sp3 sirna Search Results


91
Santa Cruz Biotechnology sp3
Figure 7. Transcriptional regulation of CPTP expression by <t>Sp1/Sp3.</t> (A) 5’ deletion analysis of the CPTP promoter in the PANC-1 cell line. A series of CPTP promoter deletion mutants were generated utilizing firefly luciferase plasmid. Each construct was co-transfected with pRL-TK plasmid as the internal control. Numbering is relative to the major transcriptional start site. (B) EMSA for the -282/-273 binding site. The assays were performed with nuclear extracts from the PANC-1 or Miacapa-2 cell lines. Competitive assays were executed with a 200-fold molar excess of unlabeled double-strand probes. Supershift assay was carried out with adding Sp1 or Sp3 antibody. The arrows show specific transcription factor binding. # indicates supershifted bands. #? indicates the position of expected supershifted Sp1 complex. (C) EMSA for the -258/-249 binding site. (D) Sp1/Sp3 interacts with the CPTP promoter in vivo was identified by ChIP assay, mouse IgG and the CPTP region (+67/+251) which does not contain binding sites of Sp1/Sp3 acted as negative control. Input, sheared DNA preceding immunoprecipitation posed as positive control. (E) RT-qPCR analysis for CPTP mRNA expression levels in the PANC-1 cells treated with mithramycin A for 24 h. (F) Knockdown of Sp1 or Sp3 decreased CPTP promoter activity. Cells transfected with pGL3(-454/-1), then transfected with Sp1 or Sp3 siRNA, and cultured for 24 h before dual-luciferase activity assay and Western blot analysis. *P < 0.05, **P < 0.01.
Sp3, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
Qiagen sirna sp3 si0004788
nSMase2 upregulation is independent of known transcriptional regulators of nSMase2. ( a ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AllStars Negative Control (AS), Sp1, <t>Sp3</t> or both together. After 24 h, cells were treated with vehicle, and 0.2 or 0.6 μ M doxorubicin. After 24 h, cells were collected and immunoblotted for nSMase2, Sp1, Sp3 and actin. ( b ) MCF7 cells were seeded in 60 mm dishes. One hour before stimulation with doxorubicin or vehicle, they were pretreated with N -acetylcysteine (NAC). Cells were collected and immunoblotted for nSMase2 and actin. ( c ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AS or CREB3L1. After 24 h, they were treated with vehicle or 0.6 μ M doxorubicin. Cells were collected and immunoblotted for nSMase2 and actin
Sirna Sp3 Si0004788, supplied by Qiagen, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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90
Panomics Inc sp1 and sp3 sirna constructs
nSMase2 upregulation is independent of known transcriptional regulators of nSMase2. ( a ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AllStars Negative Control (AS), Sp1, <t>Sp3</t> or both together. After 24 h, cells were treated with vehicle, and 0.2 or 0.6 μ M doxorubicin. After 24 h, cells were collected and immunoblotted for nSMase2, Sp1, Sp3 and actin. ( b ) MCF7 cells were seeded in 60 mm dishes. One hour before stimulation with doxorubicin or vehicle, they were pretreated with N -acetylcysteine (NAC). Cells were collected and immunoblotted for nSMase2 and actin. ( c ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AS or CREB3L1. After 24 h, they were treated with vehicle or 0.6 μ M doxorubicin. Cells were collected and immunoblotted for nSMase2 and actin
Sp1 And Sp3 Sirna Constructs, supplied by Panomics Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
B-Bridge Inc sirna sirna cocktails targeting human sp1, human sp3, or human sp7
nSMase2 upregulation is independent of known transcriptional regulators of nSMase2. ( a ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AllStars Negative Control (AS), Sp1, <t>Sp3</t> or both together. After 24 h, cells were treated with vehicle, and 0.2 or 0.6 μ M doxorubicin. After 24 h, cells were collected and immunoblotted for nSMase2, Sp1, Sp3 and actin. ( b ) MCF7 cells were seeded in 60 mm dishes. One hour before stimulation with doxorubicin or vehicle, they were pretreated with N -acetylcysteine (NAC). Cells were collected and immunoblotted for nSMase2 and actin. ( c ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AS or CREB3L1. After 24 h, they were treated with vehicle or 0.6 μ M doxorubicin. Cells were collected and immunoblotted for nSMase2 and actin
Sirna Sirna Cocktails Targeting Human Sp1, Human Sp3, Or Human Sp7, supplied by B-Bridge Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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90
Qiagen sirna sets against sp1 and sp3
nSMase2 upregulation is independent of known transcriptional regulators of nSMase2. ( a ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AllStars Negative Control (AS), Sp1, <t>Sp3</t> or both together. After 24 h, cells were treated with vehicle, and 0.2 or 0.6 μ M doxorubicin. After 24 h, cells were collected and immunoblotted for nSMase2, Sp1, Sp3 and actin. ( b ) MCF7 cells were seeded in 60 mm dishes. One hour before stimulation with doxorubicin or vehicle, they were pretreated with N -acetylcysteine (NAC). Cells were collected and immunoblotted for nSMase2 and actin. ( c ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AS or CREB3L1. After 24 h, they were treated with vehicle or 0.6 μ M doxorubicin. Cells were collected and immunoblotted for nSMase2 and actin
Sirna Sets Against Sp1 And Sp3, supplied by Qiagen, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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90
Vigene Biosciences sirnas targeting human sp3 mrnas
nSMase2 upregulation is independent of known transcriptional regulators of nSMase2. ( a ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AllStars Negative Control (AS), Sp1, <t>Sp3</t> or both together. After 24 h, cells were treated with vehicle, and 0.2 or 0.6 μ M doxorubicin. After 24 h, cells were collected and immunoblotted for nSMase2, Sp1, Sp3 and actin. ( b ) MCF7 cells were seeded in 60 mm dishes. One hour before stimulation with doxorubicin or vehicle, they were pretreated with N -acetylcysteine (NAC). Cells were collected and immunoblotted for nSMase2 and actin. ( c ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AS or CREB3L1. After 24 h, they were treated with vehicle or 0.6 μ M doxorubicin. Cells were collected and immunoblotted for nSMase2 and actin
Sirnas Targeting Human Sp3 Mrnas, supplied by Vigene Biosciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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Image Search Results


