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cervical cancer cell line hela  (ATCC)


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    Structured Review

    ATCC cervical cancer cell line hela
    Cervical Cancer Cell Line Hela, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 7925 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cervical cancer cell line hela/product/ATCC
    Average 99 stars, based on 7925 article reviews
    cervical cancer cell line hela - by Bioz Stars, 2026-03
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    ATCC cervical cancer cell line hela
    Cervical Cancer Cell Line Hela, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cervical cancer cell line hela/product/ATCC
    Average 99 stars, based on 1 article reviews
    cervical cancer cell line hela - by Bioz Stars, 2026-03
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    99
    ATCC cervical cancer cell lines hela
    HMGCS1 regulates cisplatin sensitivity and resistance <t>in</t> <t>cervical</t> cancer cells through mitochondrial localization. ( A - B ) Dose-response curves showing cell viability of wild-type (WT) and HMGCS1 knockout (KO) <t>HeLa</t> ( A ) and C33A ( B ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. Cell viability was determined using SRB assay. The corresponding Western blots below validate HMGCS1 protein knockout, using TUBA1A as a loading control. ( C - D ) Dose-response curves showing cell viability of parental and cisplatin-resistant (CisR) HeLa ( C ) and C33A ( D ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. ( E ) Western blot analysis of HMGCS1 protein expression in parental and cisplatin-resistant HeLa and C33A cells. TUBA1A was used as a loading control. ( F - G ) Dose-response curves showing cell viability of wild-type (WT) and HMGCS1 knockout (KO) cisplatin-resistant HeLa_CisR ( F ) and C33A_CisR ( G ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. ( H - I ) Western blot analysis of HMGCS1 protein expression in nuclear and mitochondrial fractions of parental and cisplatin-resistant HeLa ( H ) and C33A ( I ) cells. Lamin B1 and Tomm20 were used as nuclear and mitochondrial markers, respectively. ( A - D , F - G ) Data are presented as mean ± SD. Statistical significance of the difference between IC50 values was determined by the Extra Sum-of-Squares F-test
    Cervical Cancer Cell Lines Hela, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cervical cancer cell lines hela/product/ATCC
    Average 99 stars, based on 1 article reviews
    cervical cancer cell lines hela - by Bioz Stars, 2026-03
    99/100 stars
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    99
    ATCC hela human cervical cancer cell line
    HMGCS1 regulates cisplatin sensitivity and resistance <t>in</t> <t>cervical</t> cancer cells through mitochondrial localization. ( A - B ) Dose-response curves showing cell viability of wild-type (WT) and HMGCS1 knockout (KO) <t>HeLa</t> ( A ) and C33A ( B ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. Cell viability was determined using SRB assay. The corresponding Western blots below validate HMGCS1 protein knockout, using TUBA1A as a loading control. ( C - D ) Dose-response curves showing cell viability of parental and cisplatin-resistant (CisR) HeLa ( C ) and C33A ( D ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. ( E ) Western blot analysis of HMGCS1 protein expression in parental and cisplatin-resistant HeLa and C33A cells. TUBA1A was used as a loading control. ( F - G ) Dose-response curves showing cell viability of wild-type (WT) and HMGCS1 knockout (KO) cisplatin-resistant HeLa_CisR ( F ) and C33A_CisR ( G ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. ( H - I ) Western blot analysis of HMGCS1 protein expression in nuclear and mitochondrial fractions of parental and cisplatin-resistant HeLa ( H ) and C33A ( I ) cells. Lamin B1 and Tomm20 were used as nuclear and mitochondrial markers, respectively. ( A - D , F - G ) Data are presented as mean ± SD. Statistical significance of the difference between IC50 values was determined by the Extra Sum-of-Squares F-test
    Hela Human Cervical Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hela human cervical cancer cell line/product/ATCC
    Average 99 stars, based on 1 article reviews
    hela human cervical cancer cell line - by Bioz Stars, 2026-03
    99/100 stars
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    99
    ATCC cervical cancer hela cell line
    Detection of wild-type and mutant FZD4 on downstream signal proteins by luciferase reporter gene assay. FZD4-wild-type (FZD4-WT) and FZD4-mutant (FZD4-MU) represent the relative luciferase activity ascertained from the transfection of wild-type FZD4 plasmid and mutant FZD4 plasmid into <t>Hela</t> cells, respectively. Data are representative of three independent experiments. The experimental data are presented as the mean ± standard deviation (mean ± SD). Differences between groups were assessed using the Student’s t -test, and * P < 0.05.
    Cervical Cancer Hela Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cervical cancer hela cell line/product/ATCC
    Average 99 stars, based on 1 article reviews
    cervical cancer hela cell line - by Bioz Stars, 2026-03
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    99
    ATCC human cervical cancer cell line
    Detection of wild-type and mutant FZD4 on downstream signal proteins by luciferase reporter gene assay. FZD4-wild-type (FZD4-WT) and FZD4-mutant (FZD4-MU) represent the relative luciferase activity ascertained from the transfection of wild-type FZD4 plasmid and mutant FZD4 plasmid into <t>Hela</t> cells, respectively. Data are representative of three independent experiments. The experimental data are presented as the mean ± standard deviation (mean ± SD). Differences between groups were assessed using the Student’s t -test, and * P < 0.05.
    Human Cervical Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human cervical cancer cell line/product/ATCC
    Average 99 stars, based on 1 article reviews
    human cervical cancer cell line - by Bioz Stars, 2026-03
    99/100 stars
      Buy from Supplier

