icam 1  (ATCC)


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    Name:
    BE29G1
    Description:

    Catalog Number:
    hb-233
    Price:
    None
    Applications:
    The antiboy is useful for studies of inflammation, lymphocyte differentiation and lymphocyte activation.It can be used for purification of ICAM-1 and for staining of cell surface ICAM-1 by flow cytometry.
    Host:
    Rattus norvegicus (B cell); Mus musculus (myeloma), rat (B cell); mouse (myeloma)
    Cell Type:
    hybridoma: B lymphocyte
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    Structured Review

    ATCC icam 1
    Northern blot analyses of the expression of IL-6 and <t>ICAM-1</t> (A) and GM-CSF (B) mRNA in T. gondii -infected HRPE cells. Total cellular RNA isolated from HRPE cells at indicated time points were subjected to Northern blot analysis. The arrows indicate the positions of IL-6 (1.3 kb), ICAM-1 (3.3 kb), and GM-CSF (0.8 kb) mRNA. Lanes: control, uninfected cells incubated for 3 days; T. gondii , days 1, 2, and 3, cultures infected with T. gondii and total RNA prepared 1, 2, and 3 days p.i., respectively; dead T. gondii , cells incubated for 3 days with heat-killed T. gondii . The bottom panel shows the intensity of the 28S RNA band of an ethidium bromide-stained RNA gel.

    https://www.bioz.com/result/icam 1/product/ATCC
    Average 94 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    icam 1 - by Bioz Stars, 2020-09
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    Images

    1) Product Images from "Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells"

    Article Title: Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells

    Journal: Infection and Immunity

    doi:

    Northern blot analyses of the expression of IL-6 and ICAM-1 (A) and GM-CSF (B) mRNA in T. gondii -infected HRPE cells. Total cellular RNA isolated from HRPE cells at indicated time points were subjected to Northern blot analysis. The arrows indicate the positions of IL-6 (1.3 kb), ICAM-1 (3.3 kb), and GM-CSF (0.8 kb) mRNA. Lanes: control, uninfected cells incubated for 3 days; T. gondii , days 1, 2, and 3, cultures infected with T. gondii and total RNA prepared 1, 2, and 3 days p.i., respectively; dead T. gondii , cells incubated for 3 days with heat-killed T. gondii . The bottom panel shows the intensity of the 28S RNA band of an ethidium bromide-stained RNA gel.
    Figure Legend Snippet: Northern blot analyses of the expression of IL-6 and ICAM-1 (A) and GM-CSF (B) mRNA in T. gondii -infected HRPE cells. Total cellular RNA isolated from HRPE cells at indicated time points were subjected to Northern blot analysis. The arrows indicate the positions of IL-6 (1.3 kb), ICAM-1 (3.3 kb), and GM-CSF (0.8 kb) mRNA. Lanes: control, uninfected cells incubated for 3 days; T. gondii , days 1, 2, and 3, cultures infected with T. gondii and total RNA prepared 1, 2, and 3 days p.i., respectively; dead T. gondii , cells incubated for 3 days with heat-killed T. gondii . The bottom panel shows the intensity of the 28S RNA band of an ethidium bromide-stained RNA gel.

    Techniques Used: Northern Blot, Expressing, Infection, Isolation, Incubation, Staining

    Secretion of IL-β (A), IL-6 (B), GM-CSF (C), and ICAM-1 (D) by T. gondii -infected HRPE cells. Cell culture supernatant fluids were collected at indicated p.i. times, and the levels of IL-1β, IL-6, GM-CSF, and ICAM-1 were determined by enzyme-linked immunosorbent assay. The lower limits of detection were 0.13 pg/ml (IL-1β), 10 pg/ml (IL-6), 15.6 pg/ml (GM-CSF), and 1.6 ng/ml (ICAM-1). Results are the means ± standard error for six experiments, each with duplicate samples.
    Figure Legend Snippet: Secretion of IL-β (A), IL-6 (B), GM-CSF (C), and ICAM-1 (D) by T. gondii -infected HRPE cells. Cell culture supernatant fluids were collected at indicated p.i. times, and the levels of IL-1β, IL-6, GM-CSF, and ICAM-1 were determined by enzyme-linked immunosorbent assay. The lower limits of detection were 0.13 pg/ml (IL-1β), 10 pg/ml (IL-6), 15.6 pg/ml (GM-CSF), and 1.6 ng/ml (ICAM-1). Results are the means ± standard error for six experiments, each with duplicate samples.

    Techniques Used: Infection, Cell Culture, Enzyme-linked Immunosorbent Assay

    2) Product Images from "The adhesion receptor CD44 promotes atherosclerosis by mediating inflammatory cell recruitment and vascular cell activation"

    Article Title: The adhesion receptor CD44 promotes atherosclerosis by mediating inflammatory cell recruitment and vascular cell activation

    Journal: Journal of Clinical Investigation

    doi:

    Upregulation of VCAM-1 on vascular SMCs is an early and persistent marker of atherosclerosis. Immunohistochemistry of the arch region of aorta isolated from 6-week ( a and b ) or 16-week ( c – f ) apoE-deficient mice with anti–VCAM-1 ( a and c ), anti–ICAM-1 ( b and d ), anti–PECAM-1 ( e ), and anti-CD44 ( f ) Ab’s. VCAM-1 is selectively and markedly upregulated on the vascular SMCs in atherosclerosis-prone areas of the aorta, including on medial SMCs underlying established lesions, while ICAM-1 expression is restricted to endothelial cells. CD44 was expressed on macrophage-derived foam cells and upregulated on vascular SMCs underlying lesion. Representative sections from five to seven mice. ×100.
    Figure Legend Snippet: Upregulation of VCAM-1 on vascular SMCs is an early and persistent marker of atherosclerosis. Immunohistochemistry of the arch region of aorta isolated from 6-week ( a and b ) or 16-week ( c – f ) apoE-deficient mice with anti–VCAM-1 ( a and c ), anti–ICAM-1 ( b and d ), anti–PECAM-1 ( e ), and anti-CD44 ( f ) Ab’s. VCAM-1 is selectively and markedly upregulated on the vascular SMCs in atherosclerosis-prone areas of the aorta, including on medial SMCs underlying established lesions, while ICAM-1 expression is restricted to endothelial cells. CD44 was expressed on macrophage-derived foam cells and upregulated on vascular SMCs underlying lesion. Representative sections from five to seven mice. ×100.