Figure 7. Transcriptional regulation of CPTP expression by Sp1/Sp3. (A) 5’ deletion analysis of the CPTP promoter in the PANC-1 cell line. A series of CPTP promoter deletion mutants were generated utilizing firefly luciferase plasmid. Each construct was co-transfected with pRL-TK plasmid as the internal control. Numbering is relative to the major transcriptional start site. (B) EMSA for the -282/-273 binding site. The assays were performed with nuclear extracts from the PANC-1 or Miacapa-2 cell lines. Competitive assays were executed with a 200-fold molar excess of unlabeled double-strand probes. Supershift assay was carried out with adding Sp1 or Sp3 antibody. The arrows show specific transcription factor binding. # indicates supershifted bands. #? indicates the position of expected supershifted Sp1 complex. (C) EMSA for the -258/-249 binding site. (D) Sp1/Sp3 interacts with the CPTP promoter in vivo was identified by ChIP assay, mouse IgG and the CPTP region (+67/+251) which does not contain binding sites of Sp1/Sp3 acted as negative control. Input, sheared DNA preceding immunoprecipitation posed as positive control. (E) RT-qPCR analysis for CPTP mRNA expression levels in the PANC-1 cells treated with mithramycin A for 24 h. (F) Knockdown of Sp1 or Sp3 decreased CPTP promoter activity. Cells transfected with pGL3(-454/-1), then transfected with Sp1 or Sp3 siRNA, and cultured for 24 h before dual-luciferase activity assay and Western blot analysis. *P < 0.05, **P < 0.01.

Journal: International journal of biological sciences

Article Title: Human CPTP promotes growth and metastasis via sphingolipid metabolite ceramide and PI4KA/AKT signaling in pancreatic cancer cells.

