had no effect on GATA-1 mRNA.
|
73 |
11167015
|
Our results indicate a differential role of GATA-1 and -2 transcription factors on globin transcripts and suggest a correlation between the conservation of GATA sites in the regulatory regions and the ability of endogenous globin genes to respond to GATA transcription factors.
|
74 |
11167015
|
They also suggest that quantitative changes in the levels of GATA-1 or GATA-2 can result in alterations of globin target gene expression and may participate in the ontogenic control of the globin genes.
|
75 |
11167015
|
Levels of GATA-1/GATA-2 transcription factors modulate expression of embryonic and fetal hemoglobins.
|
76 |
11167015
|
GATA-1 and GATA-2, coexpressed in erythroid cells, are important for expression of erythroid genes.
|
77 |
11167015
|
Conserved GATA sites were found in each of the hypersensitive sites in both beta-and alpha clusters and in proximal regulatory regions of the zeta-, epsilon- and gamma-globin but not the alpha, delta or beta-globin genes.
|
78 |
11167015
|
We then tested the effect of increasing levels of GATA-1 and GATA-2 on the expression of endogenous globin genes in human erythroid cells.
|
79 |
11167015
|
Increasing GATA-1 levels in K562 cells decreased the levels of epsilon-globin mRNA but had no effect on the levels of expression of gamma, zeta or alpha-globin genes.
|
80 |
11167015
|
Increasing GATA-2 levels increased epsilon-globin and gamma-globin transcripts.
|
81 |
11167015
|
Increasing levels of GATA-1 also caused a decrease in the expression of endogenous GATA-2, while increased levels of GATA-2 had no effect on GATA-1 mRNA.
|
82 |
11167015
|
Our results indicate a differential role of GATA-1 and -2 transcription factors on globin transcripts and suggest a correlation between the conservation of GATA sites in the regulatory regions and the ability of endogenous globin genes to respond to GATA transcription factors.
|
83 |
11167015
|
They also suggest that quantitative changes in the levels of GATA-1 or GATA-2 can result in alterations of globin target gene expression and may participate in the ontogenic control of the globin genes.
|
84 |
12472594
|
GATA-1 mRNA was downregulated at a high dose and GATA-2 was dose dependently upregulated over a lower dosage range.
|
85 |
15453831
|
All three models had reduced levels of GATA-2 positive EPCs in the wound bed that was corrected by the adenoviral mediated gene transfer of PDGF.
|
86 |
19120268
|
Lowered expressions of the NF-kappaB family members in dendritic cells from NOD mice are associated with a reduced expression of GATA-2.
|
87 |
19120268
|
In the present study, we compared transcription profiles of CD11c(+) bone marrow (BM)-derived DCs from NOD mice with those from NON mice, focusing on the NF-kappaB/Rel family members and associated molecules.
|
88 |
19120268
|
The BMDCs from NOD mice displayed reduced mRNA expressions of NF-kappaB components, p65, p50, p52, and RelB, compared to NON mice: the proportions of each molecule relative to those of NON DCs were 53.9, 54.1, 54.0, and 37.0%, respectively, which were accompanied with lowered expressions of downstream immunomodulatory molecules, including IL-6, CD80, CD86, 4-1BB, and CD40.
|
89 |
19136559
|
Re-expression of GATA2 cooperates with peroxisome proliferator-activated receptor-gamma depletion to revert the adipocyte phenotype.
|
90 |
19136559
|
Nuclear peroxisome proliferator-activated receptor-gamma (PPARgamma) is required for adipocyte differentiation, but its role in mature adipocytes is less clear.
|
91 |
19136559
|
Here, we report that knockdown of PPARgamma expression in 3T3-L1 adipocytes returned the expression of most adipocyte genes to preadipocyte levels.
|
92 |
19136559
|
Surprisingly, not all adipocyte genes were reversed, and the adipocyte morphology was maintained for an extended period after PPARgamma depletion.
|
93 |
19136559
|
We identified GATA2, a transcription factor whose down-regulation early in adipogenesis is required for preadipocyte differentiation and whose levels remain low after PPARgamma knockdown.
|
94 |
19136559
|
Forced expression of GATA2 in mature adipocytes complemented PPARgamma depletion and impaired adipocyte functionality with a more preadipocyte-like gene expression profile.
|
95 |
19136559
|
These results suggest that PPARgamma-independent down-regulation of GATA2 prevents reversion of mature adipocytes after PPARgamma depletion.
|
96 |
19136559
|
Re-expression of GATA2 cooperates with peroxisome proliferator-activated receptor-gamma depletion to revert the adipocyte phenotype.
|
97 |
19136559
|
Nuclear peroxisome proliferator-activated receptor-gamma (PPARgamma) is required for adipocyte differentiation, but its role in mature adipocytes is less clear.
|
98 |
19136559
|
Here, we report that knockdown of PPARgamma expression in 3T3-L1 adipocytes returned the expression of most adipocyte genes to preadipocyte levels.
|
99 |
19136559
|
Surprisingly, not all adipocyte genes were reversed, and the adipocyte morphology was maintained for an extended period after PPARgamma depletion.
|
100 |
19136559
|
We identified GATA2, a transcription factor whose down-regulation early in adipogenesis is required for preadipocyte differentiation and whose levels remain low after PPARgamma knockdown.
