recombinant human leptin protein, cf Search Results


recombinant lep  (R&D Systems)
93
R&D Systems recombinant lep
H1650 human lung adenocarcinoma cells are PTEN-deficient and express high leptin and leptin receptor mRNA. Comparison of different lung cancer cell lines reveals H1650 cells are PTEN-deficient (A) and express the highest levels of <t>LEP</t> and its receptor LEPR mRNA (B). C, leptin and leptin receptor protein levels as a result of PTEN deletion as assessed in H1650 cells, suggesting the likely presence of a functional LEP signaling pathway in lung epithelial cells. D, dose-dependent increase in H1650 cell proliferation (∼3-fold) was observed when cells were treated for 48 h with increasing concentrations (50, 100, and 200 ng/ml; lane 2–4) of human <t>recombinant</t> LEP. E, continuous impedance sensing measurements identify greater wound closure efficiency in cells treated with 100 ng/ml leptin prior to wounding as compared with control cells without leptin. F, identification of the LEP gene core promoter region in H1650 lung cancer cell line revealed a proximal enhancer containing NRF-1 and δ-binding sites. Subconfluent cultures were transiently transfected with various promoter-reporter deletion constructs derived from 5′-upstream regulatory sequence of the LEP gene. Luciferase activity was expressed relative to the base-line luciferase activity of a promoter-less luciferase reporter construct (pGL3-Basic) set to unity. Data are represented from four independent experiments performed in triplicate (± S.E.; *, p value ≤ 0.05). G, diagrammatic representation of the most active promoter region −149 to +21 bp of the LEP gene (Luc-150), including proximal enhancers depicting the positions of NRF-1 and C/EBP sites.
Recombinant Lep, 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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human leptin  (R&D Systems)
95
R&D Systems human leptin
H1650 human lung adenocarcinoma cells are PTEN-deficient and express high leptin and leptin receptor mRNA. Comparison of different lung cancer cell lines reveals H1650 cells are PTEN-deficient (A) and express the highest levels of <t>LEP</t> and its receptor LEPR mRNA (B). C, leptin and leptin receptor protein levels as a result of PTEN deletion as assessed in H1650 cells, suggesting the likely presence of a functional LEP signaling pathway in lung epithelial cells. D, dose-dependent increase in H1650 cell proliferation (∼3-fold) was observed when cells were treated for 48 h with increasing concentrations (50, 100, and 200 ng/ml; lane 2–4) of human <t>recombinant</t> LEP. E, continuous impedance sensing measurements identify greater wound closure efficiency in cells treated with 100 ng/ml leptin prior to wounding as compared with control cells without leptin. F, identification of the LEP gene core promoter region in H1650 lung cancer cell line revealed a proximal enhancer containing NRF-1 and δ-binding sites. Subconfluent cultures were transiently transfected with various promoter-reporter deletion constructs derived from 5′-upstream regulatory sequence of the LEP gene. Luciferase activity was expressed relative to the base-line luciferase activity of a promoter-less luciferase reporter construct (pGL3-Basic) set to unity. Data are represented from four independent experiments performed in triplicate (± S.E.; *, p value ≤ 0.05). G, diagrammatic representation of the most active promoter region −149 to +21 bp of the LEP gene (Luc-150), including proximal enhancers depicting the positions of NRF-1 and C/EBP sites.
Human Leptin, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human leptin receptor  (R&D Systems)
90
R&D Systems human leptin receptor
H1650 human lung adenocarcinoma cells are PTEN-deficient and express high leptin and leptin receptor mRNA. Comparison of different lung cancer cell lines reveals H1650 cells are PTEN-deficient (A) and express the highest levels of <t>LEP</t> and its receptor LEPR mRNA (B). C, leptin and leptin receptor protein levels as a result of PTEN deletion as assessed in H1650 cells, suggesting the likely presence of a functional LEP signaling pathway in lung epithelial cells. D, dose-dependent increase in H1650 cell proliferation (∼3-fold) was observed when cells were treated for 48 h with increasing concentrations (50, 100, and 200 ng/ml; lane 2–4) of human <t>recombinant</t> LEP. E, continuous impedance sensing measurements identify greater wound closure efficiency in cells treated with 100 ng/ml leptin prior to wounding as compared with control cells without leptin. F, identification of the LEP gene core promoter region in H1650 lung cancer cell line revealed a proximal enhancer containing NRF-1 and δ-binding sites. Subconfluent cultures were transiently transfected with various promoter-reporter deletion constructs derived from 5′-upstream regulatory sequence of the LEP gene. Luciferase activity was expressed relative to the base-line luciferase activity of a promoter-less luciferase reporter construct (pGL3-Basic) set to unity. Data are represented from four independent experiments performed in triplicate (± S.E.; *, p value ≤ 0.05). G, diagrammatic representation of the most active promoter region −149 to +21 bp of the LEP gene (Luc-150), including proximal enhancers depicting the positions of NRF-1 and C/EBP sites.
Human Leptin Receptor, supplied by R&D Systems, 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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rhleptin  (R&D Systems)
86
R&D Systems rhleptin
H1650 human lung adenocarcinoma cells are PTEN-deficient and express high leptin and leptin receptor mRNA. Comparison of different lung cancer cell lines reveals H1650 cells are PTEN-deficient (A) and express the highest levels of <t>LEP</t> and its receptor LEPR mRNA (B). C, leptin and leptin receptor protein levels as a result of PTEN deletion as assessed in H1650 cells, suggesting the likely presence of a functional LEP signaling pathway in lung epithelial cells. D, dose-dependent increase in H1650 cell proliferation (∼3-fold) was observed when cells were treated for 48 h with increasing concentrations (50, 100, and 200 ng/ml; lane 2–4) of human <t>recombinant</t> LEP. E, continuous impedance sensing measurements identify greater wound closure efficiency in cells treated with 100 ng/ml leptin prior to wounding as compared with control cells without leptin. F, identification of the LEP gene core promoter region in H1650 lung cancer cell line revealed a proximal enhancer containing NRF-1 and δ-binding sites. Subconfluent cultures were transiently transfected with various promoter-reporter deletion constructs derived from 5′-upstream regulatory sequence of the LEP gene. Luciferase activity was expressed relative to the base-line luciferase activity of a promoter-less luciferase reporter construct (pGL3-Basic) set to unity. Data are represented from four independent experiments performed in triplicate (± S.E.; *, p value ≤ 0.05). G, diagrammatic representation of the most active promoter region −149 to +21 bp of the LEP gene (Luc-150), including proximal enhancers depicting the positions of NRF-1 and C/EBP sites.
Rhleptin, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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H1650 human lung adenocarcinoma cells are PTEN-deficient and express high leptin and leptin receptor mRNA. Comparison of different lung cancer cell lines reveals H1650 cells are PTEN-deficient (A) and express the highest levels of LEP and its receptor LEPR mRNA (B). C, leptin and leptin receptor protein levels as a result of PTEN deletion as assessed in H1650 cells, suggesting the likely presence of a functional LEP signaling pathway in lung epithelial cells. D, dose-dependent increase in H1650 cell proliferation (∼3-fold) was observed when cells were treated for 48 h with increasing concentrations (50, 100, and 200 ng/ml; lane 2–4) of human recombinant LEP. E, continuous impedance sensing measurements identify greater wound closure efficiency in cells treated with 100 ng/ml leptin prior to wounding as compared with control cells without leptin. F, identification of the LEP gene core promoter region in H1650 lung cancer cell line revealed a proximal enhancer containing NRF-1 and δ-binding sites. Subconfluent cultures were transiently transfected with various promoter-reporter deletion constructs derived from 5′-upstream regulatory sequence of the LEP gene. Luciferase activity was expressed relative to the base-line luciferase activity of a promoter-less luciferase reporter construct (pGL3-Basic) set to unity. Data are represented from four independent experiments performed in triplicate (± S.E.; *, p value ≤ 0.05). G, diagrammatic representation of the most active promoter region −149 to +21 bp of the LEP gene (Luc-150), including proximal enhancers depicting the positions of NRF-1 and C/EBP sites.