    Techniques Used: Marker, Immunohistochemistry, Isolation, Mouse Assay, Expressing, Derivative Assay

    3) Product Images from "Cytokine and Adhesion Molecule Expression Induced by Different Strains of Staphylococcus aureus in Type 1 Diabetic Rats: Role of Insulin"

    Article Title: Cytokine and Adhesion Molecule Expression Induced by Different Strains of Staphylococcus aureus in Type 1 Diabetic Rats: Role of Insulin

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2018.03165

    Mesenteric adhesion molecule expression after S. aureus strain ATCC 25923 infection: role of insulin. Samples were obtained from the mesentery of diabetic or non-diabetic animals treated or not treated with insulin 3 days after S. aureus ATCC 25923 infection and stained with haematoxylin (purple staining) and antibodies (brown staining, arrows) for PECAM (A) , ICAM-1 (B) , and P-selectin (C) . * blood vessel; bar = 50 μm. Quantification of immunostaining was performed with the software NIS-Elements AR. Values represent the mean total/diameter of the area ± s.e.m. of three animals/group (five fields were photographed per animal). (D) PECAM; (E) ICAM-1; (F) P-selectin expression (μm 2 ). Animals were treated with multiple doses of insulin (I2). Non-diabetic uninfected group (Cs); Non-diabetic infected group (CATCC); Non-diabetic infected and treated with I2 insulin group (CATCC+I2); Diabetic uninfected group (Ds); Diabetic infected group (DATCC); Diabetic infected; and treated with I2 insulin group (DATCC+I2). Values are shown as the mean ± SEM of 5 animals/group *** p
    Figure Legend Snippet: Mesenteric adhesion molecule expression after S. aureus strain ATCC 25923 infection: role of insulin. Samples were obtained from the mesentery of diabetic or non-diabetic animals treated or not treated with insulin 3 days after S. aureus ATCC 25923 infection and stained with haematoxylin (purple staining) and antibodies (brown staining, arrows) for PECAM (A) , ICAM-1 (B) , and P-selectin (C) . * blood vessel; bar = 50 μm. Quantification of immunostaining was performed with the software NIS-Elements AR. Values represent the mean total/diameter of the area ± s.e.m. of three animals/group (five fields were photographed per animal). (D) PECAM; (E) ICAM-1; (F) P-selectin expression (μm 2 ). Animals were treated with multiple doses of insulin (I2). Non-diabetic uninfected group (Cs); Non-diabetic infected group (CATCC); Non-diabetic infected and treated with I2 insulin group (CATCC+I2); Diabetic uninfected group (Ds); Diabetic infected group (DATCC); Diabetic infected; and treated with I2 insulin group (DATCC+I2). Values are shown as the mean ± SEM of 5 animals/group *** p

    Techniques Used: Expressing, Infection, Staining, Immunostaining, Software

    4) Product Images from "Protein C Concentrate Controls Leukocyte Recruitment during Inflammation and Improves Survival during Endotoxemia after Efficient in Vivo Activation"

    Article Title: Protein C Concentrate Controls Leukocyte Recruitment during Inflammation and Improves Survival during Endotoxemia after Efficient in Vivo Activation

    Journal: The American Journal of Pathology

    doi: 10.1016/j.ajpath.2011.07.023

    Role of intercellular adhesion molecule 1 (ICAM-1) for protein C (PC)-induced inhibition of leukocyte adhesion during tumor necrosis factor-α (TNF-α)- and trauma-induced inflammation. Leukocyte adhesion in cremaster muscle venules (per
    Figure Legend Snippet: Role of intercellular adhesion molecule 1 (ICAM-1) for protein C (PC)-induced inhibition of leukocyte adhesion during tumor necrosis factor-α (TNF-α)- and trauma-induced inflammation. Leukocyte adhesion in cremaster muscle venules (per

    Techniques Used: Inhibition

    Tumor necrosis factor-α (TNF-α)-stimulated intercellular adhesion molecule 1 (ICAM-1) expression on endothelial cells, β 2 -integrin, and CXCR2 expression on neutrophils after PC treatment. ICAM-1 expression of cultured endothelial
    Figure Legend Snippet: Tumor necrosis factor-α (TNF-α)-stimulated intercellular adhesion molecule 1 (ICAM-1) expression on endothelial cells, β 2 -integrin, and CXCR2 expression on neutrophils after PC treatment. ICAM-1 expression of cultured endothelial

    Techniques Used: Expressing, Cell Culture

    Expression of P- and E-selectin, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), thrombomodulin (TM), and endothelial protein C receptor (EPCR) in tumor necrosis factor-α (TNF-α)-stimulated cremaster
    Figure Legend Snippet: Expression of P- and E-selectin, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), thrombomodulin (TM), and endothelial protein C receptor (EPCR) in tumor necrosis factor-α (TNF-α)-stimulated cremaster

    Techniques Used: Expressing

    5) Product Images from "Cytokine and Adhesion Molecule Expression Induced by Different Strains of Staphylococcus aureus in Type 1 Diabetic Rats: Role of Insulin"

    Article Title: Cytokine and Adhesion Molecule Expression Induced by Different Strains of Staphylococcus aureus in Type 1 Diabetic Rats: Role of Insulin

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2018.03165

    Mesenteric adhesion molecule expression after S. aureus strain ATCC 25923 infection: role of insulin. Samples were obtained from the mesentery of diabetic or non-diabetic animals treated or not treated with insulin 3 days after S. aureus ATCC 25923 infection and stained with haematoxylin (purple staining) and antibodies (brown staining, arrows) for PECAM (A) , ICAM-1 (B) , and P-selectin (C) . * blood vessel; bar = 50 μm. Quantification of immunostaining was performed with the software NIS-Elements AR. Values represent the mean total/diameter of the area ± s.e.m. of three animals/group (five fields were photographed per animal). (D) PECAM; (E) ICAM-1; (F) P-selectin expression (μm 2 ). Animals were treated with multiple doses of insulin (I2). Non-diabetic uninfected group (Cs); Non-diabetic infected group (CATCC); Non-diabetic infected and treated with I2 insulin group (CATCC+I2); Diabetic uninfected group (Ds); Diabetic infected group (DATCC); Diabetic infected; and treated with I2 insulin group (DATCC+I2). Values are shown as the mean ± SEM of 5 animals/group *** p
    Figure Legend Snippet: Mesenteric adhesion molecule expression after S. aureus strain ATCC 25923 infection: role of insulin. Samples were obtained from the mesentery of diabetic or non-diabetic animals treated or not treated with insulin 3 days after S. aureus ATCC 25923 infection and stained with haematoxylin (purple staining) and antibodies (brown staining, arrows) for PECAM (A) , ICAM-1 (B) , and P-selectin (C) . * blood vessel; bar = 50 μm. Quantification of immunostaining was performed with the software NIS-Elements AR. Values represent the mean total/diameter of the area ± s.e.m. of three animals/group (five fields were photographed per animal). (D) PECAM; (E) ICAM-1; (F) P-selectin expression (μm 2 ). Animals were treated with multiple doses of insulin (I2). Non-diabetic uninfected group (Cs); Non-diabetic infected group (CATCC); Non-diabetic infected and treated with I2 insulin group (CATCC+I2); Diabetic uninfected group (Ds); Diabetic infected group (DATCC); Diabetic infected; and treated with I2 insulin group (DATCC+I2). Values are shown as the mean ± SEM of 5 animals/group *** p

    Techniques Used: Expressing, Infection, Staining, Immunostaining, Software

    6) Product Images from "Tumour necrosis factor-alpha (TNF-?) enhances lymphocyte migration into rheumatoid synovial tissue transplanted into severe combined immunodeficient (SCID) mice"