    99
    ATCC human cervical cancer cell lines hela
    Detection of wild-type and mutant FZD4 on downstream signal proteins by luciferase reporter gene assay. FZD4-wild-type (FZD4-WT) and FZD4-mutant (FZD4-MU) represent the relative luciferase activity ascertained from the transfection of wild-type FZD4 plasmid and mutant FZD4 plasmid into <t>Hela</t> cells, respectively. Data are representative of three independent experiments. The experimental data are presented as the mean ± standard deviation (mean ± SD). Differences between groups were assessed using the Student’s t -test, and * P < 0.05.
    Human Cervical Cancer Cell Lines Hela, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human cervical cancer cell lines hela/product/ATCC
    Average 99 stars, based on 1 article reviews
    human cervical cancer cell lines hela - by Bioz Stars, 2026-03
    99/100 stars
      Buy from Supplier

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    HMGCS1 regulates cisplatin sensitivity and resistance in cervical cancer cells through mitochondrial localization. ( A - B ) Dose-response curves showing cell viability of wild-type (WT) and HMGCS1 knockout (KO) HeLa ( A ) and C33A ( B ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. Cell viability was determined using SRB assay. The corresponding Western blots below validate HMGCS1 protein knockout, using TUBA1A as a loading control. ( C - D ) Dose-response curves showing cell viability of parental and cisplatin-resistant (CisR) HeLa ( C ) and C33A ( D ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. ( E ) Western blot analysis of HMGCS1 protein expression in parental and cisplatin-resistant HeLa and C33A cells. TUBA1A was used as a loading control. ( F - G ) Dose-response curves showing cell viability of wild-type (WT) and HMGCS1 knockout (KO) cisplatin-resistant HeLa_CisR ( F ) and C33A_CisR ( G ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. ( H - I ) Western blot analysis of HMGCS1 protein expression in nuclear and mitochondrial fractions of parental and cisplatin-resistant HeLa ( H ) and C33A ( I ) cells. Lamin B1 and Tomm20 were used as nuclear and mitochondrial markers, respectively. ( A - D , F - G ) Data are presented as mean ± SD. Statistical significance of the difference between IC50 values was determined by the Extra Sum-of-Squares F-test