|
101 |
19136559
|
Forced expression of GATA2 in mature adipocytes complemented PPARgamma depletion and impaired adipocyte functionality with a more preadipocyte-like gene expression profile.
|
102 |
19136559
|
These results suggest that PPARgamma-independent down-regulation of GATA2 prevents reversion of mature adipocytes after PPARgamma depletion.
|
103 |
19136559
|
Re-expression of GATA2 cooperates with peroxisome proliferator-activated receptor-gamma depletion to revert the adipocyte phenotype.
|
104 |
19136559
|
Nuclear peroxisome proliferator-activated receptor-gamma (PPARgamma) is required for adipocyte differentiation, but its role in mature adipocytes is less clear.
|
105 |
19136559
|
Here, we report that knockdown of PPARgamma expression in 3T3-L1 adipocytes returned the expression of most adipocyte genes to preadipocyte levels.
|
106 |
19136559
|
Surprisingly, not all adipocyte genes were reversed, and the adipocyte morphology was maintained for an extended period after PPARgamma depletion.
|
107 |
19136559
|
We identified GATA2, a transcription factor whose down-regulation early in adipogenesis is required for preadipocyte differentiation and whose levels remain low after PPARgamma knockdown.
|
108 |
19136559
|
Forced expression of GATA2 in mature adipocytes complemented PPARgamma depletion and impaired adipocyte functionality with a more preadipocyte-like gene expression profile.
|
109 |
19136559
|
These results suggest that PPARgamma-independent down-regulation of GATA2 prevents reversion of mature adipocytes after PPARgamma depletion.
|
110 |
19136559
|
Re-expression of GATA2 cooperates with peroxisome proliferator-activated receptor-gamma depletion to revert the adipocyte phenotype.
|
111 |
19136559
|
Nuclear peroxisome proliferator-activated receptor-gamma (PPARgamma) is required for adipocyte differentiation, but its role in mature adipocytes is less clear.
|
112 |
19136559
|
Here, we report that knockdown of PPARgamma expression in 3T3-L1 adipocytes returned the expression of most adipocyte genes to preadipocyte levels.
|
113 |
19136559
|
Surprisingly, not all adipocyte genes were reversed, and the adipocyte morphology was maintained for an extended period after PPARgamma depletion.
|
114 |
19136559
|
We identified GATA2, a transcription factor whose down-regulation early in adipogenesis is required for preadipocyte differentiation and whose levels remain low after PPARgamma knockdown.
|
115 |
19136559
|
Forced expression of GATA2 in mature adipocytes complemented PPARgamma depletion and impaired adipocyte functionality with a more preadipocyte-like gene expression profile.
|
116 |
19136559
|
These results suggest that PPARgamma-independent down-regulation of GATA2 prevents reversion of mature adipocytes after PPARgamma depletion.
|
117 |
20179324
|
Activation of canonical wingless-type MMTV integration site family (Wnt) signaling in mature adipocytes increases beta-catenin levels and leads to cell dedifferentiation and insulin resistance.
|
118 |
20179324
|
Typical adipogenic markers were reduced while undifferentiated cell markers like Pref-1/Dlk1, Wnt10b, and Gata2 were increased.
|
119 |
20179324
|
Wnt3a stabilized beta-catenin in the absence of the LRP6 receptor and with maintained axin and Dickkopf-1 protein expression.
|
120 |
20179324
|
PPARgamma was repressed and PPARgamma ligands could not restore the adipogenic markers or reduce the beta-catenin levels.
|
121 |
20179324
|
These results identify a novel pathway in mature adipose cells that is critical for maintaining the normal adipocyte phenotype and insulin sensitivity.
|
122 |
22499991
|
Downregulation of endothelial microRNA-200b supports cutaneous wound angiogenesis by desilencing GATA binding protein 2 and vascular endothelial growth factor receptor 2.
|
123 |
22705548
|
However, roles of Smad6 in hematopoiesis remained unknown in contrast to the other inhibitory Smad (I-Smad), Smad7.
|
124 |
22705548
|
Here we show that Smad6 inhibits erythropoiesis in human CD34(+) cord blood hematopoietic stem cells (HSCs).
|
125 |
22705548
|
Smad6 was specifically expressed in CD34(+) cord blood HSCs, which was correlated with the expression of BMP2/4/6/7 and BMP type I receptor (BMPRI).
|
126 |
22705548
|
BMP-specific receptor-regulated Smads (R-Smads), Smad1 and Smad5 in cooperation with Smad4 induced transcription of the Smad6 gene.
|
127 |
22705548
|
Instead of affecting cell cycle, apoptosis, self-renewal, and stemness of CD34(+) cells, Smad6 knockdown enhanced, whereas Smad6 overexpression suppressed erythropoiesis in stem cell culture and colony formation assay.
|
128 |
22705548
|
Consistently, Smad6 suppressed the expression of the genes essential for erythropoiesis, such as Kruppel-like factor 1 (erythroid) (KLF1/EKLF) and GATA binding protein 2 (GATA-2).
|
129 |
22705548
|
Promoter analyses showed that Smad6 repressed Smad5/4-induced transcription of the Klf1 gene.
|