cd54 icam 1 antibody  (Cell Signaling Technology Inc)

 
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    Name:
    CD54 ICAM 1 Antibody
    Description:
    Intercellular cell adhesion molecule 1 CD54 or ICAM 1 is a cell surface glycoprotein that belongs to the immunoglobulin superfamily IgSF of adhesion molecules CD54 is expressed at low levels in diverse cell types and is induced by cytokines TNF α interleukin 1 and bacterial lipopolysaccharide 1 Apical localization of CD54 on endothelial cells or basolateral localization on epithelial cells is a prerequisite for leukocyte trafficking through the endothelial or epithelial barrier 1 Apical expression of CD54 on epithelial cells mediates pathogen invasion as well as host defense a pattern also observed in tumors 1 CD54 also functions as a co stimulator on antigen presenting cells binding to its receptor LFA 1 leukocyte function associated antigen 1 on the surface of T cells during antigen presentation 2 Cross linking of CD54 or binding to its ligand triggers activation of Src family kinases and the Rho ROCK pathway 3 7 Phosphorylation on Tyr485 of CD54 is required for its association with SHP 2 5 SHP 2 seems essential for CD54 induced Src activation 7
    Catalog Number:
    4915
    Price:
    None
    Applications:
    Western Blot, Immunohistochemistry
    Category:
    Primary Antibodies
    Source:
    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues of human CD54 (ICAM-1) protein. Antibodies are purified by protein A and peptide affinity chromatography.
    Reactivity:
    Human
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    Structured Review

    Cell Signaling Technology Inc cd54 icam 1 antibody
    Intercellular cell adhesion molecule 1 CD54 or ICAM 1 is a cell surface glycoprotein that belongs to the immunoglobulin superfamily IgSF of adhesion molecules CD54 is expressed at low levels in diverse cell types and is induced by cytokines TNF α interleukin 1 and bacterial lipopolysaccharide 1 Apical localization of CD54 on endothelial cells or basolateral localization on epithelial cells is a prerequisite for leukocyte trafficking through the endothelial or epithelial barrier 1 Apical expression of CD54 on epithelial cells mediates pathogen invasion as well as host defense a pattern also observed in tumors 1 CD54 also functions as a co stimulator on antigen presenting cells binding to its receptor LFA 1 leukocyte function associated antigen 1 on the surface of T cells during antigen presentation 2 Cross linking of CD54 or binding to its ligand triggers activation of Src family kinases and the Rho ROCK pathway 3 7 Phosphorylation on Tyr485 of CD54 is required for its association with SHP 2 5 SHP 2 seems essential for CD54 induced Src activation 7
    https://www.bioz.com/result/cd54 icam 1 antibody/product/Cell Signaling Technology Inc
    Average 98 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    cd54 icam 1 antibody - by Bioz Stars, 2020-09
    98/100 stars

    Images

    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: The MK2/HuR signaling pathway regulates TNF-α-induced ICAM-1 expression by promoting the stabilization of ICAM-1 mRNA
    Article Snippet: .. Antibodies raised against MK2 (#3042), phospho-MK2 (Thr334, #3041), ICAM-1 (#4915) was obtained from Cell Signaling (Danvers, USA); a monoclonal antibody against HuR (ab14371) was received from Abcam (Cambridge, USA); antibodies against β-actin (P30002) and histone (P30266) were from Abmart (Shanghai, China);IL-8 ELISA Kit (BMS204/3) was received from eBioscience (San Diego, USA). .. RevertAid First Strand cDNA Synthesis Kit (#K1622) was purchased from Fermentas UAB (Vilnius, Lithuania).

    Incubation:

    Article Title: Vaspin inhibits cytokine-induced nuclear factor-kappa B activation and adhesion molecule expression via AMP-activated protein kinase activation in vascular endothelial cells
    Article Snippet: .. Membranes were incubated in blocking buffer and then with one or more of the following primary antibodies: anti-AMPK (#2532, Cell Signaling, 1:1000), anti-phosphorylated AMPK (#2531, Thr172, Cell Signaling, 1:1000), anti-acetyl-CoA carboxylase (#3662, ACC, Cell Signaling, 1:1000), anti-phosphorylated ACC (#3661, Ser79, Cell Signaling, 1:1000), anti-phosphorylated Akt (#9271, Cell Signaling, 1:1000), anti-ICAM-1 (#4915, Cell Signaling, 1:1000), anti-VCAM-1 (#12367, Cell Signaling, 1:1000), anti-E-selectin (NBP1-45545, Novus Biologicals, CO, USA), and anti-MCP-1 (ab25124, Abcam, Cambridge, UK, 1:1000) antibodies. .. For the inhibitor of NF-κB (IκB) experiments, membranes were incubated with anti-IκBα (#4812, Cell Signaling, 1:1000), anti-phosphorylated IκBα (#4812, Ser32, Cell Signaling, 1:1000), or anti-β-actin (A5316, Sigma, St. Louis, MO, USA, 1:10,000) antibodies.