    Article Title: Tumour necrosis factor-alpha (TNF-?) enhances lymphocyte migration into rheumatoid synovial tissue transplanted into severe combined immunodeficient (SCID) mice

    Journal: Clinical and Experimental Immunology

    doi: 10.1046/j.1365-2249.2000.01342.x

    (a) Intercellular adhesion molecule-1 (ICAM-1) and (b) vascular cell adhesion molecule-1 (VCAM-1) expression in the original and grafted synovial tissue, pre- (Pre-T) and post-transplantation (Post-T). Transplants were injected with PBS (control) or TNF-α (200 ng/graft). Cryostat sections (10 μm) were stained for anti-human ICAM-1 and VCAM-1 using a standard immunoperoxidase technique. The intensity of staining was assessed using an arbitrary score 0–3 with increasing intensity. (a) P =
    Figure Legend Snippet: (a) Intercellular adhesion molecule-1 (ICAM-1) and (b) vascular cell adhesion molecule-1 (VCAM-1) expression in the original and grafted synovial tissue, pre- (Pre-T) and post-transplantation (Post-T). Transplants were injected with PBS (control) or TNF-α (200 ng/graft). Cryostat sections (10 μm) were stained for anti-human ICAM-1 and VCAM-1 using a standard immunoperoxidase technique. The intensity of staining was assessed using an arbitrary score 0–3 with increasing intensity. (a) P =

    Techniques Used: Expressing, Transplantation Assay, Injection, Staining

    7) Product Images from "Interleukin-8 and Intercellular Adhesion Molecule 1 Regulation in Oral Epithelial Cells by Selected Periodontal Bacteria: Multiple Effects of Porphyromonas gingivalis via Antagonistic Mechanisms"

    Article Title: Interleukin-8 and Intercellular Adhesion Molecule 1 Regulation in Oral Epithelial Cells by Selected Periodontal Bacteria: Multiple Effects of Porphyromonas gingivalis via Antagonistic Mechanisms

    Journal: Infection and Immunity

    doi: 10.1128/IAI.69.3.1364-1372.2001

    IL-8 and ICAM-1 mRNA levels in gingival epithelial cells following bacterial challenge. Confluent HOK-18A cell monolayers were infected with F. nucleatum or various P. gingivalis strains at a MOI of 500:1. The bacterium–epithelial-cell coculture period was either 2, 4, or 6 h. RNA was isolated at 4 or 6 h after infection, and 8 to 12 μg of total RNA was subjected to Northern blot analysis. For the 2-h coculture group, the culture was washed and fresh medium containing appropriate antibiotics was added at 2 h and the cultures were further incubated for another 2 to 4 h before harvesting. For the 4- or 6-h coculture group, the bacteria were continuously cocultured with the epithelial cells to 4 or 6 h (see diagram in the bottom panel). (A) Epithelial cells were challenged with F. nucleatum 12230, P. gingivalis 381, or P. gingivalis W50 for 2 h (washed) or 6 h (continuous), and RNA was isolated at 6 h. (B and C) Epithelial cells were challenged with P. gingivalis 33277 (B) or F. nucleatum 12230 (C) for 2 h (washed) or 4 h (continuous) and RNA was isolated at 4 h. The levels of mRNA from the Northern blot analysis (shown in the top panel) are plotted and shown in the middle panel. Mock, no bacteria were added to the cultures. Fn , F. nucleatum ; Pg , P. gingivalis ; W , 2-h coculture group that was washed at the 2-h time point; C , 4- or 6-h coculture group, bacteria continuously cocultured with the epithelial cells.
    Figure Legend Snippet: IL-8 and ICAM-1 mRNA levels in gingival epithelial cells following bacterial challenge. Confluent HOK-18A cell monolayers were infected with F. nucleatum or various P. gingivalis strains at a MOI of 500:1. The bacterium–epithelial-cell coculture period was either 2, 4, or 6 h. RNA was isolated at 4 or 6 h after infection, and 8 to 12 μg of total RNA was subjected to Northern blot analysis. For the 2-h coculture group, the culture was washed and fresh medium containing appropriate antibiotics was added at 2 h and the cultures were further incubated for another 2 to 4 h before harvesting. For the 4- or 6-h coculture group, the bacteria were continuously cocultured with the epithelial cells to 4 or 6 h (see diagram in the bottom panel). (A) Epithelial cells were challenged with F. nucleatum 12230, P. gingivalis 381, or P. gingivalis W50 for 2 h (washed) or 6 h (continuous), and RNA was isolated at 6 h. (B and C) Epithelial cells were challenged with P. gingivalis 33277 (B) or F. nucleatum 12230 (C) for 2 h (washed) or 4 h (continuous) and RNA was isolated at 4 h. The levels of mRNA from the Northern blot analysis (shown in the top panel) are plotted and shown in the middle panel. Mock, no bacteria were added to the cultures. Fn , F. nucleatum ; Pg , P. gingivalis ; W , 2-h coculture group that was washed at the 2-h time point; C , 4- or 6-h coculture group, bacteria continuously cocultured with the epithelial cells.

    Techniques Used: Infection, Isolation, Northern Blot, Incubation

    8) Product Images from "Skeletal Muscle Cells Express ICAM-1 after Muscle Overload and ICAM-1 Contributes to the Ensuing Hypertrophic Response"

    Article Title: Skeletal Muscle Cells Express ICAM-1 after Muscle Overload and ICAM-1 Contributes to the Ensuing Hypertrophic Response

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0058486

    Protein synthesis, measured using the nonradioactive SUnSET technique, in plantaris muscles. A) Representative western blot (50 ug of protein/lane) of puromycin in control (CT) and 7 d overloaded muscles of wild type (WT) and ICAM-1-/- (IC) mice. B) Coomassie blue stained 10% SDS PAGE gel containing the same samples shown in panel A. C) Quantitative analysis of the relative abundance of puromycin incorporation into proteins (n = 7-8/group). #, significant interaction at 7 d of overload. *, significantly elevated at 7 d of overload compared to controls for wild type mice.
    Figure Legend Snippet: Protein synthesis, measured using the nonradioactive SUnSET technique, in plantaris muscles. A) Representative western blot (50 ug of protein/lane) of puromycin in control (CT) and 7 d overloaded muscles of wild type (WT) and ICAM-1-/- (IC) mice. B) Coomassie blue stained 10% SDS PAGE gel containing the same samples shown in panel A. C) Quantitative analysis of the relative abundance of puromycin incorporation into proteins (n = 7-8/group). #, significant interaction at 7 d of overload. *, significantly elevated at 7 d of overload compared to controls for wild type mice.

