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human bronchial epithelial cells hbec  (ATCC)


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    ATCC human bronchial epithelial cells hbec
    Human Bronchial Epithelial Cells Hbec, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 310 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+bronchial+epithelial+cells+hbec/pmc13011240-24-0-6?v=ATCC
    Average 99 stars, based on 310 article reviews
    human bronchial epithelial cells hbec - by Bioz Stars, 2026-07
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    ATCC human bronchial epithelial cells hbec
    Human Bronchial Epithelial Cells Hbec, 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
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    PromoCell bronchial epithelial cells hbecs
    A) Immunoblot of FcRn and pIgR in hNECs and <t>hBECs.</t> B, C) Relative protein expression levels by Western blotting of FcRN, pIgR, normalized to β-tublin, n = <3. D, E) Quantification of flow cytometry cell types by percentage of total cells, values are expressed as mean ± SE, n = 1/group. F, G) Transcytosis of IgG and IgA was determined using an ELISA assay. Values are expressed as mean ± SE, n = <3well/time point. *P<0.05 **P<0.01
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    Procell Inc primary human bronchial epithelial cells hbecs
    Verification of angiotensin-converting enzyme 2 (ACE2) inhibition using a series of DX600 concentrations and the corresponding viral infection efficiency in wild-type A549 (alveolar basal <t>epithelial</t> adenocarcinoma cells) ( a ), rs1788783 knockout (KO) A549 ( b ), primary human bronchial epithelial cells <t>(HBECs)</t> ( c ), and BEAS-2B (human bronchial epithelial cells) ( d ), respectively. Relative luminescence intensities are presented as mean ± standard deviation ( n = 10) from 10 biological replicates. Exact P values are shown in the figure. Reduced NPC1 expression levels using 3 distinct small interfering RNAs (siRNAs) and negative control siRNA (NC siRNA), and the corresponding viral infection efficiency in primary human bronchial epithelial cells (HBECs) ( e ) and BEAS-2B (human bronchial epithelial cells) ( f ), respectively. Viral infection was quantified by the expression levels of open reading frame 1 (ORF1) and nucleocapsid (N) genes. Data are presented as mean ± standard deviation ( n = 3) from 3 biological replicates. Statistical significance was assessed using two-sided t-tests. Source data are available in the file.
    Primary Human Bronchial Epithelial Cells Hbecs, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Verification of angiotensin-converting enzyme 2 (ACE2) inhibition using a series of DX600 concentrations and the corresponding viral infection efficiency in wild-type A549 (alveolar basal <t>epithelial</t> adenocarcinoma cells) ( a ), rs1788783 knockout (KO) A549 ( b ), primary human bronchial epithelial cells <t>(HBECs)</t> ( c ), and BEAS-2B (human bronchial epithelial cells) ( d ), respectively. Relative luminescence intensities are presented as mean ± standard deviation ( n = 10) from 10 biological replicates. Exact P values are shown in the figure. Reduced NPC1 expression levels using 3 distinct small interfering RNAs (siRNAs) and negative control siRNA (NC siRNA), and the corresponding viral infection efficiency in primary human bronchial epithelial cells (HBECs) ( e ) and BEAS-2B (human bronchial epithelial cells) ( f ), respectively. Viral infection was quantified by the expression levels of open reading frame 1 (ORF1) and nucleocapsid (N) genes. Data are presented as mean ± standard deviation ( n = 3) from 3 biological replicates. Statistical significance was assessed using two-sided t-tests. Source data are available in the file.
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    Verification of angiotensin-converting enzyme 2 (ACE2) inhibition using a series of DX600 concentrations and the corresponding viral infection efficiency in wild-type A549 (alveolar basal <t>epithelial</t> adenocarcinoma cells) ( a ), rs1788783 knockout (KO) A549 ( b ), primary human bronchial epithelial cells <t>(HBECs)</t> ( c ), and BEAS-2B (human bronchial epithelial cells) ( d ), respectively. Relative luminescence intensities are presented as mean ± standard deviation ( n = 10) from 10 biological replicates. Exact P values are shown in the figure. Reduced NPC1 expression levels using 3 distinct small interfering RNAs (siRNAs) and negative control siRNA (NC siRNA), and the corresponding viral infection efficiency in primary human bronchial epithelial cells (HBECs) ( e ) and BEAS-2B (human bronchial epithelial cells) ( f ), respectively. Viral infection was quantified by the expression levels of open reading frame 1 (ORF1) and nucleocapsid (N) genes. Data are presented as mean ± standard deviation ( n = 3) from 3 biological replicates. Statistical significance was assessed using two-sided t-tests. Source data are available in the file.
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    Procell Inc human bronchial epithelial cells hbec
    A –C Pseudovirus infection assays. Control and UHRF1 -knockout A549-ACE2 cells were infected with VSV-based pseudoviruses. D –F Virus binding and internalization assays. Cells were incubated with HCoV-229E (MOI 10). Bound or internalized virions were quantified by qRT-PCR or analyzed by confocal microscopy. Representative images from three independent experiments were shown. G , H Western blotting analysis of gene expression in gene-knockout A549 or HeLa cells. Representative images from three independent experiments were shown. I Infection efficiency of HCoV-229E (MOI 0.5, 24 h) in control and UHRF1 -knockout HeLa cells, determined by flow cytometry. J . Relative APN mRNA levels and infection efficiency of HCoV-229E (MOI 1, 12 h) in control and UHRF1 -knockout primary human bronchial <t>epithelial</t> cells <t>(HBEC).