    Journal: BMC Molecular and Cell Biology

    Article Title: Mitochondrial HMGCS1 mediates cisplatin resistance in cervical cancer through regulation of mitochondrial transcription

    doi: 10.1186/s12860-026-00566-y

    Figure Lengend Snippet: HMGCS1 regulates cisplatin sensitivity and resistance in cervical cancer cells through mitochondrial localization. ( A - B ) Dose-response curves showing cell viability of wild-type (WT) and HMGCS1 knockout (KO) HeLa ( A ) and C33A ( B ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. Cell viability was determined using SRB assay. The corresponding Western blots below validate HMGCS1 protein knockout, using TUBA1A as a loading control. ( C - D ) Dose-response curves showing cell viability of parental and cisplatin-resistant (CisR) HeLa ( C ) and C33A ( D ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. ( E ) Western blot analysis of HMGCS1 protein expression in parental and cisplatin-resistant HeLa and C33A cells. TUBA1A was used as a loading control. ( F - G ) Dose-response curves showing cell viability of wild-type (WT) and HMGCS1 knockout (KO) cisplatin-resistant HeLa_CisR ( F ) and C33A_CisR ( G ) cells treated with increasing concentrations of cisplatin for 72 h. IC50 values are indicated. ( H - I ) Western blot analysis of HMGCS1 protein expression in nuclear and mitochondrial fractions of parental and cisplatin-resistant HeLa ( H ) and C33A ( I ) cells. Lamin B1 and Tomm20 were used as nuclear and mitochondrial markers, respectively. ( A - D , F - G ) Data are presented as mean ± SD. Statistical significance of the difference between IC50 values was determined by the Extra Sum-of-Squares F-test

    Article Snippet: Cervical cancer cell lines HeLa and C33A were obtained from American Type Culture Collection (ATCC) and maintained in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin at 37 °C with 5% CO2.

    Techniques: Knock-Out, Sulforhodamine B Assay, Western Blot, Control, Expressing

    Subcellular localization of HMGCS1 determines its role in cisplatin resistance. ( A ) Immunofluorescence microscopy of HeLa and C33A cells expressing 6xHis-tagged NLS-HMGCS1 or MTS-HMGCS1. Cells were stained with DAPI (blue) for nuclei, anti-6xHis antibody (green) for tagged HMGCS1, and MitoTracker (red) for mitochondria. Merged images show the distinct subcellular localization of each construct. ( B- E ) Dose-response curves showing cell viability after cisplatin treatment (72 h) in: parental HeLa ( B ) and C33A ( C ) cells; and HMGCS1-knockout cisplatin-resistant HeLa_CisR ( D ) and C33A_CisR ( E ) cells expressing empty vector (EV), MTS-HMGCS1, or NLS-HMGCS1. Cell viability was determined using SRB assay. Data are presented as mean ± SD. IC50 values are indicated. Statistical significance was determined by pairwise comparison of the LogIC50 value for each construct against the EV control using the Extra sum-of-squares F-test, with a Bonferroni correction for multiple comparisons (*** p < 0.001, ns: not significant)

    Journal: BMC Molecular and Cell Biology

    Article Title: Mitochondrial HMGCS1 mediates cisplatin resistance in cervical cancer through regulation of mitochondrial transcription

    doi: 10.1186/s12860-026-00566-y

    Figure Lengend Snippet: Subcellular localization of HMGCS1 determines its role in cisplatin resistance. ( A ) Immunofluorescence microscopy of HeLa and C33A cells expressing 6xHis-tagged NLS-HMGCS1 or MTS-HMGCS1. Cells were stained with DAPI (blue) for nuclei, anti-6xHis antibody (green) for tagged HMGCS1, and MitoTracker (red) for mitochondria. Merged images show the distinct subcellular localization of each construct. ( B- E ) Dose-response curves showing cell viability after cisplatin treatment (72 h) in: parental HeLa ( B ) and C33A ( C ) cells; and HMGCS1-knockout cisplatin-resistant HeLa_CisR ( D ) and C33A_CisR ( E ) cells expressing empty vector (EV), MTS-HMGCS1, or NLS-HMGCS1. Cell viability was determined using SRB assay. Data are presented as mean ± SD. IC50 values are indicated. Statistical significance was determined by pairwise comparison of the LogIC50 value for each construct against the EV control using the Extra sum-of-squares F-test, with a Bonferroni correction for multiple comparisons (*** p < 0.001, ns: not significant)

    Article Snippet: Cervical cancer cell lines HeLa and C33A were obtained from American Type Culture Collection (ATCC) and maintained in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin at 37 °C with 5% CO2.

