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pcs 100 010 • vascular cell basal medium  (ATCC)


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    Structured Review

    ATCC pcs 100 010 • vascular cell basal medium
    Pcs 100 010 • Vascular Cell Basal Medium, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 283 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pcs 100 010 • vascular cell basal medium/product/ATCC
    Average 96 stars, based on 283 article reviews
    pcs 100 010 • vascular cell basal medium - by Bioz Stars, 2026-03
    96/100 stars

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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    ATCC human normal hepatocytes
    Inhibition of cell viability and colony formation, and induction of apoptosis by riluzole. (A) Expression of stem cell markers in HCC CSCs. CSCs were stained with CD44 and CD133 antibody and the expression of CD44 and CD133 was measured by immunocytochemistry. (B, C) HCC cell lines (HepG2 and Hep3B), cancer stem cells (CSCs), and human normal <t>hepatocytes</t> were seeded in 96‐well plates, treated with or without riluzole (0–40 μM) for 72 h, and cell viability was measured by CellTiter‐Glo Luminescent Cell Viability Assay (Promega). (D) Colony formation. HCC cell lines (HepG2, Hep3B, SNU‐382 and SNU‐475) and CSCs were treated with riluzole (0–20 μM). Number of colonies formed at 21 days was counted under a microscope. (E) Normal human hepatocytes, HCC cell lines (HepG2 and Hep3B) and CSCs were treated with riluzole (0–20 μM) for 72 h. Apoptosis was measured by TUNEL assay. Data represent mean ± SD ( n = 4). *, # and % = significantly different from control and each other; p < 0.05.
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    ATCC keratinocyte growth kit
    Inhibition of cell viability and colony formation, and induction of apoptosis by riluzole. (A) Expression of stem cell markers in HCC CSCs. CSCs were stained with CD44 and CD133 antibody and the expression of CD44 and CD133 was measured by immunocytochemistry. (B, C) HCC cell lines (HepG2 and Hep3B), cancer stem cells (CSCs), and human normal <t>hepatocytes</t> were seeded in 96‐well plates, treated with or without riluzole (0–40 μM) for 72 h, and cell viability was measured by CellTiter‐Glo Luminescent Cell Viability Assay (Promega). (D) Colony formation. HCC cell lines (HepG2, Hep3B, SNU‐382 and SNU‐475) and CSCs were treated with riluzole (0–20 μM). Number of colonies formed at 21 days was counted under a microscope. (E) Normal human hepatocytes, HCC cell lines (HepG2 and Hep3B) and CSCs were treated with riluzole (0–20 μM) for 72 h. Apoptosis was measured by TUNEL assay. Data represent mean ± SD ( n = 4). *, # and % = significantly different from control and each other; p < 0.05.
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    ATCC dermal cell basal medium
    Inhibition of cell viability and colony formation, and induction of apoptosis by riluzole. (A) Expression of stem cell markers in HCC CSCs. CSCs were stained with CD44 and CD133 antibody and the expression of CD44 and CD133 was measured by immunocytochemistry. (B, C) HCC cell lines (HepG2 and Hep3B), cancer stem cells (CSCs), and human normal <t>hepatocytes</t> were seeded in 96‐well plates, treated with or without riluzole (0–40 μM) for 72 h, and cell viability was measured by CellTiter‐Glo Luminescent Cell Viability Assay (Promega). (D) Colony formation. HCC cell lines (HepG2, Hep3B, SNU‐382 and SNU‐475) and CSCs were treated with riluzole (0–20 μM). Number of colonies formed at 21 days was counted under a microscope. (E) Normal human hepatocytes, HCC cell lines (HepG2 and Hep3B) and CSCs were treated with riluzole (0–20 μM) for 72 h. Apoptosis was measured by TUNEL assay. Data represent mean ± SD ( n = 4). *, # and % = significantly different from control and each other; p < 0.05.
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    ATCC human gingival epithelial cell line
    Photomicrograph of gingival <t>epithelial</t> cells used in the study at 80% confluence under an inverted microscope showing a characteristic cobblestone appearance. scale bar 100 µm.
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    ATCC human kidney epithelial cell line
    Photomicrograph of gingival <t>epithelial</t> cells used in the study at 80% confluence under an inverted microscope showing a characteristic cobblestone appearance. scale bar 100 µm.
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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for epithelial damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: The Cell Surface