doi: 10.7150/ijbs.70007

Figure Lengend Snippet: Figure 7. Transcriptional regulation of CPTP expression by Sp1/Sp3. (A) 5’ deletion analysis of the CPTP promoter in the PANC-1 cell line. A series of CPTP promoter deletion mutants were generated utilizing firefly luciferase plasmid. Each construct was co-transfected with pRL-TK plasmid as the internal control. Numbering is relative to the major transcriptional start site. (B) EMSA for the -282/-273 binding site. The assays were performed with nuclear extracts from the PANC-1 or Miacapa-2 cell lines. Competitive assays were executed with a 200-fold molar excess of unlabeled double-strand probes. Supershift assay was carried out with adding Sp1 or Sp3 antibody. The arrows show specific transcription factor binding. # indicates supershifted bands. #? indicates the position of expected supershifted Sp1 complex. (C) EMSA for the -258/-249 binding site. (D) Sp1/Sp3 interacts with the CPTP promoter in vivo was identified by ChIP assay, mouse IgG and the CPTP region (+67/+251) which does not contain binding sites of Sp1/Sp3 acted as negative control. Input, sheared DNA preceding immunoprecipitation posed as positive control. (E) RT-qPCR analysis for CPTP mRNA expression levels in the PANC-1 cells treated with mithramycin A for 24 h. (F) Knockdown of Sp1 or Sp3 decreased CPTP promoter activity. Cells transfected with pGL3(-454/-1), then transfected with Sp1 or Sp3 siRNA, and cultured for 24 h before dual-luciferase activity assay and Western blot analysis. *P < 0.05, **P < 0.01.

Article Snippet: Small interfering RNA targeted to Sp1 or Sp3 (Santa Cruz Biotechnology, Inc.) was used to knockdown the expression levels of Sp1 and Sp3, respectively.

Techniques: Expressing, Generated, Luciferase, Plasmid Preparation, Construct, Transfection, Control, Binding Assay, In Vivo, Negative Control, Immunoprecipitation, Positive Control, Quantitative RT-PCR, Knockdown, Activity Assay, Cell Culture, Western Blot

Figure 8. Sp3 attenuates the decrease in cell proliferation, migration and invasion induced by CPTP knockdown. (A) Decreased cell viability in CPTP knockdown PC cells was restored by Sp3 overexpression. The cell viability was measured using a CCK-8 assay. (B-C) Sp3 overexpression rescued the decrease in cell motility in CPTP knockdown PC cells. (D) Sp3 overexpression rescued upregulation of epithelial-related markers and downregulation of mesenchymal-related markers expression induced by CPTP knockdown as detected by Western blot analysis. *P < 0.05, **P < 0.01, ***P < 0.001. ns, not significant.

Journal: International journal of biological sciences

Article Title: Human CPTP promotes growth and metastasis via sphingolipid metabolite ceramide and PI4KA/AKT signaling in pancreatic cancer cells.

doi: 10.7150/ijbs.70007

Figure Lengend Snippet: Figure 8. Sp3 attenuates the decrease in cell proliferation, migration and invasion induced by CPTP knockdown. (A) Decreased cell viability in CPTP knockdown PC cells was restored by Sp3 overexpression. The cell viability was measured using a CCK-8 assay. (B-C) Sp3 overexpression rescued the decrease in cell motility in CPTP knockdown PC cells. (D) Sp3 overexpression rescued upregulation of epithelial-related markers and downregulation of mesenchymal-related markers expression induced by CPTP knockdown as detected by Western blot analysis. *P < 0.05, **P < 0.01, ***P < 0.001. ns, not significant.

Article Snippet: Small interfering RNA targeted to Sp1 or Sp3 (Santa Cruz Biotechnology, Inc.) was used to knockdown the expression levels of Sp1 and Sp3, respectively.

Techniques: Migration, Knockdown, Over Expression, CCK-8 Assay, Expressing, Western Blot

Figure 9. Sp1/Sp3 expression is concurrently increased with CPTP expression in PC tissues. Representative images and IHC scores of Sp1 (A-B) or Sp3 (C-D) expression in PC (90 cases) and adjacent normal tissues (60 cases) were detected using IHC. Scale bar, 500 μm. Correlation analysis of protein expression in PC tissue samples between CPTP and Sp1 (E) or Sp3 (F). *P < 0.05, **P < 0.01, ***P < 0.001.

