human ahr shrna plasmids Search Results


human ahr shrna plasmids  (OriGene)
90
OriGene human ahr shrna plasmids
Human Ahr Shrna Plasmids, 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
https://www.bioz.com/result/human ahr shrna plasmids/product/OriGene
Average 90 stars, based on 1 article reviews
human ahr shrna plasmids - by Bioz Stars, 2026-03
90/100 stars
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human ahr  (OriGene)
90
OriGene human ahr
Long-term canonical activation of <t>AhR</t> drives melanoma resistance to BRAFi. a Graphical representation of AhR function controlling melanoma cell sensitivity or resistance during BRAFi treatment. A high level of heterogeneity is observed among melanomas with a high proportion of highly differentiated and β-cells sensitive to BRAFi (induction of pigmentation by AhR: β signature) and a weak number of undifferentiated and α-cells resistant to BRAFi (induction of α signature and resistance genes). These persister cells constitute a cell reservoir leading to melanoma relapse. b Graphical model of AhR activation by BRAFi and α-ligands, with α-ligands dictating melanoma resistance. c Expression heatmap for resistant genes in 501Mel cells treated for 7–14 days with TCDD (10 nM). d 501 melanoma cells (501Mel) were pre-treated daily or not for 2 weeks with TCDD (10 nM) and treated 4 days with increasing concentrations of Vem in order to establish cell density measurements and calculate IC50 (sensitivity to Vem). Values, calculated with GraphPad (PRISM6.0 ® ), represent the IC50 of Vem for control cells (without TCDD pre-treatment) or after 2 weeks of TCDD. e Expression heatmap for β-, α-, and resistance genes in 501Mel cells invalidated or not for AhR by CRISPR/Cas9 before or 48 h after treatment with Vem (1 μM). f Expression Heatmap for β-, α-, and resistance genes in 501Mel and SKMEL28 (R) cells knocked-down for AhR or ARNT using siRNA. The human silhouettes have been adapted (change of color background) from Servier Medical Art, licensed under a CC BY 3.0 FR [ https://smart.servier.com/smart_image/shape-29/ ]
Human Ahr, 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
https://www.bioz.com/result/human ahr/product/OriGene
Average 90 stars, based on 1 article reviews
human ahr - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier

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Long-term canonical activation of AhR drives melanoma resistance to BRAFi. a Graphical representation of AhR function controlling melanoma cell sensitivity or resistance during BRAFi treatment. A high level of heterogeneity is observed among melanomas with a high proportion of highly differentiated and β-cells sensitive to BRAFi (induction of pigmentation by AhR: β signature) and a weak number of undifferentiated and α-cells resistant to BRAFi (induction of α signature and resistance genes). These persister cells constitute a cell reservoir leading to melanoma relapse. b Graphical model of AhR activation by BRAFi and α-ligands, with α-ligands dictating melanoma resistance. c Expression heatmap for resistant genes in 501Mel cells treated for 7–14 days with TCDD (10 nM). d 501 melanoma cells (501Mel) were pre-treated daily or not for 2 weeks with TCDD (10 nM) and treated 4 days with increasing concentrations of Vem in order to establish cell density measurements and calculate IC50 (sensitivity to Vem). Values, calculated with GraphPad (PRISM6.0 ® ), represent the IC50 of Vem for control cells (without TCDD pre-treatment) or after 2 weeks of TCDD. e Expression heatmap for β-, α-, and resistance genes in 501Mel cells invalidated or not for AhR by CRISPR/Cas9 before or 48 h after treatment with Vem (1 μM). f Expression Heatmap for β-, α-, and resistance genes in 501Mel and SKMEL28 (R) cells knocked-down for AhR or ARNT using siRNA. The human silhouettes have been adapted (change of color background) from Servier Medical Art, licensed under a CC BY 3.0 FR [ https://smart.servier.com/smart_image/shape-29/ ]

Journal: Nature Communications

Article Title: Sustained activation of the Aryl hydrocarbon Receptor transcription factor promotes resistance to BRAF-inhibitors in melanoma

doi: 10.1038/s41467-018-06951-2

Figure Lengend Snippet: Long-term canonical activation of AhR drives melanoma resistance to BRAFi. a Graphical representation of AhR function controlling melanoma cell sensitivity or resistance during BRAFi treatment. A high level of heterogeneity is observed among melanomas with a high proportion of highly differentiated and β-cells sensitive to BRAFi (induction of pigmentation by AhR: β signature) and a weak number of undifferentiated and α-cells resistant to BRAFi (induction of α signature and resistance genes). These persister cells constitute a cell reservoir leading to melanoma relapse. b Graphical model of AhR activation by BRAFi and α-ligands, with α-ligands dictating melanoma resistance. c Expression heatmap for resistant genes in 501Mel cells treated for 7–14 days with TCDD (10 nM). d 501 melanoma cells (501Mel) were pre-treated daily or not for 2 weeks with TCDD (10 nM) and treated 4 days with increasing concentrations of Vem in order to establish cell density measurements and calculate IC50 (sensitivity to Vem). Values, calculated with GraphPad (PRISM6.0 ® ), represent the IC50 of Vem for control cells (without TCDD pre-treatment) or after 2 weeks of TCDD. e Expression heatmap for β-, α-, and resistance genes in 501Mel cells invalidated or not for AhR by CRISPR/Cas9 before or 48 h after treatment with Vem (1 μM). f Expression Heatmap for β-, α-, and resistance genes in 501Mel and SKMEL28 (R) cells knocked-down for AhR or ARNT using siRNA. The human silhouettes have been adapted (change of color background) from Servier Medical Art, licensed under a CC BY 3.0 FR [ https://smart.servier.com/smart_image/shape-29/ ]

Article Snippet: Plasmids encoding shRNA targeting human AhR (TL320259, 29mer shRNA constructs in lentiviral GFP vector) were purchased from Origene, Rockville, MD.

Techniques: Activation Assay, Expressing, CRISPR