    Article Title: Reduction of Endothelial Nitric Oxide Increases the Adhesiveness of Constitutive Endothelial Membrane ICAM-1 through Src-Mediated Phosphorylation
    Article Snippet: .. The membranes were then incubated at room temperature in Odyssey blocking buffer (LiCor BioSciences) for 1 h, followed by incubations with primary antibodies [1:1,000 for anti-VE-Cadherin (Cat # 2500, Cell Signaling), anti ICAM-1 (1:1,000, Cat # 4915S, Cell Signaling or Cat # 554966, BD Pharmingen), and anti-β-actin (Cat # 8457, Cell Signaling), 1:500 for anti-p-ICAM-1 (phospho Y512, ab51033, Abcam)] at 4°C overnight, and secondary antibodies [1:10,000 for IRDye800-conjugated anti-mouse and anti-rabbit antibodies (Cat # 925-68071 and 925-32211, LiCor BioSciences)] at room temperature for 1 h. Images were visualized using a LiCor Odyssey Scanner and the bands were quantified using Image Studio software (LiCor BioSciences). ..

    Article Title: Exosome-Transmitted miR-25 Induced by H. pylori Promotes Vascular Endothelial Cell Injury by Targeting KLF2
    Article Snippet: .. The PVDF membranes were incubated with VCAM-1 (Cell Signaling Technology, CST, Boston, USA, #32653); ICAM-1 (CST, #4915); CD63 (Abcam, Shanghai, China, ab134045); KLF2 (Abcam, ab203591); or GAPDH (CST, #5174) antibodies overnight at 4°C, and then incubated with secondary antibodies (goat anti-rabbit or mouse) (ZSGB-BIO, Beijing, China) for 1 h. The PVDF membranes were then exposed in a chemiluminescence instrument (Bio-Rad ChemiDoc XRS+, USA) using the SuperSignal West Dura Extended Duration Substrate Kit (Thermo, Scientific, Beijing, China). .. Cell and Bacterial Culture The GES-1 and HEK293 cell lines were purchased from the American Type Culture Collection (ATCC).

    Blocking Assay:

    Article Title: Vaspin inhibits cytokine-induced nuclear factor-kappa B activation and adhesion molecule expression via AMP-activated protein kinase activation in vascular endothelial cells
    Article Snippet: .. Membranes were incubated in blocking buffer and then with one or more of the following primary antibodies: anti-AMPK (#2532, Cell Signaling, 1:1000), anti-phosphorylated AMPK (#2531, Thr172, Cell Signaling, 1:1000), anti-acetyl-CoA carboxylase (#3662, ACC, Cell Signaling, 1:1000), anti-phosphorylated ACC (#3661, Ser79, Cell Signaling, 1:1000), anti-phosphorylated Akt (#9271, Cell Signaling, 1:1000), anti-ICAM-1 (#4915, Cell Signaling, 1:1000), anti-VCAM-1 (#12367, Cell Signaling, 1:1000), anti-E-selectin (NBP1-45545, Novus Biologicals, CO, USA), and anti-MCP-1 (ab25124, Abcam, Cambridge, UK, 1:1000) antibodies. .. For the inhibitor of NF-κB (IκB) experiments, membranes were incubated with anti-IκBα (#4812, Cell Signaling, 1:1000), anti-phosphorylated IκBα (#4812, Ser32, Cell Signaling, 1:1000), or anti-β-actin (A5316, Sigma, St. Louis, MO, USA, 1:10,000) antibodies.

    Article Title: Reduction of Endothelial Nitric Oxide Increases the Adhesiveness of Constitutive Endothelial Membrane ICAM-1 through Src-Mediated Phosphorylation
    Article Snippet: .. The membranes were then incubated at room temperature in Odyssey blocking buffer (LiCor BioSciences) for 1 h, followed by incubations with primary antibodies [1:1,000 for anti-VE-Cadherin (Cat # 2500, Cell Signaling), anti ICAM-1 (1:1,000, Cat # 4915S, Cell Signaling or Cat # 554966, BD Pharmingen), and anti-β-actin (Cat # 8457, Cell Signaling), 1:500 for anti-p-ICAM-1 (phospho Y512, ab51033, Abcam)] at 4°C overnight, and secondary antibodies [1:10,000 for IRDye800-conjugated anti-mouse and anti-rabbit antibodies (Cat # 925-68071 and 925-32211, LiCor BioSciences)] at room temperature for 1 h. Images were visualized using a LiCor Odyssey Scanner and the bands were quantified using Image Studio software (LiCor BioSciences). ..

