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    ATCC human microvascular endothelial cells humec
    The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human <t>endothelial</t> and epithelial cells. The endogenous IFITMs mRNA levels in <t>HuMEC</t> ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).
    Human Microvascular Endothelial Cells Humec, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 54 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "IFITM1 inhibits Henipavirus membrane fusion by trapping ephrinB2 receptors in fusion-unfavorable membrane nanodomains"

    Article Title: IFITM1 inhibits Henipavirus membrane fusion by trapping ephrinB2 receptors in fusion-unfavorable membrane nanodomains

    Journal: bioRxiv

    doi: 10.64898/2026.05.06.723334

    The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human endothelial and epithelial cells. The endogenous IFITMs mRNA levels in HuMEC ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).
    Figure Legend Snippet: The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human endothelial and epithelial cells. The endogenous IFITMs mRNA levels in HuMEC ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).

    Techniques Used: Transfection, Expressing, Knockdown, Western Blot, Control, Luciferase, Virus, Labeling



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    The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human <t>endothelial</t> and epithelial cells. The endogenous IFITMs mRNA levels in <t>HuMEC</t> ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).
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    The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human endothelial and epithelial cells. The endogenous IFITMs mRNA levels in HuMEC ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).

    Journal: bioRxiv

    Article Title: IFITM1 inhibits Henipavirus membrane fusion by trapping ephrinB2 receptors in fusion-unfavorable membrane nanodomains

    doi: 10.64898/2026.05.06.723334

    Figure Lengend Snippet: The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human endothelial and epithelial cells. The endogenous IFITMs mRNA levels in HuMEC ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).

    Article Snippet: Human microvascular endothelial cells (HuMEC) (ATCC CRL-4060) were cultured in Vascular cell basal medium (ATCC, PCS-100-030) with Microvascular endothelial cell growth kit – BBE (ATCC, PCS-110-040) and 0.5 ug/ml puromycin (10 mg/ml stock, Gibco A1138-03).

    Techniques: Transfection, Expressing, Knockdown, Western Blot, Control, Luciferase, Virus, Labeling