    Techniques: Immunofluorescence, Microscopy, Expressing, Staining, Construct, Knock-Out, Plasmid Preparation, Sulforhodamine B Assay, Comparison, Control

    Mitochondrial HMGCS1 enhances oxidative phosphorylation and regulates redox homeostasis in cisplatin-resistant cervical cancer cells. ( A , C ) Mitochondrial respiration profiles showing oxygen consumption rate (OCR) in parental and cisplatin-resistant (CisR) HeLa ( A ) and C33A ( C ) cells. Sequential addition of oligomycin (O), FCCP (F), and rotenone/antimycin A (R/A) is indicated by arrows. ( B , D ) Quantification of basal and maximal respiratory capacity in parental and cisplatin-resistant HeLa ( B ) and C33A ( D ) cells. ( E ) Relative intracellular cholesterol levels in parental and cisplatin-resistant HeLa and C33A cells as measured by a commercial cholesterol assay kit. ( F , H ) Mitochondrial respiration profiles of wild-type (WT), HMGCS1-knockout (KO), and KO cells expressing NLS-HMGCS1 (KO + NLS) or MTS-HMGCS1 (KO + MTS) in HeLa_CisR ( F ) and C33A_CisR ( H ) cells. ( G , I ) Quantification of basal and maximal respiratory capacity in WT, KO, and rescued HeLa_CisR ( G ) and C33A_CisR ( I ) cells. ( J) Relative ROS levels in wild-type, HMGCS1-knockout, and rescued HeLa_CisR and C33A_CisR cells measured by measured by ROS Deep Red fluorescence. Data are presented as mean ± SD. Statistical significance for panels G , I , and J was determined by One-way ANOVA with Dunnett’s multiple comparisons test. Comparisons in panels B , D , and E were made using Student’s t-test: ** p < 0.01, *** p < 0.001, ns: not significant, by Student’s t-test

    Journal: BMC Molecular and Cell Biology

    Article Title: Mitochondrial HMGCS1 mediates cisplatin resistance in cervical cancer through regulation of mitochondrial transcription

    doi: 10.1186/s12860-026-00566-y

    Figure Lengend Snippet: Mitochondrial HMGCS1 enhances oxidative phosphorylation and regulates redox homeostasis in cisplatin-resistant cervical cancer cells. ( A , C ) Mitochondrial respiration profiles showing oxygen consumption rate (OCR) in parental and cisplatin-resistant (CisR) HeLa ( A ) and C33A ( C ) cells. Sequential addition of oligomycin (O), FCCP (F), and rotenone/antimycin A (R/A) is indicated by arrows. ( B , D ) Quantification of basal and maximal respiratory capacity in parental and cisplatin-resistant HeLa ( B ) and C33A ( D ) cells. ( E ) Relative intracellular cholesterol levels in parental and cisplatin-resistant HeLa and C33A cells as measured by a commercial cholesterol assay kit. ( F , H ) Mitochondrial respiration profiles of wild-type (WT), HMGCS1-knockout (KO), and KO cells expressing NLS-HMGCS1 (KO + NLS) or MTS-HMGCS1 (KO + MTS) in HeLa_CisR ( F ) and C33A_CisR ( H ) cells. ( G , I ) Quantification of basal and maximal respiratory capacity in WT, KO, and rescued HeLa_CisR ( G ) and C33A_CisR ( I ) cells. ( J) Relative ROS levels in wild-type, HMGCS1-knockout, and rescued HeLa_CisR and C33A_CisR cells measured by measured by ROS Deep Red fluorescence. Data are presented as mean ± SD. Statistical significance for panels G , I , and J was determined by One-way ANOVA with Dunnett’s multiple comparisons test. Comparisons in panels B , D , and E were made using Student’s t-test: ** p < 0.01, *** p < 0.001, ns: not significant, by Student’s t-test

    Article Snippet: Cervical cancer cell lines HeLa and C33A were obtained from American Type Culture Collection (ATCC) and maintained in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin at 37 °C with 5% CO2.

