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caco 2bbe  (ATCC)


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    Structured Review

    ATCC caco 2bbe
    Pharmacological inhibition of NM II motor activity promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . Confluent differentiated HT-29cF8 (A and <t>B)</t> <t>Caco-2BBE</t> (C and D) cell monolayers were exposed to EPEC (MOI 5:1) for 3 h in the presence of either vehicle, blebbistatin (50 µM) or 4-HAP (100 µM). Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (A and C) or a colony forming assay (B and D). Mean ± SEM of combined data from three independent experiments, n = 9; **** p < 0.001; scale bar = 20 μm.
    Caco 2bbe, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 476 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/caco 2bbe/product/ATCC
    Average 95 stars, based on 476 article reviews
    caco 2bbe - by Bioz Stars, 2026-03
    95/100 stars

    Images

    1) Product Images from "Myosin IIA motor regulates attaching-effacing bacteria interactions with intestinal epithelium"

    Article Title: Myosin IIA motor regulates attaching-effacing bacteria interactions with intestinal epithelium

    Journal: Gut Microbes

    doi: 10.1080/19490976.2026.2638002

    Pharmacological inhibition of NM II motor activity promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . Confluent differentiated HT-29cF8 (A and B) Caco-2BBE (C and D) cell monolayers were exposed to EPEC (MOI 5:1) for 3 h in the presence of either vehicle, blebbistatin (50 µM) or 4-HAP (100 µM). Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (A and C) or a colony forming assay (B and D). Mean ± SEM of combined data from three independent experiments, n = 9; **** p < 0.001; scale bar = 20 μm.
    Figure Legend Snippet: Pharmacological inhibition of NM II motor activity promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . Confluent differentiated HT-29cF8 (A and B) Caco-2BBE (C and D) cell monolayers were exposed to EPEC (MOI 5:1) for 3 h in the presence of either vehicle, blebbistatin (50 µM) or 4-HAP (100 µM). Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (A and C) or a colony forming assay (B and D). Mean ± SEM of combined data from three independent experiments, n = 9; **** p < 0.001; scale bar = 20 μm.

    Techniques Used: Inhibition, Activity Assay, In Vitro, Immunofluorescence, Labeling, Confocal Microscopy

    CRISPR-Cas9-mediated knockout of NM IIA promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . (A and D) Immunoblotting analysis of NM IIA and NM IIC expression in HT-29cF8 and Caco-2BBE cells with CRISPR/Cas9-mediated knockout of NM IIA using two different sgRNAs. (B–E). Control and NM IIA knockout HT-29 (B and C) and Caco-2 (E and F) cells were infected with EPEC (MOI 5:1) for 3 h. Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (B and E) or colony forming assay (C and F). Mean ± SEM of combined data from three independent experiments, n = 9; *** p < 0.001, **** p < 0.0001; scale bar = 20 μm.
    Figure Legend Snippet: CRISPR-Cas9-mediated knockout of NM IIA promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . (A and D) Immunoblotting analysis of NM IIA and NM IIC expression in HT-29cF8 and Caco-2BBE cells with CRISPR/Cas9-mediated knockout of NM IIA using two different sgRNAs. (B–E). Control and NM IIA knockout HT-29 (B and C) and Caco-2 (E and F) cells were infected with EPEC (MOI 5:1) for 3 h. Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (B and E) or colony forming assay (C and F). Mean ± SEM of combined data from three independent experiments, n = 9; *** p < 0.001, **** p < 0.0001; scale bar = 20 μm.

    Techniques Used: CRISPR, Knock-Out, In Vitro, Western Blot, Expressing, Control, Infection, Immunofluorescence, Labeling, Confocal Microscopy