    Techniques Used: Western Blot, Mouse Assay, Staining, SDS Page

    Measures of skeletal muscle hypertrophy. A) Wet plantaris mass in control and overloaded mice (n = 16-20/group). B) Total protein in muscle homogenates of control (n = 6/group) and overloaded mice (n = 8/group). C) Mean cross-sectional area of normal myofibers in control (n = 1813 and 1697 myofibers for wild type and ICAM-1-/- mice, respectively)/strain) and 14 d overloaded (n = 2617 and 1096 myofibers for wild type and ICAM-1-/- mice, respectively) muscles. D) Frequency distribution of the size of normal myofibers at 14 d of overload #, significant interaction at 14 and 21 d of overload. *, significantly higher at 14 and/or 21 d of overload relative to respective controls.
    Figure Legend Snippet: Measures of skeletal muscle hypertrophy. A) Wet plantaris mass in control and overloaded mice (n = 16-20/group). B) Total protein in muscle homogenates of control (n = 6/group) and overloaded mice (n = 8/group). C) Mean cross-sectional area of normal myofibers in control (n = 1813 and 1697 myofibers for wild type and ICAM-1-/- mice, respectively)/strain) and 14 d overloaded (n = 2617 and 1096 myofibers for wild type and ICAM-1-/- mice, respectively) muscles. D) Frequency distribution of the size of normal myofibers at 14 d of overload #, significant interaction at 14 and 21 d of overload. *, significantly higher at 14 and/or 21 d of overload relative to respective controls.

    Techniques Used: Mouse Assay

    Satellite cells/myoblasts and regenerating myofibers after muscle overload. A) Representative western blot (30 ug of protein/lane) of Pax7 (60 kDa) in control (CT) and overloaded (3, 7 and 14 d) muscles of wild type (WT) and ICAM-1-/- (IC) mice. B) Quantitative analysis of the relative abundance of Pax7 protein (n = 6–8/group). #, significant interaction at 3 d of overload. *, significantly elevated at each overload time point compared to control levels for both wild type and ICAM-1-/- mice. C) Regenerating myofibers expressed as a percentage of the total number of myofibers. #, significant interaction at 7 d of overload.
    Figure Legend Snippet: Satellite cells/myoblasts and regenerating myofibers after muscle overload. A) Representative western blot (30 ug of protein/lane) of Pax7 (60 kDa) in control (CT) and overloaded (3, 7 and 14 d) muscles of wild type (WT) and ICAM-1-/- (IC) mice. B) Quantitative analysis of the relative abundance of Pax7 protein (n = 6–8/group). #, significant interaction at 3 d of overload. *, significantly elevated at each overload time point compared to control levels for both wild type and ICAM-1-/- mice. C) Regenerating myofibers expressed as a percentage of the total number of myofibers. #, significant interaction at 7 d of overload.

    Techniques Used: Western Blot, Mouse Assay

    ICAM-1 expression by cultured skeletal muscle cells. A) Representative flow cytometric quadrant plots of control and TNF-α treated (10 ng/ml for 24 h) cultures of myoblasts. ICAM-1 was detected using a phycoerythrin (PE) conjugated antibody; whereas, myoblasts were identified using an AlexaFlour® 649 (AF649) α7 antibody. ICAM-1 was not expressed by C2C12 and primary myoblasts in control cultures; whereas, TNF-α treatment caused ICAM-1 to be expressed by 30% and 15% of C2C12 and primary myoblasts, respectively. B) Representative western blots for ICAM-1 expression in C212 and primary cells treated with differentiation medium for up to 6 d (20 ug of protein/lane). A cell lysate of a myeloid cell line (RAW 264.7 cells; 5 ug of protein) was used a positive control (+CT). Membranes were probed for α-tubulin (50 kDa) to serve as a control for sample loading. ICAM-1 was not detected in differentiating or differentiated cultures. C) Representative western blot for ICAM-1 after treating proliferating myoblasts or differentiated myotubes (4 d in differentiation medium) with TNF-α (10 ng/ml for 24 h) (20 ug of protein/lane). TNF-α treatment resulted in a ICAM-1 band that was of the same molecule weight (110 kDa) as those found in plantaris muscles from control (CT) and 7 d overloaded (7 d) wild type mice (15 ug of protein/lane).
    Figure Legend Snippet: ICAM-1 expression by cultured skeletal muscle cells. A) Representative flow cytometric quadrant plots of control and TNF-α treated (10 ng/ml for 24 h) cultures of myoblasts. ICAM-1 was detected using a phycoerythrin (PE) conjugated antibody; whereas, myoblasts were identified using an AlexaFlour® 649 (AF649) α7 antibody. ICAM-1 was not expressed by C2C12 and primary myoblasts in control cultures; whereas, TNF-α treatment caused ICAM-1 to be expressed by 30% and 15% of C2C12 and primary myoblasts, respectively. B) Representative western blots for ICAM-1 expression in C212 and primary cells treated with differentiation medium for up to 6 d (20 ug of protein/lane). A cell lysate of a myeloid cell line (RAW 264.7 cells; 5 ug of protein) was used a positive control (+CT). Membranes were probed for α-tubulin (50 kDa) to serve as a control for sample loading. ICAM-1 was not detected in differentiating or differentiated cultures. C) Representative western blot for ICAM-1 after treating proliferating myoblasts or differentiated myotubes (4 d in differentiation medium) with TNF-α (10 ng/ml for 24 h) (20 ug of protein/lane). TNF-α treatment resulted in a ICAM-1 band that was of the same molecule weight (110 kDa) as those found in plantaris muscles from control (CT) and 7 d overloaded (7 d) wild type mice (15 ug of protein/lane).

    Techniques Used: Expressing, Cell Culture, Flow Cytometry, Western Blot, Positive Control, Mouse Assay

    ICAM-1 localization in 7 and 14 d overloaded muscles of wild type mice. Representative images from confocal microscopy. A) ICAM-1 (green) was found to be co-localized to CD31+ endothelial cells (cyan) and to be associated with the membrane of myofibers (WGA+; red). Cells (DAPI+; blue) in the interstitium were also found to express ICAM-1 (arrow). Column labeled as “MERGED” represents an overlay of the ICAM-1, CD31, WGA and DAPI images. B) Higher magnification clearly revealed the colocalization of ICAM-1 (green) with the membrane marker WGA (red) in overloaded muscles. Column labeled as “MERGED” include images of ICAM-1, WGA, and DAPI.
    Figure Legend Snippet: ICAM-1 localization in 7 and 14 d overloaded muscles of wild type mice. Representative images from confocal microscopy. A) ICAM-1 (green) was found to be co-localized to CD31+ endothelial cells (cyan) and to be associated with the membrane of myofibers (WGA+; red). Cells (DAPI+; blue) in the interstitium were also found to express ICAM-1 (arrow). Column labeled as “MERGED” represents an overlay of the ICAM-1, CD31, WGA and DAPI images. B) Higher magnification clearly revealed the colocalization of ICAM-1 (green) with the membrane marker WGA (red) in overloaded muscles. Column labeled as “MERGED” include images of ICAM-1, WGA, and DAPI.

    Techniques Used: Mouse Assay, Confocal Microscopy, Whole Genome Amplification, Labeling, Marker

    ICAM-1 and CD11b localization in 7 d overloaded muscle of wild type mice. Representative images from confocal microscopy. ICAM-1 (green) and CD11b (red) co-localized on the membrane of myofibers (arrow) and CD11b+ cells were closely associated with ICAM-1+ myofibers (arrowhead). Numerous CD11b+ cells residing in overloaded muscles expressed ICAM-1.
    Figure Legend Snippet: ICAM-1 and CD11b localization in 7 d overloaded muscle of wild type mice. Representative images from confocal microscopy. ICAM-1 (green) and CD11b (red) co-localized on the membrane of myofibers (arrow) and CD11b+ cells were closely associated with ICAM-1+ myofibers (arrowhead). Numerous CD11b+ cells residing in overloaded muscles expressed ICAM-1.

