hela cell line Search Results


94
Genecopoeia hela c abl ko cells
Hela C Abl Ko Cells, supplied by Genecopoeia, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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hela c abl ko cells - by Bioz Stars, 2026-07
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BPS Bioscience hela hace2 reporter cells
Hela Hace2 Reporter Cells, supplied by BPS Bioscience, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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BPS Bioscience gas reporter luc hela cell line ifn γ jak stat1 pathway
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Gas Reporter Luc Hela Cell Line Ifn γ Jak Stat1 Pathway, supplied by BPS Bioscience, 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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Average 93 stars, based on 1 article reviews
gas reporter luc hela cell line ifn γ jak stat1 pathway - by Bioz Stars, 2026-07
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94
Genecopoeia hela cell line
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Hela Cell Line, supplied by Genecopoeia, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
China Center for Type Culture Collection human cervical adenocarcinoma cell line hela
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Human Cervical Adenocarcinoma Cell Line Hela, supplied by China Center for Type Culture Collection, 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/product/hela+cell+line/pm29375707-33-2-11?v=China+Center+for+Type+Culture+Collection
Average 90 stars, based on 1 article reviews
human cervical adenocarcinoma cell line hela - by Bioz Stars, 2026-07
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European Collection of Authenticated Cell Cultures hela cell line ecacc general cell collection
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Hela Cell Line Ecacc General Cell Collection, supplied by European Collection of Authenticated Cell Cultures, 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/product/hela+cell+line/pm34078930-103-1-8?v=European+Collection+of+Authenticated+Cell+Cultures
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hela cell line ecacc general cell collection - by Bioz Stars, 2026-07
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European Collection of Authenticated Cell Cultures human cervical carcinoma (hela) cells
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Human Cervical Carcinoma (Hela) Cells, supplied by European Collection of Authenticated Cell Cultures, 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/product/hela+cell+line/pm37111627-38-0-9?v=European+Collection+of+Authenticated+Cell+Cultures
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human cervical carcinoma (hela) cells - by Bioz Stars, 2026-07
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China Center for Type Culture Collection cell line hela (cervical adenocarcinoma, cadc)
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Cell Line Hela (Cervical Adenocarcinoma, Cadc), supplied by China Center for Type Culture Collection, 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/product/hela+cell+line/pm39793896-174-5-17?v=China+Center+for+Type+Culture+Collection
Average 90 stars, based on 1 article reviews
cell line hela (cervical adenocarcinoma, cadc) - by Bioz Stars, 2026-07
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DS Pharma Biomedical human cervical cancer cell line hela
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Human Cervical Cancer Cell Line Hela, supplied by DS Pharma Biomedical, 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/product/hela+cell+line/us09664671-1000-1-9?v=DS+Pharma+Biomedical
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human cervical cancer cell line hela - by Bioz Stars, 2026-07
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National Centre for Cell Science cervical cancer cell line hela (p53 degraded/hpv18-e6 positive)
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Cervical Cancer Cell Line Hela (P53 Degraded/Hpv18 E6 Positive), supplied by National Centre for Cell Science, 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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National Centre for Cell Science ht-29
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Ht 29, supplied by National Centre for Cell Science, 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/product/hela+cell+line/10__7897_slash_2230___8407__080458-52-10-18?v=National+Centre+for+Cell+Science
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ht-29 - by Bioz Stars, 2026-07
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Inex Pharmaceuticals hela-luc stable cell line
a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in <t>IFN-γ-JAK1/2-STAT1</t> HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.
Hela Luc Stable Cell Line, supplied by Inex Pharmaceuticals, 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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a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in IFN-γ-JAK1/2-STAT1 HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Rational design of a JAK1-selective siRNA inhibitor for the modulation of autoimmunity in the skin

doi: 10.1038/s41467-023-42714-4

Figure Lengend Snippet: a Activity of 3033 on JAK family enzymes. Human HEL 92.1.7 cells were treated with siRNA at 1.5 μM for 72 h, and mRNA levels of JAK1, JAK2, JAK3, and TYK2 were measured using the QuantiGene 2.0 assay ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, **** P < 0.0001, ns: not significant). b Ruxolitinib inhibits JAK1 and JAK2 to prevent the pathogenesis of vitiligo driven by IFN-γ signaling. c mRNA expression of IFN-γ-inducible chemokines CXCL9, 10, and 11. Cells were first treated with siRNA or ruxolitinib at 1.5 μM for 72 h, and then stimulated with recombinant human IFN-γ for 24 h ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). d , e Chemical engineering of 3033 for skin delivery. Terminal nucleotides were stabilized with phosphorothioate backbone modifications for nuclease stability ( d ). Human HeLa cells were transfected with DCA-siRNAs for 72 h through lipofectamine RNAiMax-mediated uptake and mRNA levels were measured using the QuantiGene 2.0 assay ( n = 3 biologically independent samples, mean ± s.d.; two-way ANOVA multiple comparison, * P < 0.05). f Molecular modeling (PyMOL 2) of DCA-siRNA 3033 in scaffold 2, si3033. g – i ruxolitinib and si3033 both reduce luciferase activity in IFN-γ-JAK1/2-STAT1 HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; one-way ANOVA, ** P < 0.01, **** P < 0.0001). Cells were treated with ruxolitinib or siRNA for 72 h and then stimulated with IFN-γ for 18 h. si3033 was transfected to the HeLa reporter cells using lipofectamine RNAiMax. j JAK1 and JAK2 mRNA expression in si3033-treated and untreated HeLa reporter cells ( n = 7 biologically independent samples, mean ± s.d.; two-sided unpaired t test, **** P < 0.0001, ns: not significant). Source data are provided as a Source Data file.

Article Snippet: GAS reporter (Luc)-HeLa cell line (IFN-γ/JAK/STAT1 pathway) was purchased from BPS Bioscience (#79041).

Techniques: Activity Assay, Expressing, Recombinant, Transfection, Comparison, Luciferase