</t> mRNA levels were analyzed by qRT-PCR, and infectivity was determined by flow cytometry. K Temporal expression of APN in UHRF1 -knockout A549 cells. Cell lysates were collected at different days post-transduction of sgRNA-expressing lentivirus and analyzed by western blotting. Representative images from three independent experiments were shown. L Surface expression of APN analyzed by flow cytometry in A549 cells edited with control or UHRF1 sgRNA. M Relative APN mRNA levels analyzed by qRT-PCR in A549 cells edited with control or UHRF1 sgRNA. N Relative APN mRNA levels analyzed by qRT-PCR in A549 cells treated with UHRF1 inhibitor UF146 for 2 days. O Control and two APN -knockout A549 clonal cell lines were edited with control or UHRF1 sgRNA, and infected with HCoV-229E (MOI 0.5, 24 h). Infectivity was determined by flow cytometry. P UHRF1 -knockout cells were pre-treated with 5 μg/ml APN-blocking antibody or isotype control for 1 h, then infected with HCoV-229E (MOI 0.5, 24 h) in the presence of antibody. qRT-PCR was performed to determine the relative levels of HCoV-229E N gene. Error bars represent standard deviations from three independent experiments ( n = 3), and each performed in duplicate. Unpaired, two-sided t-test ( A – C , I , J , M ); two-way ANOVA with Sidak’s test ( D, O ); one-way ANOVA with Sidak’s test ( N , P ); mean ± s.d.; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, not significant.
    Human Bronchial Epithelial Cells Hbec, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC primary hbec
    A –C Pseudovirus infection assays. Control and UHRF1 -knockout A549-ACE2 cells were infected with VSV-based pseudoviruses. D –F Virus binding and internalization assays. Cells were incubated with HCoV-229E (MOI 10). Bound or internalized virions were quantified by qRT-PCR or analyzed by confocal microscopy. Representative images from three independent experiments were shown. G , H Western blotting analysis of gene expression in gene-knockout A549 or HeLa cells. Representative images from three independent experiments were shown. I Infection efficiency of HCoV-229E (MOI 0.5, 24 h) in control and UHRF1 -knockout HeLa cells, determined by flow cytometry. J . Relative APN mRNA levels and infection efficiency of HCoV-229E (MOI 1, 12 h) in control and UHRF1 -knockout primary human bronchial <t>epithelial</t> cells <t>(HBEC).</t> mRNA levels were analyzed by qRT-PCR, and infectivity was determined by flow cytometry. K Temporal expression of APN in UHRF1 -knockout A549 cells. Cell lysates were collected at different days post-transduction of sgRNA-expressing lentivirus and analyzed by western blotting. Representative images from three independent experiments were shown. L Surface expression of APN analyzed by flow cytometry in A549 cells edited with control or UHRF1 sgRNA. M Relative APN mRNA levels analyzed by qRT-PCR in A549 cells edited with control or UHRF1 sgRNA. N Relative APN mRNA levels analyzed by qRT-PCR in A549 cells treated with UHRF1 inhibitor UF146 for 2 days. O Control and two APN -knockout A549 clonal cell lines were edited with control or UHRF1 sgRNA, and infected with HCoV-229E (MOI 0.5, 24 h). Infectivity was determined by flow cytometry. P UHRF1 -knockout cells were pre-treated with 5 μg/ml APN-blocking antibody or isotype control for 1 h, then infected with HCoV-229E (MOI 0.5, 24 h) in the presence of antibody. qRT-PCR was performed to determine the relative levels of HCoV-229E N gene. Error bars represent standard deviations from three independent experiments ( n = 3), and each performed in duplicate. Unpaired, two-sided t-test ( A – C , I , J , M ); two-way ANOVA with Sidak’s test ( D, O ); one-way ANOVA with Sidak’s test ( N , P ); mean ± s.d.; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, not significant.
    Primary Hbec, 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
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    ATCC human bronchial epithelial cells hbec kt
    A –C Pseudovirus infection assays. Control and UHRF1 -knockout A549-ACE2 cells were infected with VSV-based pseudoviruses. D –F Virus binding and internalization assays. Cells were incubated with HCoV-229E (MOI 10). Bound or internalized virions were quantified by qRT-PCR or analyzed by confocal microscopy. Representative images from three independent experiments were shown. G , H Western blotting analysis of gene expression in gene-knockout A549 or HeLa cells. Representative images from three independent experiments were shown. I Infection efficiency of HCoV-229E (MOI 0.5, 24 h) in control and UHRF1 -knockout HeLa cells, determined by flow cytometry. J . Relative APN mRNA levels and infection efficiency of HCoV-229E (MOI 1, 12 h) in control and UHRF1 -knockout primary human bronchial <t>epithelial</t> cells <t>(HBEC).</t> mRNA levels were analyzed by qRT-PCR, and infectivity was determined by flow cytometry. K Temporal expression of APN in UHRF1 -knockout A549 cells. Cell lysates were collected at different days post-transduction of sgRNA-expressing lentivirus and analyzed by western blotting. Representative images from three independent experiments were shown. L Surface expression of APN analyzed by flow cytometry in A549 cells edited with control or UHRF1 sgRNA. M Relative APN mRNA levels analyzed by qRT-PCR in A549 cells edited with control or UHRF1 sgRNA. N Relative APN mRNA levels analyzed by qRT-PCR in A549 cells treated with UHRF1 inhibitor UF146 for 2 days. O Control and two APN -knockout A549 clonal cell lines were edited with control or UHRF1 sgRNA, and infected with HCoV-229E (MOI 0.5, 24 h). Infectivity was determined by flow cytometry. P UHRF1 -knockout cells were pre-treated with 5 μg/ml APN-blocking antibody or isotype control for 1 h, then infected with HCoV-229E (MOI 0.5, 24 h) in the presence of antibody. qRT-PCR was performed to determine the relative levels of HCoV-229E N gene. Error bars represent standard deviations from three independent experiments ( n = 3), and each performed in duplicate. Unpaired, two-sided t-test ( A – C , I , J , M ); two-way ANOVA with Sidak’s test ( D, O ); one-way ANOVA with Sidak’s test ( N , P ); mean ± s.d.; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, not significant.
    Human Bronchial Epithelial Cells Hbec Kt, 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
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    Image Search Results