    Techniques Used: Mouse Assay, Confocal Microscopy

    Gene and protein expression of ICAM-1. A) Fold change in ICAM-1 gene expression (n = 8/group). Gene transcripts tended (p = 0.054) to be lower at 14 d relative to 3 d of overload for both strains of mice. B) Representative western blot of ICAM-1 (110 kDa) in control and overloaded (3, 7, and 14 d) muscles of wild type and CD18-/- mice (15 ug of protein/lane). C) Quantitative analysis of ICAM-1 protein (n = 7/group). *, significantly elevated at each overload time point compared to control levels for both strains of mice.
    Figure Legend Snippet: Gene and protein expression of ICAM-1. A) Fold change in ICAM-1 gene expression (n = 8/group). Gene transcripts tended (p = 0.054) to be lower at 14 d relative to 3 d of overload for both strains of mice. B) Representative western blot of ICAM-1 (110 kDa) in control and overloaded (3, 7, and 14 d) muscles of wild type and CD18-/- mice (15 ug of protein/lane). C) Quantitative analysis of ICAM-1 protein (n = 7/group). *, significantly elevated at each overload time point compared to control levels for both strains of mice.

    Techniques Used: Expressing, Mouse Assay, Western Blot

    ICAM-1 expression by satellite cells/myoblasts. A) Confocal images of wild type muscle overloaded for 7 d. Arrow indicates a presumptive satellite cell that is positive for ICAM-1. B) Representative plots from flow cytometric analysis of cells isolated from control and 7 d overloaded muscles of wild type mice. ICAM-1 was detected using a phycoerythrin (PE) conjugated antibody; whereas, satellite cells/myoblasts were identified using an AlexaFlour® 649 (AF649) α7 antibody. Satellite cells/myoblasts were operational defined as CD45 neg CD31 neg integrin α7+cells. C) Flow cytometric determination of ICAM-1 expression by satellite cells/myoblasts (CD45 neg CD31 neg integrin α7+ICAM-1+) expressed relative to muscle mass (mg). *, significantly higher for 7 d overloaded muscles (n = 6) compared to control muscles (n = 4).
    Figure Legend Snippet: ICAM-1 expression by satellite cells/myoblasts. A) Confocal images of wild type muscle overloaded for 7 d. Arrow indicates a presumptive satellite cell that is positive for ICAM-1. B) Representative plots from flow cytometric analysis of cells isolated from control and 7 d overloaded muscles of wild type mice. ICAM-1 was detected using a phycoerythrin (PE) conjugated antibody; whereas, satellite cells/myoblasts were identified using an AlexaFlour® 649 (AF649) α7 antibody. Satellite cells/myoblasts were operational defined as CD45 neg CD31 neg integrin α7+cells. C) Flow cytometric determination of ICAM-1 expression by satellite cells/myoblasts (CD45 neg CD31 neg integrin α7+ICAM-1+) expressed relative to muscle mass (mg). *, significantly higher for 7 d overloaded muscles (n = 6) compared to control muscles (n = 4).

    Techniques Used: Expressing, Flow Cytometry, Isolation, Mouse Assay

    Myeloid cell accumulation in plantaris muscles. A) Neutrophil concentrations (Ly6G+ cells/mm 3 ; n = 6–8/group). *, elevated relative to respective controls. #, higher for wild type compared to ICAM-1-/- mice at 7 d of overload. B) Macrophage concentrations (F4/80+ cells/mm 3 ; n = 6-8/group). *, elevated relative to controls.
    Figure Legend Snippet: Myeloid cell accumulation in plantaris muscles. A) Neutrophil concentrations (Ly6G+ cells/mm 3 ; n = 6–8/group). *, elevated relative to respective controls. #, higher for wild type compared to ICAM-1-/- mice at 7 d of overload. B) Macrophage concentrations (F4/80+ cells/mm 3 ; n = 6-8/group). *, elevated relative to controls.

    Techniques Used: Mouse Assay

    ICAM-1 localization in control muscle of wild type mice. Representative images from confocal microscopy. A) ICAM-1 (green), B) WGA (membrane marker; red) and ICAM-1 (green), C) CD31 (endothelial cell marker; purple), and D) Merged image of ICAM-1 (panel A), and CD31 (panel C). Co-localization analysis revealed that the majority (90–95%) of the ICAM-1 labeling in control muscles was expressed by CD31+ endothelial cells. ICAM-1 was not found on the membrane of myofibers in control muscles.
    Figure Legend Snippet: ICAM-1 localization in control muscle of wild type mice. Representative images from confocal microscopy. A) ICAM-1 (green), B) WGA (membrane marker; red) and ICAM-1 (green), C) CD31 (endothelial cell marker; purple), and D) Merged image of ICAM-1 (panel A), and CD31 (panel C). Co-localization analysis revealed that the majority (90–95%) of the ICAM-1 labeling in control muscles was expressed by CD31+ endothelial cells. ICAM-1 was not found on the membrane of myofibers in control muscles.

    Techniques Used: Mouse Assay, Confocal Microscopy, Whole Genome Amplification, Marker, Labeling

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    Article Snippet: .. Murine vasculature was identified using species-specific rat anti-mouse MoAbs against either ICAM-1 (HB233; ATCC, Rockville, MD) or CD31 (PharMingen, San Diego, CA) and standard immunoperoxidase or immunofluorescence methods were used as described below. .. Cryostat sections of the transplants were immunostained for both human vasculature (VWFVIII; Dako) and murine vasculature (CD31; PharMingen) using either single or double immunoperoxidase methods as described below.

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    Article Snippet: .. The KM201 and HB-233 hybridomas (ATCC), which produce mAbs against mouse CD44 and intracellular adhesion molecule (ICAM)-1, respectively, were both cultured in DMEM with 10% FBS. .. Partially purified mAbs were obtained by 50% (NH4 )2 SO4 precipitation of the hybridoma culture media.

