wnt1 Search Results


90
OriGene mouse e2f1 cdna
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
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94
Proteintech anti wnt1
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
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93
Santa Cruz Biotechnology polyclonal anti wnt1 antibody
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
Polyclonal Anti Wnt1 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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92
Addgene inc plenti6 slc7a11 xct v5
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
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93
Addgene inc aav9 hsyn soma gcamp8f
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
Aav9 Hsyn Soma Gcamp8f, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
Cusabio elisa kits
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
Elisa Kits, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
R&D Systems goat anti wnt 1
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
Goat Anti Wnt 1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
OriGene wnt 1 lentivirus
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
Wnt 1 Lentivirus, supplied by OriGene, 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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93
Addgene inc pcdna wnt1
Figure 6 <t>E2F1</t> promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase
Pcdna Wnt1, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech wisp1
The top 20 genes in odontoblasts.
Wisp1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology human wnt1
miR-329 decreases proliferation in PTC cells, while the overexpression of <t>WNT1</t> rescued this effect. (A) TPC-1 and BCPAP cells were transfected with miR-329 mimic or miR-NC and WNT1 plasmid, the expression level of miR-329 was detected via quantitative polymerase chain reaction. RNU48 served as an internal control. The cell viability of (B) TPC-1 and (C) BCPAP cells was determined by a CCK-8 assay. The proliferation of (D) TPC-1 and (E) BCPAP cells was assessed by colony formation assays. (F) Western blot assays were performed to confirm the WNT1 protein expression in TPC-1 and BCPAP cells. *P<0.05. PTC, papillary thyroid cancer; miR, microRNA; NC, negative control.
Human Wnt1, supplied by Santa Cruz Biotechnology, 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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91
Novus Biologicals nbp1 51575
miR-329 decreases proliferation in PTC cells, while the overexpression of <t>WNT1</t> rescued this effect. (A) TPC-1 and BCPAP cells were transfected with miR-329 mimic or miR-NC and WNT1 plasmid, the expression level of miR-329 was detected via quantitative polymerase chain reaction. RNU48 served as an internal control. The cell viability of (B) TPC-1 and (C) BCPAP cells was determined by a CCK-8 assay. The proliferation of (D) TPC-1 and (E) BCPAP cells was assessed by colony formation assays. (F) Western blot assays were performed to confirm the WNT1 protein expression in TPC-1 and BCPAP cells. *P<0.05. PTC, papillary thyroid cancer; miR, microRNA; NC, negative control.
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Image Search Results


Figure 6 E2F1 promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase

Journal: Cell death and differentiation

Article Title: E2F1-regulated miR-30b suppresses Cyclophilin D and protects heart from ischemia/reperfusion injury and necrotic cell death.

doi: 10.1038/cdd.2014.165

Figure Lengend Snippet: Figure 6 E2F1 promotes necrosis through miR-30b and CypD. (a) E2F1 levels are increased in cardiomyocytes exposed to H2O2. Cardiomyocytes were exposed to H2O2. Cells were harvested at the indicated times for the analysis of E2F1 levels by immunoblot. (b) Knockdown of E2F1 reduces necrotic cell death induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc. Twenty-four hours after infection, cells were treated with H2O2. PI exclusion was analyzed. *Po0.05 versus H2O2 alone. (c) The levels of E2F1 are increased in myocardial I/R. Mice were induced to undergo cardiac I/R at the indicated times as described in Materials and Methods. E2F1 levels were analyzed by immunoblot. (d and e) E2F1 knockout mice attenuates myocyte necrosis and myocardial infarction upon I/R. WTand E2F1 knockout mice were subjected to I/R as described in Materials and Methods. Myocyte necrosis (d) and myocardial infarction (e) were analyzed. *Po0.05 versus WT+I/R. (f and g) CypD TP attenuates the inhibitory effect of E2F1 knockdown on CypD expression and necrotic responses induced by H2O2. Cardiomyocytes were infected with adenoviral E2F1-siRNA or E2F1-sc, transfected with the TP (CypD-TP miR-30b) or the control (CypD-TP control) and then exposed to H2O2. CypD expression (f) was analyzed by immunoblot. Necrosis was assessed by PI exclusion assay (g). *Po0.05. GAPDH, glyceraldehyde 3-phosphate dehydrogenase

Article Snippet: Mouse E2F1 cDNA was from Origene (Rockville, MD, USA).

Techniques: Western Blot, Knockdown, Infection, Knock-Out, Expressing, Transfection, Control, Exclusion Assay

The top 20 genes in odontoblasts.

Journal: Frontiers in Physiology

Article Title: Atlas of human dental pulp cells at multiple spatial and temporal levels based on single-cell sequencing analysis

doi: 10.3389/fphys.2022.993478

Figure Lengend Snippet: The top 20 genes in odontoblasts.

Article Snippet: The following antibodies were used in our study: CD163 (1:500, Abcam, United States), SLC12A2 (1:100, Proteintech, China), ST8SIA1 (1:100, Proteintech), CD24 (1: 50, Santa Cruz, United States), WISP1 (1:100, Proteintech), CD146/MCAM (1: 250, Abcam), and CD90 (1:200, Abcam).