    A) Immunoblot of FcRn and pIgR in hNECs and hBECs. B, C) Relative protein expression levels by Western blotting of FcRN, pIgR, normalized to β-tublin, n = <3. D, E) Quantification of flow cytometry cell types by percentage of total cells, values are expressed as mean ± SE, n = 1/group. F, G) Transcytosis of IgG and IgA was determined using an ELISA assay. Values are expressed as mean ± SE, n = <3well/time point. *P<0.05 **P<0.01

    Journal: bioRxiv

    Article Title: Antibody Transcytosis and Neutralizing Activity in Respiratory Epithelial Cells

    doi: 10.64898/2026.05.25.727697

    Figure Lengend Snippet: A) Immunoblot of FcRn and pIgR in hNECs and hBECs. B, C) Relative protein expression levels by Western blotting of FcRN, pIgR, normalized to β-tublin, n = <3. D, E) Quantification of flow cytometry cell types by percentage of total cells, values are expressed as mean ± SE, n = 1/group. F, G) Transcytosis of IgG and IgA was determined using an ELISA assay. Values are expressed as mean ± SE, n = <3well/time point. *P<0.05 **P<0.01

    Article Snippet: Human nasal epithelial cells (hNECs) or bronchial epithelial cells (hBECs) (Promocell) were grown to confluence in 24-well Falcon filter inserts (0.4-uM pore; 0.33cm 2 ; Becton Dickinson) using PneumaCultTM-Ex Plus Medium (Stemcell, Cat# 05001).