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  • icam 1  (ATCC)
    92
    ATCC icam 1
    Northern blot analyses of the expression of IL-6 and <t>ICAM-1</t> (A) and GM-CSF (B) mRNA in T. gondii -infected HRPE cells. Total cellular RNA isolated from HRPE cells at indicated time points were subjected to Northern blot analysis. The arrows indicate the positions of IL-6 (1.3 kb), ICAM-1 (3.3 kb), and GM-CSF (0.8 kb) mRNA. Lanes: control, uninfected cells incubated for 3 days; T. gondii , days 1, 2, and 3, cultures infected with T. gondii and total RNA prepared 1, 2, and 3 days p.i., respectively; dead T. gondii , cells incubated for 3 days with heat-killed T. gondii . The bottom panel shows the intensity of the 28S RNA band of an ethidium bromide-stained RNA gel.
    Icam 1, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human icam 1
    Deletion of RKIKK motif inhibits leukocyte adhesion and transmigration under shear-flow condition. (A) Attachment of human PBLs to COS-7 <t>ICAM-1</t> mutants under shear-flow condition. PBLs (1 × 10 6 cells/ml) were incubated with COS-7 transfectants
    Human Icam 1, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC pmx dc sign 3a
    DENV internalization and infectivity in wt <t>DC-SIGN</t> compared to mutant cells. A. % virus internalized for <t>DC-SIGN-3A</t> cells as compared to wt DC-SIGN cells (upper panel); the same comparison for DC-SIGN-Δ35 cells (lower panel). B. DENV infection at 24h of wt DC-SIGN, DC-SIGN-3A (upper panel) and DC-SIGN-Δ35 (lower panel) expressing cells at MOIs of 1, 3 and 10.
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    Northern blot analyses of the expression of IL-6 and ICAM-1 (A) and GM-CSF (B) mRNA in T. gondii -infected HRPE cells. Total cellular RNA isolated from HRPE cells at indicated time points were subjected to Northern blot analysis. The arrows indicate the positions of IL-6 (1.3 kb), ICAM-1 (3.3 kb), and GM-CSF (0.8 kb) mRNA. Lanes: control, uninfected cells incubated for 3 days; T. gondii , days 1, 2, and 3, cultures infected with T. gondii and total RNA prepared 1, 2, and 3 days p.i., respectively; dead T. gondii , cells incubated for 3 days with heat-killed T. gondii . The bottom panel shows the intensity of the 28S RNA band of an ethidium bromide-stained RNA gel.

    Journal: Infection and Immunity

    Article Title: Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells

    doi:

    Figure Lengend Snippet: Northern blot analyses of the expression of IL-6 and ICAM-1 (A) and GM-CSF (B) mRNA in T. gondii -infected HRPE cells. Total cellular RNA isolated from HRPE cells at indicated time points were subjected to Northern blot analysis. The arrows indicate the positions of IL-6 (1.3 kb), ICAM-1 (3.3 kb), and GM-CSF (0.8 kb) mRNA. Lanes: control, uninfected cells incubated for 3 days; T. gondii , days 1, 2, and 3, cultures infected with T. gondii and total RNA prepared 1, 2, and 3 days p.i., respectively; dead T. gondii , cells incubated for 3 days with heat-killed T. gondii . The bottom panel shows the intensity of the 28S RNA band of an ethidium bromide-stained RNA gel.

    Article Snippet: Human IL-6 , ICAM-1 , and GM-CSF (clone GMCSF, pCSF-1; American Type Culture Collection, Manassas, Va.) cDNA probes were labeled by the random primer method with digoxigenin-dUTP (Dig DNA labeling and detection kit; Boehringer Mannheim, Indianapolis, Ind.).

    Techniques: Northern Blot, Expressing, Infection, Isolation, Incubation, Staining

    Secretion of IL-β (A), IL-6 (B), GM-CSF (C), and ICAM-1 (D) by T. gondii -infected HRPE cells. Cell culture supernatant fluids were collected at indicated p.i. times, and the levels of IL-1β, IL-6, GM-CSF, and ICAM-1 were determined by enzyme-linked immunosorbent assay. The lower limits of detection were 0.13 pg/ml (IL-1β), 10 pg/ml (IL-6), 15.6 pg/ml (GM-CSF), and 1.6 ng/ml (ICAM-1). Results are the means ± standard error for six experiments, each with duplicate samples.

    Journal: Infection and Immunity

    Article Title: Toxoplasma gondii Infection Induces Gene Expression and Secretion of Interleukin 1 (IL-1), IL-6, Granulocyte-Macrophage Colony-Stimulating Factor, and Intercellular Adhesion Molecule 1 by Human Retinal Pigment Epithelial Cells

    doi:

    Figure Lengend Snippet: Secretion of IL-β (A), IL-6 (B), GM-CSF (C), and ICAM-1 (D) by T. gondii -infected HRPE cells. Cell culture supernatant fluids were collected at indicated p.i. times, and the levels of IL-1β, IL-6, GM-CSF, and ICAM-1 were determined by enzyme-linked immunosorbent assay. The lower limits of detection were 0.13 pg/ml (IL-1β), 10 pg/ml (IL-6), 15.6 pg/ml (GM-CSF), and 1.6 ng/ml (ICAM-1). Results are the means ± standard error for six experiments, each with duplicate samples.

    Article Snippet: Human IL-6 , ICAM-1 , and GM-CSF (clone GMCSF, pCSF-1; American Type Culture Collection, Manassas, Va.) cDNA probes were labeled by the random primer method with digoxigenin-dUTP (Dig DNA labeling and detection kit; Boehringer Mannheim, Indianapolis, Ind.).

    Techniques: Infection, Cell Culture, Enzyme-linked Immunosorbent Assay

    Affinity and antigen-density dependent activation of Jurkat CAR T cells in vitro . ( a ) Top, histograms depicting 8 μm latex beads coupled with known amounts of R6.5 antibody conjugated with cy5.5 (10 3 –10 7 antibodies per bead). The level of shift after incubation with R6.5 (black) from non-labeled (grey) was used to estimate ICAM-1 density in each indicated target cell line. 8505 C/-ICAM-1; 8505 C cells with ICAM-1 gene inactivation by CRISPR/Cas9. 8505 C/LPS, 8505 C cells were incubated with LPS to induce overexpression of ICAM-1. ( b ) CD25 expression in Jurkat CAR T cells (WT, F292A, F292G, and TM) after co-incubation with different target cell lines for 24 h (n = 3–4). p

    Journal: Scientific Reports

    Article Title: Micromolar affinity CAR T cells to ICAM-1 achieves rapid tumor elimination while avoiding systemic toxicity

    doi: 10.1038/s41598-017-14749-3

    Figure Lengend Snippet: Affinity and antigen-density dependent activation of Jurkat CAR T cells in vitro . ( a ) Top, histograms depicting 8 μm latex beads coupled with known amounts of R6.5 antibody conjugated with cy5.5 (10 3 –10 7 antibodies per bead). The level of shift after incubation with R6.5 (black) from non-labeled (grey) was used to estimate ICAM-1 density in each indicated target cell line. 8505 C/-ICAM-1; 8505 C cells with ICAM-1 gene inactivation by CRISPR/Cas9. 8505 C/LPS, 8505 C cells were incubated with LPS to induce overexpression of ICAM-1. ( b ) CD25 expression in Jurkat CAR T cells (WT, F292A, F292G, and TM) after co-incubation with different target cell lines for 24 h (n = 3–4). p

    Article Snippet: ICAM-1 and CAR expression quantification ICAM-1 expression on various cell lines was determined using a mouse anti-human R6.5 monoclonal antibody (10 µg/ml) obtained from hybridoma (ATCC).