    Techniques: Phospho-proteomics, Cholesterol Assay, Knock-Out, Expressing, Fluorescence

    Mitochondrial HMGCS1 enhances mtDNA-encoded gene expression without affecting mtDNA copy number in cisplatin-resistant cells. ( A - B ) Relative mRNA expression levels of mtDNA-encoded respiratory complex genes (MT-ND1, MT-ND5, MT-CO1, MT-CYB, and MT-ATP6) in HeLa_CisR ( A ) and C33A_CisR ( B ) cells with indicated HMGCS1 status: wild-type (WT), knockout (KO), nuclear-localized HMGCS1 (NLS), or mitochondria-targeted HMGCS1 (MTS). ( C ) Relative mtDNA copy number quantification in HeLa_CisR and C33A_CisR cells with different HMGCS1 status. Data are presented as mean ± SD. Statistical significance was determined using Two-way ANOVA ( A , B ) or One-way ANOVA ( C ), followed by Dunnett’s multiple comparisons test: *** p < 0.001, ns: not significant

    Journal: BMC Molecular and Cell Biology

    Article Title: Mitochondrial HMGCS1 mediates cisplatin resistance in cervical cancer through regulation of mitochondrial transcription

    doi: 10.1186/s12860-026-00566-y

    Figure Lengend Snippet: Mitochondrial HMGCS1 enhances mtDNA-encoded gene expression without affecting mtDNA copy number in cisplatin-resistant cells. ( A - B ) Relative mRNA expression levels of mtDNA-encoded respiratory complex genes (MT-ND1, MT-ND5, MT-CO1, MT-CYB, and MT-ATP6) in HeLa_CisR ( A ) and C33A_CisR ( B ) cells with indicated HMGCS1 status: wild-type (WT), knockout (KO), nuclear-localized HMGCS1 (NLS), or mitochondria-targeted HMGCS1 (MTS). ( C ) Relative mtDNA copy number quantification in HeLa_CisR and C33A_CisR cells with different HMGCS1 status. Data are presented as mean ± SD. Statistical significance was determined using Two-way ANOVA ( A , B ) or One-way ANOVA ( C ), followed by Dunnett’s multiple comparisons test: *** p < 0.001, ns: not significant

    Article Snippet: Cervical cancer cell lines HeLa and C33A were obtained from American Type Culture Collection (ATCC) and maintained in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin at 37 °C with 5% CO2.

    Techniques: Gene Expression, Expressing, Knock-Out

    HMGCS1 inhibitor and mitochondrial transcription inhibitor synergize with cisplatin in drug-resistant cervical cancer cells. ( A - D ) Dose-response curves showing cell viability of cisplatin-resistant cells treated with increasing concentrations of cisplatin alone (DMSO control) or in combination with 2 µM hymeglusin or 1 µM IMT1B. Curves are shown for parental HeLa_CisR ( A ) and C33A_CisR ( B ) cells, and for their HMGCS1 knockout (KO) counterparts, HeLa_CisR HMGCS1 KO ( C ) and C33A_CisR HMGCS1 KO ( D ). IC50 values are indicated for each treatment condition. Statistical significance was determined by pairwise comparison of the LogIC50 value for each construct against the EV control using the Extra sum-of-squares F-test, with a Bonferroni correction for multiple comparisons (*** p < 0.001, ns: not significant). ( E - H ) Synergy analysis of drug combinations in resistant cells using the Bliss independence model. Heat maps show synergy scores for various concentration combinations of cisplatin with hymeglusin in ( E ) HeLa_CisR and ( F ) C33A_CisR cells, or with IMT1B in ( G ) HeLa_CisR and ( H ) C33A_CisR cells. Positive values (blue) indicate synergistic interactions, values near zero (white) indicate additive effects, and negative values (red) indicate antagonistic interactions