Techniques:

miR-329 decreases proliferation in PTC cells, while the overexpression of WNT1 rescued this effect. (A) TPC-1 and BCPAP cells were transfected with miR-329 mimic or miR-NC and WNT1 plasmid, the expression level of miR-329 was detected via quantitative polymerase chain reaction. RNU48 served as an internal control. The cell viability of (B) TPC-1 and (C) BCPAP cells was determined by a CCK-8 assay. The proliferation of (D) TPC-1 and (E) BCPAP cells was assessed by colony formation assays. (F) Western blot assays were performed to confirm the WNT1 protein expression in TPC-1 and BCPAP cells. *P<0.05. PTC, papillary thyroid cancer; miR, microRNA; NC, negative control.

Journal: Oncology Letters

Article Title: miR-329 inhibits papillary thyroid cancer progression via direct targeting WNT1

doi: 10.3892/ol.2018.9102

Figure Lengend Snippet: miR-329 decreases proliferation in PTC cells, while the overexpression of WNT1 rescued this effect. (A) TPC-1 and BCPAP cells were transfected with miR-329 mimic or miR-NC and WNT1 plasmid, the expression level of miR-329 was detected via quantitative polymerase chain reaction. RNU48 served as an internal control. The cell viability of (B) TPC-1 and (C) BCPAP cells was determined by a CCK-8 assay. The proliferation of (D) TPC-1 and (E) BCPAP cells was assessed by colony formation assays. (F) Western blot assays were performed to confirm the WNT1 protein expression in TPC-1 and BCPAP cells. *P<0.05. PTC, papillary thyroid cancer; miR, microRNA; NC, negative control.

Article Snippet: WNT1 overexpression plasmid was achieved using pcDNA3.1/WNT1 transfection. siRNA targeting human Wnt1 was obtained from Santa Cruz Biotechnology, Inc., (sc-36839; Dallas, TX, USA). siWnt1 (5 nmol) was transfected into the cells according to the manufacturer's protocol.

Techniques: Over Expression, Transfection, Plasmid Preparation, Expressing, Real-time Polymerase Chain Reaction, Control, CCK-8 Assay, Western Blot, Negative Control

miR-329 overexpression decreases cell migration and invasion in TPC-1 and BCPAP cells, while WNT1 overexpression rescued this effect. (A-D) TPC-1 and BCPAP cells were co-transfected with either miR-329 mimic or miR-NC and WNT1 plasmid. Transwell assays were conducted and quantified. Migrated and invasive cells were fixed, stained and counted and images were captured (magnification, ×200). (A) Images and (B) quantification of TPC-1 cell migration and invasion in the lower chamber. (C) Images and (D) quantification of BCPAP cell migration and invasion in the lower chamber. *P<0.05. miR, microRNA; NC, negative control.

Journal: Oncology Letters

Article Title: miR-329 inhibits papillary thyroid cancer progression via direct targeting WNT1

doi: 10.3892/ol.2018.9102

Figure Lengend Snippet: miR-329 overexpression decreases cell migration and invasion in TPC-1 and BCPAP cells, while WNT1 overexpression rescued this effect. (A-D) TPC-1 and BCPAP cells were co-transfected with either miR-329 mimic or miR-NC and WNT1 plasmid. Transwell assays were conducted and quantified. Migrated and invasive cells were fixed, stained and counted and images were captured (magnification, ×200). (A) Images and (B) quantification of TPC-1 cell migration and invasion in the lower chamber. (C) Images and (D) quantification of BCPAP cell migration and invasion in the lower chamber. *P<0.05. miR, microRNA; NC, negative control.

Article Snippet: WNT1 overexpression plasmid was achieved using pcDNA3.1/WNT1 transfection. siRNA targeting human Wnt1 was obtained from Santa Cruz Biotechnology, Inc., (sc-36839; Dallas, TX, USA). siWnt1 (5 nmol) was transfected into the cells according to the manufacturer's protocol.

Techniques: Over Expression, Migration, Transfection, Plasmid Preparation, Staining, Negative Control

WNT1 is a direct target gene of miR-329. (A) Sequence alignment of miR-329 with 3′untranslated region of WNT1 predicted by TargetScan. (B) The mRNA expression level of WNT1 in TPC-1 and BCPAP cells was analyzed by quantitative polymerase chain reaction. GAPDH served as the control. (C) Western blot analysis was used to analyze the protein expression of WNT1 in TPC-1 and BCPAP cells. GAPDH served as the control. Luciferase activity of (D) TPC-1 and (E) BCPAP cells was examined via luciferase reporter assay. (F) Spearman's correlation analysis examined the correlations between the mRNA expression level of WNT1 and miR-329 in PTC tissues. *P<0.05. miR, microRNA; NC, negative control; WT, wild type; MUT, mutant.