    Techniques: Activation Assay, In Vitro, Incubation, Labeling, CRISPR, Over Expression, Expressing

    Analysis of systemic toxicity by flow cytometry and histology. ( a ) Flow cytometry analysis of total cells harvested from the lungs of non treated (No T) or treated (TM CAR) mice. GFP and CD3 were used as markers of 8505 C tumor and T cells, respectively. Mice treated with TM CAR T cells were sacrificed at different time points to represent the association between tumor burden and TM CAR T cells. ( b ) Lung tissues harvested from untreated mice and mice treated with TM and F292A CAR T cells were processed for H E, GFP and CD3 staining. The scale bar in each image is 2 mm. Tissue sacrifice time points are indicated on the left. For example, X20T10 represents 20 days post tumor x enograft and 10 days post T cell infusion. ( c ) Murine ICAM-1 expression in lung cells harvested from tumor-bearing mice after treatment with TM CAR T cells.

    Journal: Scientific Reports

    Article Title: Micromolar affinity CAR T cells to ICAM-1 achieves rapid tumor elimination while avoiding systemic toxicity

    doi: 10.1038/s41598-017-14749-3

    Figure Lengend Snippet: Analysis of systemic toxicity by flow cytometry and histology. ( a ) Flow cytometry analysis of total cells harvested from the lungs of non treated (No T) or treated (TM CAR) mice. GFP and CD3 were used as markers of 8505 C tumor and T cells, respectively. Mice treated with TM CAR T cells were sacrificed at different time points to represent the association between tumor burden and TM CAR T cells. ( b ) Lung tissues harvested from untreated mice and mice treated with TM and F292A CAR T cells were processed for H E, GFP and CD3 staining. The scale bar in each image is 2 mm. Tissue sacrifice time points are indicated on the left. For example, X20T10 represents 20 days post tumor x enograft and 10 days post T cell infusion. ( c ) Murine ICAM-1 expression in lung cells harvested from tumor-bearing mice after treatment with TM CAR T cells.

    Article Snippet: ICAM-1 and CAR expression quantification ICAM-1 expression on various cell lines was determined using a mouse anti-human R6.5 monoclonal antibody (10 µg/ml) obtained from hybridoma (ATCC).

    Techniques: Flow Cytometry, Cytometry, Mouse Assay, Staining, Expressing

    Construction of ICAM-1 specific CARs with step-wise, 10 6 -fold variations in affinity. ( a ) Schematic of LFA-1 in complex with ICAM-1. α and β chains, and modular domains of LFA-1 integrin are labeled. I domain of α chain is denoted with a dotted box. Metal ions necessary for LFA-1 and ICAM-1 interaction are shown in circles. ( b ) Structural model of LFA-1 I domain and the N-terminal domain of ICAM-1 (D1) are drawn in ribbon diagram. N and C-termini, and mutational hot spots are indicated. ( c ) SPR sensogram of I domain variants binding to immobilized human ICAM-1, except F265S/F292G*, which was flowed over murine ICAM-1 (adapted from Fig. 2 of Jin et al . 27 , and Fig. 1 of Wong et al . 28 ). ( d ) A schematic of the lentivirus vector encoding I domain CAR. LTR = long terminal repeat; SD = splice donor; SA = splice acceptor; ψ + = packaging signal; SS = signal sequence; TM = transmembrane; Cyt = cytosolic domain. ( e ) Anti-Myc antibody binding to Jurkat T cells transduced with Myc-tagged CARs (TM, F292G, F292A, and WT I domain). NT = non-transduced. ( f ) Recombinant ICAM-1-Fc binding to CARs expressed in HEK 293 T cells. ( g ) V-bottom adhesion assay measuring relative binding affinities between I domain CARs expressed in Jurkat T cells and soluble human (top) and murine (bottom) ICAM-1 (CD54) coated surfaces. n = 3; p

    Journal: Scientific Reports

    Article Title: Micromolar affinity CAR T cells to ICAM-1 achieves rapid tumor elimination while avoiding systemic toxicity

    doi: 10.1038/s41598-017-14749-3

    Figure Lengend Snippet: Construction of ICAM-1 specific CARs with step-wise, 10 6 -fold variations in affinity. ( a ) Schematic of LFA-1 in complex with ICAM-1. α and β chains, and modular domains of LFA-1 integrin are labeled. I domain of α chain is denoted with a dotted box. Metal ions necessary for LFA-1 and ICAM-1 interaction are shown in circles. ( b ) Structural model of LFA-1 I domain and the N-terminal domain of ICAM-1 (D1) are drawn in ribbon diagram. N and C-termini, and mutational hot spots are indicated. ( c ) SPR sensogram of I domain variants binding to immobilized human ICAM-1, except F265S/F292G*, which was flowed over murine ICAM-1 (adapted from Fig. 2 of Jin et al . 27 , and Fig. 1 of Wong et al . 28 ). ( d ) A schematic of the lentivirus vector encoding I domain CAR. LTR = long terminal repeat; SD = splice donor; SA = splice acceptor; ψ + = packaging signal; SS = signal sequence; TM = transmembrane; Cyt = cytosolic domain. ( e ) Anti-Myc antibody binding to Jurkat T cells transduced with Myc-tagged CARs (TM, F292G, F292A, and WT I domain). NT = non-transduced. ( f ) Recombinant ICAM-1-Fc binding to CARs expressed in HEK 293 T cells. ( g ) V-bottom adhesion assay measuring relative binding affinities between I domain CARs expressed in Jurkat T cells and soluble human (top) and murine (bottom) ICAM-1 (CD54) coated surfaces. n = 3; p

    Article Snippet: ICAM-1 and CAR expression quantification ICAM-1 expression on various cell lines was determined using a mouse anti-human R6.5 monoclonal antibody (10 µg/ml) obtained from hybridoma (ATCC).

    Techniques: Labeling, SPR Assay, Binding Assay, Plasmid Preparation, Sequencing, Transduction, Recombinant, Cell Adhesion Assay

    Deletion of RKIKK motif inhibits leukocyte adhesion and transmigration under shear-flow condition. (A) Attachment of human PBLs to COS-7 ICAM-1 mutants under shear-flow condition. PBLs (1 × 10 6 cells/ml) were incubated with COS-7 transfectants

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: Deletion of RKIKK motif inhibits leukocyte adhesion and transmigration under shear-flow condition. (A) Attachment of human PBLs to COS-7 ICAM-1 mutants under shear-flow condition. PBLs (1 × 10 6 cells/ml) were incubated with COS-7 transfectants

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Transmigration Assay, Flow Cytometry, Incubation

    The RKIKK motif is critical for ICAM-1–mediated, ring-shaped membrane projection upon binding to LFA-1 on leukocytes. COS-7 cells expressing wt-IC1_GFP or IC1ΔRKIKK_GFP were incubated with CBR-LFA-1/2 mAb-activated PBMCs for various times

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: The RKIKK motif is critical for ICAM-1–mediated, ring-shaped membrane projection upon binding to LFA-1 on leukocytes. COS-7 cells expressing wt-IC1_GFP or IC1ΔRKIKK_GFP were incubated with CBR-LFA-1/2 mAb-activated PBMCs for various times

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Binding Assay, Expressing, Incubation