    Software:

    Article Title: Reduction of Endothelial Nitric Oxide Increases the Adhesiveness of Constitutive Endothelial Membrane ICAM-1 through Src-Mediated Phosphorylation
    Article Snippet: .. The membranes were then incubated at room temperature in Odyssey blocking buffer (LiCor BioSciences) for 1 h, followed by incubations with primary antibodies [1:1,000 for anti-VE-Cadherin (Cat # 2500, Cell Signaling), anti ICAM-1 (1:1,000, Cat # 4915S, Cell Signaling or Cat # 554966, BD Pharmingen), and anti-β-actin (Cat # 8457, Cell Signaling), 1:500 for anti-p-ICAM-1 (phospho Y512, ab51033, Abcam)] at 4°C overnight, and secondary antibodies [1:10,000 for IRDye800-conjugated anti-mouse and anti-rabbit antibodies (Cat # 925-68071 and 925-32211, LiCor BioSciences)] at room temperature for 1 h. Images were visualized using a LiCor Odyssey Scanner and the bands were quantified using Image Studio software (LiCor BioSciences). ..

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    Cell Signaling Technology Inc icam 1
    APN attenuated TNF-α induced nitrotyrosine formation (A) and <t>ICAM-1</t> expression (B) in control cells cultured with normal glucose/normal lipid (Control). After 72 hours of HUVEC exposure to HG/HL, APN failed to reduce TNF-α mediated nitrotyrosine
    Icam 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/icam 1/product/Cell Signaling Technology Inc
    Average 93 stars, based on 26 article reviews
    Price from $9.99 to $1999.99
    icam 1 - by Bioz Stars, 2020-09
    93/100 stars
      Buy from Supplier

    91
    Cell Signaling Technology Inc antibody against icam 1
    p-STAT3 upregulates <t>ICAM-1</t> expression in GSC11 cells under hypoxic conditions ( A ) Western blotting revealed that ICAM-1 is expressed in multiple human glioma stem cell lines. ( B ) Western blotting revealed that the ICAM-1 expression level in GSC11 cells increased in a time-dependent manner under hypoxic conditions. ( C ) Western blotting revealed that ICAM-1 was expressed in GSC11 cells treated with or without LY, U0126, SU, or AZD1480 under hypoxic conditions. ( D ) Western blotting revealed the p-STAT3 expression level in the nuclear fraction of GSC11 cells treated with or without AZD1480 under hypoxic conditions.
    Antibody Against Icam 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibody against icam 1/product/Cell Signaling Technology Inc
    Average 91 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    antibody against icam 1 - by Bioz Stars, 2020-09
    91/100 stars
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    92
    Cell Signaling Technology Inc anti icam 1
    Effect of 9t18:1 and 11t18:1 on gene expression of <t>ICAM-1,</t> VCAM-1 and IL-6 of leptin/9c11t-CLA treated HUVECs. ( A ) The effect of 11t18:1 on expression of ICAM-1, VCAM-1 and IL-6 in leptin treated HUVECs. HUVECs were treated or without leptin (75 nmol/L) for 24 h and then cultured with 11t18:1(25, 50, 100 μmol/L) for 24 h. ( B ) The effect of 9t18:1 on expression of ICAM-1, VCAM-1 and IL-6 in 9c11tCLA treated HUVECs. HUVECs were treated or non-treated with 9c11tCLA (5, 25, 50 μmol/L) and then cultured with 9t18:1 (100 μmol/L) for 24 h. ( C ) The effect of 11t18:1 + leptin on expression of ICAM-1, VCAM-1 and IL-6 in 9c11tCLA treated HUVECs. HUVECs were treated or non-treated with 9c11tCLA (5, 25, 50 μmol/L) and then cultured with the group of 11t18:1 (100 μmol/L) + leptin (75 nmol/L) for 24 h. ( D ) The effect of 9t18:1 on expression of ICAM-1, VCAM-1 and IL-6 of leptin treated HUVECs. HUVECs were treated or non-treated with leptin (75 nmol/L) and then cultured with 9t18:1 (100 μmol/L) and 11t18:1 (100 μmol/L) for 24 h. a–g Data were presented as mean ± SD, values not sharing a common superscript denote significant difference ( P
    Anti Icam 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti icam 1/product/Cell Signaling Technology Inc
    Average 92 stars, based on 13 article reviews
    Price from $9.99 to $1999.99
    anti icam 1 - by Bioz Stars, 2020-09
    92/100 stars
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    Image Search Results