    Loss of intestinal epithelial NM IIC does not affect A/E bacterial interactions with the intestinal epithelium in vitro and in vivo . (A) Immunoblotting analysis of NM IIC and NM IIA expression in Caco-2BBE cells with CRISPR/Cas9-mediated knockout of NM IIC using two different sgRNAs. (B and C) Control and NM IIC knockout Caco-2 cells were infected with EPEC (MOI 5:1) for 3 h. Bacterial attachment to IECs was determined by either immunofluorescence labeling/confocal microscopy of LPS (B) or a colony-forming assay (C). Mean ± SEM of combined data from two independent experiments, n = 6; ns, not significant. (D) Immunoblotting analysis of NM IIC and NM IIA expression in the colonic epithelial scrapes of NM IIC knockout and control mice. Mean ± SEM, n = 4; * p < 0.05 (E–H) Control and NM IIC KO mice were gavaged with C. rodentium at 1 × 10 9 CFU per mouse. (E) Bacterial shedding in fecal pellets was examined at the indicated times of infection. (F) Bacterial colonization of the colon and cecum was determined on day 14 of infection. (G) The change in the body weight of the control and C. rodentium -infected animals determined over time. Mean ± SEM, n = 8. (H) Colonic crypt length was measured in the control and C. rodentium -infected mice on day 14 after bacterial administration. Mean ± SEM, n = 3–8; ** p < 0.001, **** p < 0.0001; scale bar = 20 μm.
    Figure Legend Snippet: Loss of intestinal epithelial NM IIC does not affect A/E bacterial interactions with the intestinal epithelium in vitro and in vivo . (A) Immunoblotting analysis of NM IIC and NM IIA expression in Caco-2BBE cells with CRISPR/Cas9-mediated knockout of NM IIC using two different sgRNAs. (B and C) Control and NM IIC knockout Caco-2 cells were infected with EPEC (MOI 5:1) for 3 h. Bacterial attachment to IECs was determined by either immunofluorescence labeling/confocal microscopy of LPS (B) or a colony-forming assay (C). Mean ± SEM of combined data from two independent experiments, n = 6; ns, not significant. (D) Immunoblotting analysis of NM IIC and NM IIA expression in the colonic epithelial scrapes of NM IIC knockout and control mice. Mean ± SEM, n = 4; * p < 0.05 (E–H) Control and NM IIC KO mice were gavaged with C. rodentium at 1 × 10 9 CFU per mouse. (E) Bacterial shedding in fecal pellets was examined at the indicated times of infection. (F) Bacterial colonization of the colon and cecum was determined on day 14 of infection. (G) The change in the body weight of the control and C. rodentium -infected animals determined over time. Mean ± SEM, n = 8. (H) Colonic crypt length was measured in the control and C. rodentium -infected mice on day 14 after bacterial administration. Mean ± SEM, n = 3–8; ** p < 0.001, **** p < 0.0001; scale bar = 20 μm.

    Techniques Used: In Vitro, In Vivo, Western Blot, Expressing, CRISPR, Knock-Out, Control, Infection, Immunofluorescence, Labeling, Confocal Microscopy

    Loss of NM IIA attenuates basal stress fiber assembly in EPEC-infected intestinal epithelial cells. Control and NM IIA knockout HT-29cF8 (A and B) and Caco-2BBE (C and D) cells were infected with EPEC (MOI 5:1) for 3 h. The cells were fixed and fluorescently labeled for F-actin (green). Representative confocal images (A and C) and quantification of F-actin intensity at the cell base (B and D) are shown. Arrows point at basal stress fiber assembly in EPEC-infected control epithelial cell monolayers. Arrowheads indicate poor stress fiber assembly in the infected NM IIA knockout cells. Mean ± SEM, n = 4–6; ** p < 0.01, **** p < 0.0001; scale bar = 20 μm.
    Figure Legend Snippet: Loss of NM IIA attenuates basal stress fiber assembly in EPEC-infected intestinal epithelial cells. Control and NM IIA knockout HT-29cF8 (A and B) and Caco-2BBE (C and D) cells were infected with EPEC (MOI 5:1) for 3 h. The cells were fixed and fluorescently labeled for F-actin (green). Representative confocal images (A and C) and quantification of F-actin intensity at the cell base (B and D) are shown. Arrows point at basal stress fiber assembly in EPEC-infected control epithelial cell monolayers. Arrowheads indicate poor stress fiber assembly in the infected NM IIA knockout cells. Mean ± SEM, n = 4–6; ** p < 0.01, **** p < 0.0001; scale bar = 20 μm.