Journal: Oncology Letters

Article Title: miR-329 inhibits papillary thyroid cancer progression via direct targeting WNT1

doi: 10.3892/ol.2018.9102

Figure Lengend Snippet: WNT1 is a direct target gene of miR-329. (A) Sequence alignment of miR-329 with 3′untranslated region of WNT1 predicted by TargetScan. (B) The mRNA expression level of WNT1 in TPC-1 and BCPAP cells was analyzed by quantitative polymerase chain reaction. GAPDH served as the control. (C) Western blot analysis was used to analyze the protein expression of WNT1 in TPC-1 and BCPAP cells. GAPDH served as the control. Luciferase activity of (D) TPC-1 and (E) BCPAP cells was examined via luciferase reporter assay. (F) Spearman's correlation analysis examined the correlations between the mRNA expression level of WNT1 and miR-329 in PTC tissues. *P<0.05. miR, microRNA; NC, negative control; WT, wild type; MUT, mutant.

Article Snippet: WNT1 overexpression plasmid was achieved using pcDNA3.1/WNT1 transfection. siRNA targeting human Wnt1 was obtained from Santa Cruz Biotechnology, Inc., (sc-36839; Dallas, TX, USA). siWnt1 (5 nmol) was transfected into the cells according to the manufacturer's protocol.

Techniques: Sequencing, Expressing, Real-time Polymerase Chain Reaction, Control, Western Blot, Luciferase, Activity Assay, Reporter Assay, Negative Control, Mutagenesis

WNT1 silencing inhibits PTC cell viability, proliferation, migration and invasion in vitro . (A) Western blot analysis examined the expression of WNT1 in the TPC-1 and BCPAP cells transfected with siWNT1 or sicontrol. Cell viability in (B) TPC-1 and (C) BCPAP cells was examined via a CCK-8 assay. (D) Proliferation was examined by a colony formation assay. The migration and invasion capability of in (E) TPC-1 and (F) BCPAP cells was determined by Transwell migration and invasion assays. *P<0.05. si, short interfering RNA. PTC, papillary thyroid cancer.

Journal: Oncology Letters

Article Title: miR-329 inhibits papillary thyroid cancer progression via direct targeting WNT1

doi: 10.3892/ol.2018.9102

Figure Lengend Snippet: WNT1 silencing inhibits PTC cell viability, proliferation, migration and invasion in vitro . (A) Western blot analysis examined the expression of WNT1 in the TPC-1 and BCPAP cells transfected with siWNT1 or sicontrol. Cell viability in (B) TPC-1 and (C) BCPAP cells was examined via a CCK-8 assay. (D) Proliferation was examined by a colony formation assay. The migration and invasion capability of in (E) TPC-1 and (F) BCPAP cells was determined by Transwell migration and invasion assays. *P<0.05. si, short interfering RNA. PTC, papillary thyroid cancer.

Article Snippet: WNT1 overexpression plasmid was achieved using pcDNA3.1/WNT1 transfection. siRNA targeting human Wnt1 was obtained from Santa Cruz Biotechnology, Inc., (sc-36839; Dallas, TX, USA). siWnt1 (5 nmol) was transfected into the cells according to the manufacturer's protocol.

Techniques: Migration, In Vitro, Western Blot, Expressing, Transfection, CCK-8 Assay, Colony Assay, Small Interfering RNA

miR-329 inhibits tumor growth in vivo via downregulation of WNT1. (A) Images of tumors derived from the BCPAP-miR-329 and BCPAP-miR-NC groups. (B) Tumor volume was analyzed every 7 days for 42 days following injection. (C) Tumor weight in BCPAP-miR-329 and BCPAP-miR-NC groups. (D) qPCR was used to determine the (D) miR-329 and (E) WNT1 expression in each treatment group. *P<0.05. miR, microRNA; NC, negative control; qPCR, quantitative polymerase chain reaction.

Journal: Oncology Letters

Article Title: miR-329 inhibits papillary thyroid cancer progression via direct targeting WNT1

doi: 10.3892/ol.2018.9102

Figure Lengend Snippet: miR-329 inhibits tumor growth in vivo via downregulation of WNT1. (A) Images of tumors derived from the BCPAP-miR-329 and BCPAP-miR-NC groups. (B) Tumor volume was analyzed every 7 days for 42 days following injection. (C) Tumor weight in BCPAP-miR-329 and BCPAP-miR-NC groups. (D) qPCR was used to determine the (D) miR-329 and (E) WNT1 expression in each treatment group. *P<0.05. miR, microRNA; NC, negative control; qPCR, quantitative polymerase chain reaction.

Article Snippet: WNT1 overexpression plasmid was achieved using pcDNA3.1/WNT1 transfection. siRNA targeting human Wnt1 was obtained from Santa Cruz Biotechnology, Inc., (sc-36839; Dallas, TX, USA). siWnt1 (5 nmol) was transfected into the cells according to the manufacturer's protocol.

Techniques: In Vivo, Derivative Assay, Injection, Expressing, Negative Control, Real-time Polymerase Chain Reaction