    Techniques: Western Blot, Expressing, Flow Cytometry, Enzyme-linked Immunosorbent Assay

    Verification of angiotensin-converting enzyme 2 (ACE2) inhibition using a series of DX600 concentrations and the corresponding viral infection efficiency in wild-type A549 (alveolar basal epithelial adenocarcinoma cells) ( a ), rs1788783 knockout (KO) A549 ( b ), primary human bronchial epithelial cells (HBECs) ( c ), and BEAS-2B (human bronchial epithelial cells) ( d ), respectively. Relative luminescence intensities are presented as mean ± standard deviation ( n = 10) from 10 biological replicates. Exact P values are shown in the figure. Reduced NPC1 expression levels using 3 distinct small interfering RNAs (siRNAs) and negative control siRNA (NC siRNA), and the corresponding viral infection efficiency in primary human bronchial epithelial cells (HBECs) ( e ) and BEAS-2B (human bronchial epithelial cells) ( f ), respectively. Viral infection was quantified by the expression levels of open reading frame 1 (ORF1) and nucleocapsid (N) genes. Data are presented as mean ± standard deviation ( n = 3) from 3 biological replicates. Statistical significance was assessed using two-sided t-tests. Source data are available in the file.

    Journal: Nature Communications

    Article Title: AI-guided multi-omics analysis identifies NPC1-modulated susceptibility to SARS-CoV-2 infection under PM 2.5 exposure

    doi: 10.1038/s41467-026-71196-3

    Figure Lengend Snippet: Verification of angiotensin-converting enzyme 2 (ACE2) inhibition using a series of DX600 concentrations and the corresponding viral infection efficiency in wild-type A549 (alveolar basal epithelial adenocarcinoma cells) ( a ), rs1788783 knockout (KO) A549 ( b ), primary human bronchial epithelial cells (HBECs) ( c ), and BEAS-2B (human bronchial epithelial cells) ( d ), respectively. Relative luminescence intensities are presented as mean ± standard deviation ( n = 10) from 10 biological replicates. Exact P values are shown in the figure. Reduced NPC1 expression levels using 3 distinct small interfering RNAs (siRNAs) and negative control siRNA (NC siRNA), and the corresponding viral infection efficiency in primary human bronchial epithelial cells (HBECs) ( e ) and BEAS-2B (human bronchial epithelial cells) ( f ), respectively. Viral infection was quantified by the expression levels of open reading frame 1 (ORF1) and nucleocapsid (N) genes. Data are presented as mean ± standard deviation ( n = 3) from 3 biological replicates. Statistical significance was assessed using two-sided t-tests. Source data are available in the file.

    Article Snippet: Primary human bronchial epithelial cells (HBECs) were provided by Procell Life Science & Technology Co., Ltd (China, #CP-H009).

    Techniques: Inhibition, Infection, Knock-Out, Standard Deviation, Expressing, Negative Control