    Techniques Used: Infection, Control, Knock-Out, Labeling



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    Pharmacological inhibition of NM II motor activity promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . Confluent differentiated HT-29cF8 (A and B) Caco-2BBE (C and D) cell monolayers were exposed to EPEC (MOI 5:1) for 3 h in the presence of either vehicle, blebbistatin (50 µM) or 4-HAP (100 µM). Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (A and C) or a colony forming assay (B and D). Mean ± SEM of combined data from three independent experiments, n = 9; **** p < 0.001; scale bar = 20 μm.

    Journal: Gut Microbes

    Article Title: Myosin IIA motor regulates attaching-effacing bacteria interactions with intestinal epithelium

    doi: 10.1080/19490976.2026.2638002

    Figure Lengend Snippet: Pharmacological inhibition of NM II motor activity promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . Confluent differentiated HT-29cF8 (A and B) Caco-2BBE (C and D) cell monolayers were exposed to EPEC (MOI 5:1) for 3 h in the presence of either vehicle, blebbistatin (50 µM) or 4-HAP (100 µM). Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (A and C) or a colony forming assay (B and D). Mean ± SEM of combined data from three independent experiments, n = 9; **** p < 0.001; scale bar = 20 μm.

    Article Snippet: Caco-2BBE (cat. #CRL-2102) and Cos-7 (cat. #CRL-1651) were purchased from ATCC.

    Techniques: Inhibition, Activity Assay, In Vitro, Immunofluorescence, Labeling, Confocal Microscopy

    CRISPR-Cas9-mediated knockout of NM IIA promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . (A and D) Immunoblotting analysis of NM IIA and NM IIC expression in HT-29cF8 and Caco-2BBE cells with CRISPR/Cas9-mediated knockout of NM IIA using two different sgRNAs. (B–E). Control and NM IIA knockout HT-29 (B and C) and Caco-2 (E and F) cells were infected with EPEC (MOI 5:1) for 3 h. Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (B and E) or colony forming assay (C and F). Mean ± SEM of combined data from three independent experiments, n = 9; *** p < 0.001, **** p < 0.0001; scale bar = 20 μm.

    Journal: Gut Microbes

    Article Title: Myosin IIA motor regulates attaching-effacing bacteria interactions with intestinal epithelium

    doi: 10.1080/19490976.2026.2638002

    Figure Lengend Snippet: CRISPR-Cas9-mediated knockout of NM IIA promotes EPEC attachment to model intestinal epithelial cell monolayers in vitro . (A and D) Immunoblotting analysis of NM IIA and NM IIC expression in HT-29cF8 and Caco-2BBE cells with CRISPR/Cas9-mediated knockout of NM IIA using two different sgRNAs. (B–E). Control and NM IIA knockout HT-29 (B and C) and Caco-2 (E and F) cells were infected with EPEC (MOI 5:1) for 3 h. Bacterial attachment to IEC was determined by either immunofluorescence labeling/confocal microscopy of LPS (B and E) or colony forming assay (C and F). Mean ± SEM of combined data from three independent experiments, n = 9; *** p < 0.001, **** p < 0.0001; scale bar = 20 μm.

    Article Snippet: Caco-2BBE (cat. #CRL-2102) and Cos-7 (cat. #CRL-1651) were purchased from ATCC.

    Techniques: CRISPR, Knock-Out, In Vitro, Western Blot, Expressing, Control, Infection, Immunofluorescence, Labeling, Confocal Microscopy

    Loss of intestinal epithelial NM IIC does not affect A/E bacterial interactions with the intestinal epithelium in vitro and in vivo . (A) Immunoblotting analysis of NM IIC and NM IIA expression in Caco-2BBE cells with CRISPR/Cas9-mediated knockout of NM IIC using two different sgRNAs. (B and C) Control and NM IIC knockout Caco-2 cells were infected with EPEC (MOI 5:1) for 3 h. Bacterial attachment to IECs was determined by either immunofluorescence labeling/confocal microscopy of LPS (B) or a colony-forming assay (C). Mean ± SEM of combined data from two independent experiments, n = 6; ns, not significant. (D) Immunoblotting analysis of NM IIC and NM IIA expression in the colonic epithelial scrapes of NM IIC knockout and control mice. Mean ± SEM, n = 4; * p < 0.05 (E–H) Control and NM IIC KO mice were gavaged with C. rodentium at 1 × 10 9 CFU per mouse. (E) Bacterial shedding in fecal pellets was examined at the indicated times of infection. (F) Bacterial colonization of the colon and cecum was determined on day 14 of infection. (G) The change in the body weight of the control and C. rodentium -infected animals determined over time. Mean ± SEM, n = 8. (H) Colonic crypt length was measured in the control and C. rodentium -infected mice on day 14 after bacterial administration. Mean ± SEM, n = 3–8; ** p < 0.001, **** p < 0.0001; scale bar = 20 μm.