    Article Title: Compromising UPD-sugar nucleotide biosynthesis attenuates Candida albicans viability, virulence and drug sensitivity

    doi: 10.1016/j.tcsw.2026.100170

    Figure Lengend Snippet: Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for epithelial damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: Human epithelial cells derived from a vulvar squamous cell carcinoma (A-431 cell line; ATCC No.: CRL-1555) were cultured and maintained in DMEM medium supplemented with 10% ( v /v) heat inactivated foetal calf serum, 5% penicillin and 5% streptomycin.

    Techniques: Lactate Dehydrogenase Assay, Incubation, Activity Assay, Control, Infection, Injection

    Inhibition of cell viability and colony formation, and induction of apoptosis by riluzole. (A) Expression of stem cell markers in HCC CSCs. CSCs were stained with CD44 and CD133 antibody and the expression of CD44 and CD133 was measured by immunocytochemistry. (B, C) HCC cell lines (HepG2 and Hep3B), cancer stem cells (CSCs), and human normal hepatocytes were seeded in 96‐well plates, treated with or without riluzole (0–40 μM) for 72 h, and cell viability was measured by CellTiter‐Glo Luminescent Cell Viability Assay (Promega). (D) Colony formation. HCC cell lines (HepG2, Hep3B, SNU‐382 and SNU‐475) and CSCs were treated with riluzole (0–20 μM). Number of colonies formed at 21 days was counted under a microscope. (E) Normal human hepatocytes, HCC cell lines (HepG2 and Hep3B) and CSCs were treated with riluzole (0–20 μM) for 72 h. Apoptosis was measured by TUNEL assay. Data represent mean ± SD ( n = 4). *, # and % = significantly different from control and each other; p < 0.05.

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Regulation of Autophagy and Metabolism in Hepatocellular Carcinoma: Involvement of Wnt‐β‐Catenin Pathway

    doi: 10.1111/jcmm.71070

    Figure Lengend Snippet: Inhibition of cell viability and colony formation, and induction of apoptosis by riluzole. (A) Expression of stem cell markers in HCC CSCs. CSCs were stained with CD44 and CD133 antibody and the expression of CD44 and CD133 was measured by immunocytochemistry. (B, C) HCC cell lines (HepG2 and Hep3B), cancer stem cells (CSCs), and human normal hepatocytes were seeded in 96‐well plates, treated with or without riluzole (0–40 μM) for 72 h, and cell viability was measured by CellTiter‐Glo Luminescent Cell Viability Assay (Promega). (D) Colony formation. HCC cell lines (HepG2, Hep3B, SNU‐382 and SNU‐475) and CSCs were treated with riluzole (0–20 μM). Number of colonies formed at 21 days was counted under a microscope. (E) Normal human hepatocytes, HCC cell lines (HepG2 and Hep3B) and CSCs were treated with riluzole (0–20 μM) for 72 h. Apoptosis was measured by TUNEL assay. Data represent mean ± SD ( n = 4). *, # and % = significantly different from control and each other; p < 0.05.

    Article Snippet: Human normal hepatocytes were purchased from ATCC.

    Techniques: Inhibition, Expressing, Staining, Immunocytochemistry, Cell Viability Assay, Microscopy, TUNEL Assay, Control

    Photomicrograph of gingival epithelial cells used in the study at 80% confluence under an inverted microscope showing a characteristic cobblestone appearance. scale bar 100 µm.

    Journal: Scientific Reports

    Article Title: The potential cytotoxic effect of recent universal adhesives with modified monomeric compositions on human gingival epithelial cells

    doi: 10.1038/s41598-026-38054-0

    Figure Lengend Snippet: Photomicrograph of gingival epithelial cells used in the study at 80% confluence under an inverted microscope showing a characteristic cobblestone appearance. scale bar 100 µm.

    Article Snippet: A human gingival epithelial cell line (ATCC CRL-3397) which was purchased from Nawah Scientific Inc. (Mokatam, Cairo, Egypt) was used in this study.

    Techniques: Inverted Microscopy