Journal: International journal of biological sciences

Article Title: Human CPTP promotes growth and metastasis via sphingolipid metabolite ceramide and PI4KA/AKT signaling in pancreatic cancer cells.

doi: 10.7150/ijbs.70007

Figure Lengend Snippet: Figure 9. Sp1/Sp3 expression is concurrently increased with CPTP expression in PC tissues. Representative images and IHC scores of Sp1 (A-B) or Sp3 (C-D) expression in PC (90 cases) and adjacent normal tissues (60 cases) were detected using IHC. Scale bar, 500 μm. Correlation analysis of protein expression in PC tissue samples between CPTP and Sp1 (E) or Sp3 (F). *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Small interfering RNA targeted to Sp1 or Sp3 (Santa Cruz Biotechnology, Inc.) was used to knockdown the expression levels of Sp1 and Sp3, respectively.

Techniques: Expressing

Figure 10. Schematic diagram illustrating the proposed mechanism of CPTP in PC cells. CPTP expression affects the levels of sphingolipid metabolite ceramide as well as the PI4KA/AKT signaling pathways. At the point when CPTP expression is upregulated, activation of the PI4KA/AKT signaling pathway and decreased levels of the sphingolipid metabolite ceramide promote PC cell growth and metastasis, respectively. Furthermore, in PC cells, the transcription factors Sp1 and Sp3 operate as upstream positive regulators of CPTP expression. Cer, ceramide.

Journal: International journal of biological sciences

Article Title: Human CPTP promotes growth and metastasis via sphingolipid metabolite ceramide and PI4KA/AKT signaling in pancreatic cancer cells.

doi: 10.7150/ijbs.70007

Figure Lengend Snippet: Figure 10. Schematic diagram illustrating the proposed mechanism of CPTP in PC cells. CPTP expression affects the levels of sphingolipid metabolite ceramide as well as the PI4KA/AKT signaling pathways. At the point when CPTP expression is upregulated, activation of the PI4KA/AKT signaling pathway and decreased levels of the sphingolipid metabolite ceramide promote PC cell growth and metastasis, respectively. Furthermore, in PC cells, the transcription factors Sp1 and Sp3 operate as upstream positive regulators of CPTP expression. Cer, ceramide.

Article Snippet: Small interfering RNA targeted to Sp1 or Sp3 (Santa Cruz Biotechnology, Inc.) was used to knockdown the expression levels of Sp1 and Sp3, respectively.

Techniques: Expressing, Protein-Protein interactions, Activation Assay

nSMase2 upregulation is independent of known transcriptional regulators of nSMase2. ( a ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AllStars Negative Control (AS), Sp1, Sp3 or both together. After 24 h, cells were treated with vehicle, and 0.2 or 0.6 μ M doxorubicin. After 24 h, cells were collected and immunoblotted for nSMase2, Sp1, Sp3 and actin. ( b ) MCF7 cells were seeded in 60 mm dishes. One hour before stimulation with doxorubicin or vehicle, they were pretreated with N -acetylcysteine (NAC). Cells were collected and immunoblotted for nSMase2 and actin. ( c ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AS or CREB3L1. After 24 h, they were treated with vehicle or 0.6 μ M doxorubicin. Cells were collected and immunoblotted for nSMase2 and actin

Journal: Cell Death & Disease

Article Title: P53-dependent upregulation of neutral sphingomyelinase-2: role in doxorubicin-induced growth arrest

doi: 10.1038/cddis.2015.268

Figure Lengend Snippet: nSMase2 upregulation is independent of known transcriptional regulators of nSMase2. ( a ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AllStars Negative Control (AS), Sp1, Sp3 or both together. After 24 h, cells were treated with vehicle, and 0.2 or 0.6 μ M doxorubicin. After 24 h, cells were collected and immunoblotted for nSMase2, Sp1, Sp3 and actin. ( b ) MCF7 cells were seeded in 60 mm dishes. One hour before stimulation with doxorubicin or vehicle, they were pretreated with N -acetylcysteine (NAC). Cells were collected and immunoblotted for nSMase2 and actin. ( c ) MCF7 cells were seeded in 60 mm dishes and transfected with siRNA to AS or CREB3L1. After 24 h, they were treated with vehicle or 0.6 μ M doxorubicin. Cells were collected and immunoblotted for nSMase2 and actin

Article Snippet: All other siRNAs, CHEK1 (SI00024570), CHEK2 (SI00095305), ATM (SI00000840), ATR (SI00023107), Sp1 (SI150983) and Sp3 (SI0004788) were from Qiagen (Hiden, Germany).

Techniques: Transfection, Negative Control