    Journal: Gut Microbes

    Article Title: Myosin IIA motor regulates attaching-effacing bacteria interactions with intestinal epithelium

    doi: 10.1080/19490976.2026.2638002

    Figure Lengend Snippet: Loss of intestinal epithelial NM IIC does not affect A/E bacterial interactions with the intestinal epithelium in vitro and in vivo . (A) Immunoblotting analysis of NM IIC and NM IIA expression in Caco-2BBE cells with CRISPR/Cas9-mediated knockout of NM IIC using two different sgRNAs. (B and C) Control and NM IIC knockout Caco-2 cells were infected with EPEC (MOI 5:1) for 3 h. Bacterial attachment to IECs was determined by either immunofluorescence labeling/confocal microscopy of LPS (B) or a colony-forming assay (C). Mean ± SEM of combined data from two independent experiments, n = 6; ns, not significant. (D) Immunoblotting analysis of NM IIC and NM IIA expression in the colonic epithelial scrapes of NM IIC knockout and control mice. Mean ± SEM, n = 4; * p < 0.05 (E–H) Control and NM IIC KO mice were gavaged with C. rodentium at 1 × 10 9 CFU per mouse. (E) Bacterial shedding in fecal pellets was examined at the indicated times of infection. (F) Bacterial colonization of the colon and cecum was determined on day 14 of infection. (G) The change in the body weight of the control and C. rodentium -infected animals determined over time. Mean ± SEM, n = 8. (H) Colonic crypt length was measured in the control and C. rodentium -infected mice on day 14 after bacterial administration. Mean ± SEM, n = 3–8; ** p < 0.001, **** p < 0.0001; scale bar = 20 μm.

    Article Snippet: Caco-2BBE (cat. #CRL-2102) and Cos-7 (cat. #CRL-1651) were purchased from ATCC.

    Techniques: In Vitro, In Vivo, Western Blot, Expressing, CRISPR, Knock-Out, Control, Infection, Immunofluorescence, Labeling, Confocal Microscopy

    Loss of NM IIA attenuates basal stress fiber assembly in EPEC-infected intestinal epithelial cells. Control and NM IIA knockout HT-29cF8 (A and B) and Caco-2BBE (C and D) cells were infected with EPEC (MOI 5:1) for 3 h. The cells were fixed and fluorescently labeled for F-actin (green). Representative confocal images (A and C) and quantification of F-actin intensity at the cell base (B and D) are shown. Arrows point at basal stress fiber assembly in EPEC-infected control epithelial cell monolayers. Arrowheads indicate poor stress fiber assembly in the infected NM IIA knockout cells. Mean ± SEM, n = 4–6; ** p < 0.01, **** p < 0.0001; scale bar = 20 μm.

    Journal: Gut Microbes

    Article Title: Myosin IIA motor regulates attaching-effacing bacteria interactions with intestinal epithelium

    doi: 10.1080/19490976.2026.2638002

    Figure Lengend Snippet: Loss of NM IIA attenuates basal stress fiber assembly in EPEC-infected intestinal epithelial cells. Control and NM IIA knockout HT-29cF8 (A and B) and Caco-2BBE (C and D) cells were infected with EPEC (MOI 5:1) for 3 h. The cells were fixed and fluorescently labeled for F-actin (green). Representative confocal images (A and C) and quantification of F-actin intensity at the cell base (B and D) are shown. Arrows point at basal stress fiber assembly in EPEC-infected control epithelial cell monolayers. Arrowheads indicate poor stress fiber assembly in the infected NM IIA knockout cells. Mean ± SEM, n = 4–6; ** p < 0.01, **** p < 0.0001; scale bar = 20 μm.

    Article Snippet: Caco-2BBE (cat. #CRL-2102) and Cos-7 (cat. #CRL-1651) were purchased from ATCC.

    Techniques: Infection, Control, Knock-Out, Labeling