    Journal: BMC Molecular and Cell Biology

    Article Title: Mitochondrial HMGCS1 mediates cisplatin resistance in cervical cancer through regulation of mitochondrial transcription

    doi: 10.1186/s12860-026-00566-y

    Figure Lengend Snippet: HMGCS1 inhibitor and mitochondrial transcription inhibitor synergize with cisplatin in drug-resistant cervical cancer cells. ( A - D ) Dose-response curves showing cell viability of cisplatin-resistant cells treated with increasing concentrations of cisplatin alone (DMSO control) or in combination with 2 µM hymeglusin or 1 µM IMT1B. Curves are shown for parental HeLa_CisR ( A ) and C33A_CisR ( B ) cells, and for their HMGCS1 knockout (KO) counterparts, HeLa_CisR HMGCS1 KO ( C ) and C33A_CisR HMGCS1 KO ( D ). IC50 values are indicated for each treatment condition. Statistical significance was determined by pairwise comparison of the LogIC50 value for each construct against the EV control using the Extra sum-of-squares F-test, with a Bonferroni correction for multiple comparisons (*** p < 0.001, ns: not significant). ( E - H ) Synergy analysis of drug combinations in resistant cells using the Bliss independence model. Heat maps show synergy scores for various concentration combinations of cisplatin with hymeglusin in ( E ) HeLa_CisR and ( F ) C33A_CisR cells, or with IMT1B in ( G ) HeLa_CisR and ( H ) C33A_CisR cells. Positive values (blue) indicate synergistic interactions, values near zero (white) indicate additive effects, and negative values (red) indicate antagonistic interactions

    Article Snippet: Cervical cancer cell lines HeLa and C33A were obtained from American Type Culture Collection (ATCC) and maintained in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin at 37 °C with 5% CO2.

    Techniques: Control, Knock-Out, Comparison, Construct, Concentration Assay

    Detection of wild-type and mutant FZD4 on downstream signal proteins by luciferase reporter gene assay. FZD4-wild-type (FZD4-WT) and FZD4-mutant (FZD4-MU) represent the relative luciferase activity ascertained from the transfection of wild-type FZD4 plasmid and mutant FZD4 plasmid into Hela cells, respectively. Data are representative of three independent experiments. The experimental data are presented as the mean ± standard deviation (mean ± SD). Differences between groups were assessed using the Student’s t -test, and * P < 0.05.

    Journal: Scientific Reports

    Article Title: A novel variant p.Y250C of FZD4 influences Norrine/β-catenin signaling pathway that associates with familial exudative vitreoretinopathy (FEVR)

    doi: 10.1038/s41598-025-34442-0

    Figure Lengend Snippet: Detection of wild-type and mutant FZD4 on downstream signal proteins by luciferase reporter gene assay. FZD4-wild-type (FZD4-WT) and FZD4-mutant (FZD4-MU) represent the relative luciferase activity ascertained from the transfection of wild-type FZD4 plasmid and mutant FZD4 plasmid into Hela cells, respectively. Data are representative of three independent experiments. The experimental data are presented as the mean ± standard deviation (mean ± SD). Differences between groups were assessed using the Student’s t -test, and * P < 0.05.

    Article Snippet: The human cervical cancer HeLa cell line was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) and maintained at a temperature of 37 °C in Dulbecco’s Modified Eagle Medium (DMEM) enriched with 10% Fetal Bovine Serum (FBS) and 1% penicillin/streptomycin.

    Techniques: Mutagenesis, Luciferase, Reporter Gene Assay, Activity Assay, Transfection, Plasmid Preparation, Standard Deviation

    Immunostaining for FZD4 and Calnexin. The immunostaining for wild-type or mutant FZD4 and Calnexin in Hela cells. FZD4 protein shows in the green image on the left side of the panel; Calnexin displays with red image; nucleus shows in the blue image; the merge of them shows on the right side. Scale bar: 10 μm. Magnification: × 50.