Journal: The Journal of Biological Chemistry

Article Title: Loss of Phosphatase and Tensin Homolog (PTEN) Induces Leptin-mediated Leptin Gene Expression

doi: 10.1074/jbc.M113.481523

Figure Lengend Snippet: H1650 human lung adenocarcinoma cells are PTEN-deficient and express high leptin and leptin receptor mRNA. Comparison of different lung cancer cell lines reveals H1650 cells are PTEN-deficient (A) and express the highest levels of LEP and its receptor LEPR mRNA (B). C, leptin and leptin receptor protein levels as a result of PTEN deletion as assessed in H1650 cells, suggesting the likely presence of a functional LEP signaling pathway in lung epithelial cells. D, dose-dependent increase in H1650 cell proliferation (∼3-fold) was observed when cells were treated for 48 h with increasing concentrations (50, 100, and 200 ng/ml; lane 2–4) of human recombinant LEP. E, continuous impedance sensing measurements identify greater wound closure efficiency in cells treated with 100 ng/ml leptin prior to wounding as compared with control cells without leptin. F, identification of the LEP gene core promoter region in H1650 lung cancer cell line revealed a proximal enhancer containing NRF-1 and δ-binding sites. Subconfluent cultures were transiently transfected with various promoter-reporter deletion constructs derived from 5′-upstream regulatory sequence of the LEP gene. Luciferase activity was expressed relative to the base-line luciferase activity of a promoter-less luciferase reporter construct (pGL3-Basic) set to unity. Data are represented from four independent experiments performed in triplicate (± S.E.; *, p value ≤ 0.05). G, diagrammatic representation of the most active promoter region −149 to +21 bp of the LEP gene (Luc-150), including proximal enhancers depicting the positions of NRF-1 and C/EBP sites.

Article Snippet: H1650 cells were grown on electric cell substrate impedance sensing 8-well plate arrays (8W1E; Applied Biophysics, Troy, NY) in growth media with serum until fully confluent, after which the media were replaced with serum-free media for 24 h. Serum-deprived cells were treated with 100 ng/ml of human recombinant LEP (R&D Systems, Minneapolis, MN) for 2 h prior to wounding.

Techniques: Comparison, Functional Assay, Recombinant, Binding Assay, Transfection, Construct, Derivative Assay, Sequencing, Luciferase, Activity Assay