    Schematic representation of C-terminally mutated ICAM-1-GFP constructs and their expression on the surface of cells. (A) Wild-type and mutant ICAM-1 proteins fused to GFP. IgSF domains 1–5 (EXT), transmembrane domain (TM), intracellular domain

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: Schematic representation of C-terminally mutated ICAM-1-GFP constructs and their expression on the surface of cells. (A) Wild-type and mutant ICAM-1 proteins fused to GFP. IgSF domains 1–5 (EXT), transmembrane domain (TM), intracellular domain

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Construct, Expressing, Mutagenesis

    ICAM-1–induced microvillar organization requires ERM activity. COS-7 cells were transfected with the indicated cDNAs (wt-IC1_GFP; Wt-Ezrin in pDesRed = Wt-Ezrin_RFP; DN-Ezrin in pDesRed = DN-Ezrin_RFP; Wt-PECAM-1 in pCDNA3.1 = Wt-PECAM-1; Wt-PECAM-1

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: ICAM-1–induced microvillar organization requires ERM activity. COS-7 cells were transfected with the indicated cDNAs (wt-IC1_GFP; Wt-Ezrin in pDesRed = Wt-Ezrin_RFP; DN-Ezrin in pDesRed = DN-Ezrin_RFP; Wt-PECAM-1 in pCDNA3.1 = Wt-PECAM-1; Wt-PECAM-1

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Activity Assay, Transfection

    The proposed model of leukocyte adhesion on and transmigration through endothelial cells. The RKIKK motif in the intracellular domain plays a critical role not only for the physical distribution of ICAM-1 on the microvilli but also for the microvillar

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: The proposed model of leukocyte adhesion on and transmigration through endothelial cells. The RKIKK motif in the intracellular domain plays a critical role not only for the physical distribution of ICAM-1 on the microvilli but also for the microvillar

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Transmigration Assay

    ICAM-1 induces microvillar elongation in COS-7 cells. (A) Overexpression of ICAM-1 induces F-actin and microvillar elongation. COS-7 cells were transiently transfected with 1 μg of plasmid producing wild-type ICAM-1 fused to GFP protein. The cells

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: ICAM-1 induces microvillar elongation in COS-7 cells. (A) Overexpression of ICAM-1 induces F-actin and microvillar elongation. COS-7 cells were transiently transfected with 1 μg of plasmid producing wild-type ICAM-1 fused to GFP protein. The cells

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Over Expression, Transfection, Plasmid Preparation

    ICAM-1 is colocalized with F-actin, ezrin, and moesin in microvilli. COS-7 cells expressing wt-IC1_GFP or IC1ΔCTD_GFP were fixed and stained with TRITC-phalloidin (A) or with anti-ezrin (B) or anti-moesin (C) antibodies, followed by incubation

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: ICAM-1 is colocalized with F-actin, ezrin, and moesin in microvilli. COS-7 cells expressing wt-IC1_GFP or IC1ΔCTD_GFP were fixed and stained with TRITC-phalloidin (A) or with anti-ezrin (B) or anti-moesin (C) antibodies, followed by incubation

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Expressing, Staining, Incubation

    Characterization of COS-7 cell lines that were transfected with cDNAs containing wild-type ICAM-1 or ICAM-1–lacking intracellular domain. (A) Immunofluorescence staining and confocal imaging of COS-7 cells expressing wild-type ICAM-1 (wt-IC1 in

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: Characterization of COS-7 cell lines that were transfected with cDNAs containing wild-type ICAM-1 or ICAM-1–lacking intracellular domain. (A) Immunofluorescence staining and confocal imaging of COS-7 cells expressing wild-type ICAM-1 (wt-IC1 in

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Transfection, Immunofluorescence, Staining, Imaging, Expressing

    Deletion of RKIKK motif inhibits leukocyte transmigration but not adhesion under static-flow condition. (A) Attachment of human PBLs to COS-7 ICAM-1 mutants under static-flow condition. PBLs were incubated with COS-7 ICAM-1 mutants in the presence or

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: Deletion of RKIKK motif inhibits leukocyte transmigration but not adhesion under static-flow condition. (A) Attachment of human PBLs to COS-7 ICAM-1 mutants under static-flow condition. PBLs were incubated with COS-7 ICAM-1 mutants in the presence or

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Transmigration Assay, Flow Cytometry, Incubation

    Association of ezrin with the RKIKK motif of ICAM-1. COS-7 cells (1 × 10 7 ) expressing wt-IC1, IC1ΔCTD, or IC1ΔRKIKK were transfected with the cDNA encoding wt-ezrin. Cells were lysed and immunoprecipitated with the R6.5-bead conjugates.

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: Association of ezrin with the RKIKK motif of ICAM-1. COS-7 cells (1 × 10 7 ) expressing wt-IC1, IC1ΔCTD, or IC1ΔRKIKK were transfected with the cDNA encoding wt-ezrin. Cells were lysed and immunoprecipitated with the R6.5-bead conjugates.

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Expressing, Transfection, Immunoprecipitation

    Leukocyte adhesion to and migration through TNF-α/SDF-1α–activated monolayers of endothelial cells in the presence of penetratin-ICAM-1 peptides. (A) Understatic adhesion and transmigration of PBLs. Left, Human PBLs were incubated

    Journal:

    Article Title:

    doi: 10.1091/mbc.E06-08-0744

    Figure Lengend Snippet: Leukocyte adhesion to and migration through TNF-α/SDF-1α–activated monolayers of endothelial cells in the presence of penetratin-ICAM-1 peptides. (A) Understatic adhesion and transmigration of PBLs. Left, Human PBLs were incubated

    Article Snippet: Antibody to human ICAM-1 (R6.5) was purified from R6.5 hybridoma (ATCC HB-9580), and anti-GFP was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Techniques: Migration, Transmigration Assay, Incubation

    DENV internalization and infectivity in wt DC-SIGN compared to mutant cells. A. % virus internalized for DC-SIGN-3A cells as compared to wt DC-SIGN cells (upper panel); the same comparison for DC-SIGN-Δ35 cells (lower panel). B. DENV infection at 24h of wt DC-SIGN, DC-SIGN-3A (upper panel) and DC-SIGN-Δ35 (lower panel) expressing cells at MOIs of 1, 3 and 10.

    Journal: Traffic (Copenhagen, Denmark)

    Article Title: Beyond attachment: roles of DC-SIGN in dengue virus infection

    doi: 10.1111/tra.12469

    Figure Lengend Snippet: DENV internalization and infectivity in wt DC-SIGN compared to mutant cells. A. % virus internalized for DC-SIGN-3A cells as compared to wt DC-SIGN cells (upper panel); the same comparison for DC-SIGN-Δ35 cells (lower panel). B. DENV infection at 24h of wt DC-SIGN, DC-SIGN-3A (upper panel) and DC-SIGN-Δ35 (lower panel) expressing cells at MOIs of 1, 3 and 10.

    Article Snippet: NIH3T3 cells were transduced with the two plasmids, pMX-DC-SIGN-Δ35 and pMX-DC-SIGN-3A, using the Phoenix-ECO retroviral packaging system (ATCC CRL-3214), respectively.

    Techniques: Infection, Mutagenesis, Expressing