    A –C Pseudovirus infection assays. Control and UHRF1 -knockout A549-ACE2 cells were infected with VSV-based pseudoviruses. D –F Virus binding and internalization assays. Cells were incubated with HCoV-229E (MOI 10). Bound or internalized virions were quantified by qRT-PCR or analyzed by confocal microscopy. Representative images from three independent experiments were shown. G , H Western blotting analysis of gene expression in gene-knockout A549 or HeLa cells. Representative images from three independent experiments were shown. I Infection efficiency of HCoV-229E (MOI 0.5, 24 h) in control and UHRF1 -knockout HeLa cells, determined by flow cytometry. J . Relative APN mRNA levels and infection efficiency of HCoV-229E (MOI 1, 12 h) in control and UHRF1 -knockout primary human bronchial epithelial cells (HBEC). mRNA levels were analyzed by qRT-PCR, and infectivity was determined by flow cytometry. K Temporal expression of APN in UHRF1 -knockout A549 cells. Cell lysates were collected at different days post-transduction of sgRNA-expressing lentivirus and analyzed by western blotting. Representative images from three independent experiments were shown. L Surface expression of APN analyzed by flow cytometry in A549 cells edited with control or UHRF1 sgRNA. M Relative APN mRNA levels analyzed by qRT-PCR in A549 cells edited with control or UHRF1 sgRNA. N Relative APN mRNA levels analyzed by qRT-PCR in A549 cells treated with UHRF1 inhibitor UF146 for 2 days. O Control and two APN -knockout A549 clonal cell lines were edited with control or UHRF1 sgRNA, and infected with HCoV-229E (MOI 0.5, 24 h). Infectivity was determined by flow cytometry. P UHRF1 -knockout cells were pre-treated with 5 μg/ml APN-blocking antibody or isotype control for 1 h, then infected with HCoV-229E (MOI 0.5, 24 h) in the presence of antibody. qRT-PCR was performed to determine the relative levels of HCoV-229E N gene. Error bars represent standard deviations from three independent experiments ( n = 3), and each performed in duplicate. Unpaired, two-sided t-test ( A – C , I , J , M ); two-way ANOVA with Sidak’s test ( D, O ); one-way ANOVA with Sidak’s test ( N , P ); mean ± s.d.; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, not significant.

    Journal: Nature Communications

    Article Title: UHRF1 restricts HCoV-229E infection through epigenetic silencing of the viral receptor APN

    doi: 10.1038/s41467-025-64977-9

    Figure Lengend Snippet: A –C Pseudovirus infection assays. Control and UHRF1 -knockout A549-ACE2 cells were infected with VSV-based pseudoviruses. D –F Virus binding and internalization assays. Cells were incubated with HCoV-229E (MOI 10). Bound or internalized virions were quantified by qRT-PCR or analyzed by confocal microscopy. Representative images from three independent experiments were shown. G , H Western blotting analysis of gene expression in gene-knockout A549 or HeLa cells. Representative images from three independent experiments were shown. I Infection efficiency of HCoV-229E (MOI 0.5, 24 h) in control and UHRF1 -knockout HeLa cells, determined by flow cytometry. J . Relative APN mRNA levels and infection efficiency of HCoV-229E (MOI 1, 12 h) in control and UHRF1 -knockout primary human bronchial epithelial cells (HBEC). mRNA levels were analyzed by qRT-PCR, and infectivity was determined by flow cytometry. K Temporal expression of APN in UHRF1 -knockout A549 cells. Cell lysates were collected at different days post-transduction of sgRNA-expressing lentivirus and analyzed by western blotting. Representative images from three independent experiments were shown. L Surface expression of APN analyzed by flow cytometry in A549 cells edited with control or UHRF1 sgRNA. M Relative APN mRNA levels analyzed by qRT-PCR in A549 cells edited with control or UHRF1 sgRNA. N Relative APN mRNA levels analyzed by qRT-PCR in A549 cells treated with UHRF1 inhibitor UF146 for 2 days. O Control and two APN -knockout A549 clonal cell lines were edited with control or UHRF1 sgRNA, and infected with HCoV-229E (MOI 0.5, 24 h). Infectivity was determined by flow cytometry. P UHRF1 -knockout cells were pre-treated with 5 μg/ml APN-blocking antibody or isotype control for 1 h, then infected with HCoV-229E (MOI 0.5, 24 h) in the presence of antibody. qRT-PCR was performed to determine the relative levels of HCoV-229E N gene. Error bars represent standard deviations from three independent experiments ( n = 3), and each performed in duplicate. Unpaired, two-sided t-test ( A – C , I , J , M ); two-way ANOVA with Sidak’s test ( D, O ); one-way ANOVA with Sidak’s test ( N , P ); mean ± s.d.; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, not significant.

    Article Snippet: For validation in primary human bronchial epithelial cells (HBEC) (Procell #CP-H009) , , cells were prepared from fresh human bronchi of healthy donors.

    Techniques: Infection, Control, Knock-Out, Virus, Binding Assay, Incubation, Quantitative RT-PCR, Confocal Microscopy, Western Blot, Gene Expression, Gene Knockout, Flow Cytometry, Expressing, Transduction, Blocking Assay