    Journal: Scientific Reports

    Article Title: A novel variant p.Y250C of FZD4 influences Norrine/β-catenin signaling pathway that associates with familial exudative vitreoretinopathy (FEVR)

    doi: 10.1038/s41598-025-34442-0

    Figure Lengend Snippet: Immunostaining for FZD4 and Calnexin. The immunostaining for wild-type or mutant FZD4 and Calnexin in Hela cells. FZD4 protein shows in the green image on the left side of the panel; Calnexin displays with red image; nucleus shows in the blue image; the merge of them shows on the right side. Scale bar: 10 μm. Magnification: × 50.

    Article Snippet: The human cervical cancer HeLa cell line was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) and maintained at a temperature of 37 °C in Dulbecco’s Modified Eagle Medium (DMEM) enriched with 10% Fetal Bovine Serum (FBS) and 1% penicillin/streptomycin.

    Techniques: Immunostaining, Mutagenesis

    Subcellular localizations and nuclear entry ratios of wild-type and mutant FZD4 proteins. ( A – C ) Subcellular localization of wild-type FZD4 protein express throughout the cytoplasm in HeLa cells, without highlights. ( D – F ) Subcellular localization of wild-type FZD4 protein aggregate on cell membrane and cytoplasm of HeLa cells, with highlights. ( G – I ) Subcellular localization of mutant FZD4 protein express throughout the cytoplasm in HeLa cells, without highlights. ( J – L ) Subcellular localization of mutant FZD4 protein aggregate on nucleic membrane and nucleus of HeLa cells, with highlights. The highlights represent the aggregation of GFP-labeled FZD4 protein. FZD4 protein shows in the green image on the left side of the panel; nucleus shows in the blue image in the middle; the merge of them shows on the right side. M: The ratio of wild-type FZD4 and mutant FZD4 proteins entering the nucleus. FZD4-WT represents the proportion of wild-type FZD4 protein entering the nucleus, while FZD4-MUT denotes the proportion of mutant FZD4 protein entering the nucleus. * P < 0.05. Scale bar: 5 μm. Magnification: × 50.

    Journal: Scientific Reports

    Article Title: A novel variant p.Y250C of FZD4 influences Norrine/β-catenin signaling pathway that associates with familial exudative vitreoretinopathy (FEVR)

    doi: 10.1038/s41598-025-34442-0

    Figure Lengend Snippet: Subcellular localizations and nuclear entry ratios of wild-type and mutant FZD4 proteins. ( A – C ) Subcellular localization of wild-type FZD4 protein express throughout the cytoplasm in HeLa cells, without highlights. ( D – F ) Subcellular localization of wild-type FZD4 protein aggregate on cell membrane and cytoplasm of HeLa cells, with highlights. ( G – I ) Subcellular localization of mutant FZD4 protein express throughout the cytoplasm in HeLa cells, without highlights. ( J – L ) Subcellular localization of mutant FZD4 protein aggregate on nucleic membrane and nucleus of HeLa cells, with highlights. The highlights represent the aggregation of GFP-labeled FZD4 protein. FZD4 protein shows in the green image on the left side of the panel; nucleus shows in the blue image in the middle; the merge of them shows on the right side. M: The ratio of wild-type FZD4 and mutant FZD4 proteins entering the nucleus. FZD4-WT represents the proportion of wild-type FZD4 protein entering the nucleus, while FZD4-MUT denotes the proportion of mutant FZD4 protein entering the nucleus. * P < 0.05. Scale bar: 5 μm. Magnification: × 50.

    Article Snippet: The human cervical cancer HeLa cell line was obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) and maintained at a temperature of 37 °C in Dulbecco’s Modified Eagle Medium (DMEM) enriched with 10% Fetal Bovine Serum (FBS) and 1% penicillin/streptomycin.

    Techniques: Mutagenesis, Membrane, Labeling