    APN attenuated TNF-α induced nitrotyrosine formation (A) and ICAM-1 expression (B) in control cells cultured with normal glucose/normal lipid (Control). After 72 hours of HUVEC exposure to HG/HL, APN failed to reduce TNF-α mediated nitrotyrosine

    Journal: Free radical biology & medicine

    Article Title: High Glucose/High Lipids Impair Vascular Adiponectin Function via Inhibition of Caveolin-1/AdipoR1 Signalsome Formation

    doi: 10.1016/j.freeradbiomed.2015.09.005

    Figure Lengend Snippet: APN attenuated TNF-α induced nitrotyrosine formation (A) and ICAM-1 expression (B) in control cells cultured with normal glucose/normal lipid (Control). After 72 hours of HUVEC exposure to HG/HL, APN failed to reduce TNF-α mediated nitrotyrosine

    Article Snippet: Antibodies against APN receptor 1 (AdipoR1), APN receptor 2 (AdipoR2), endothelial NO synthase (eNOS), AMP activated protein kinase (AMPK), Akt, ICAM-1, GAPDH, eNOS phosphorylated at Ser1177, phosphorylated AMPK, and phosphorylated Akt were from Cell Signaling Technology (Beverly, MA).

    Techniques: Expressing, Cell Culture

    Expression of intercellular adhesion molecule 1 (ICAM-1) in hapalindole H (Hap H)-treated PC-3 cells.

    Journal: Anticancer research

    Article Title: Hapalindole H Induces Apoptosis as an Inhibitor of NF-κB and Affects the Intrinsic Mitochondrial Pathway in PC-3 Androgen-insensitive Prostate Cancer Cells

    doi: 10.21873/anticanres.12595

    Figure Lengend Snippet: Expression of intercellular adhesion molecule 1 (ICAM-1) in hapalindole H (Hap H)-treated PC-3 cells.

    Article Snippet: Primary antibodies (anti-NF-κBp65 and p50, anti-IκB kinase (anti-IKKα), anti-IKKβ, intercellular adhesion molecule-1 (ICAM-1), and anti-caspase-3) were purchased from Cell Signaling Technologies (Beverly, MA, USA).

    Techniques: Expressing

    p-STAT3 upregulates ICAM-1 expression in GSC11 cells under hypoxic conditions ( A ) Western blotting revealed that ICAM-1 is expressed in multiple human glioma stem cell lines. ( B ) Western blotting revealed that the ICAM-1 expression level in GSC11 cells increased in a time-dependent manner under hypoxic conditions. ( C ) Western blotting revealed that ICAM-1 was expressed in GSC11 cells treated with or without LY, U0126, SU, or AZD1480 under hypoxic conditions. ( D ) Western blotting revealed the p-STAT3 expression level in the nuclear fraction of GSC11 cells treated with or without AZD1480 under hypoxic conditions.

    Journal: Oncotarget

    Article Title: Targeting intercellular adhesion molecule-1 prolongs survival in mice bearing bevacizumab-resistant glioblastoma

    doi: 10.18632/oncotarget.18859

    Figure Lengend Snippet: p-STAT3 upregulates ICAM-1 expression in GSC11 cells under hypoxic conditions ( A ) Western blotting revealed that ICAM-1 is expressed in multiple human glioma stem cell lines. ( B ) Western blotting revealed that the ICAM-1 expression level in GSC11 cells increased in a time-dependent manner under hypoxic conditions. ( C ) Western blotting revealed that ICAM-1 was expressed in GSC11 cells treated with or without LY, U0126, SU, or AZD1480 under hypoxic conditions. ( D ) Western blotting revealed the p-STAT3 expression level in the nuclear fraction of GSC11 cells treated with or without AZD1480 under hypoxic conditions.

    Article Snippet: Blots were incubated with the primary antibody against ICAM-1 (1:1000; Cell signaling Technology, Danvers, MA), GFP (1:1000, CST), p-STAT3 (1:1000, Cell signaling), Tubulin (1:3000; Sigma), p-AKT (1: 1000, Cell signaling Technology, Danvers, MA), AKT (1: 1000, Cell signaling).

    Techniques: Expressing, Western Blot

    ICAM-1 knockdown inhibits macrophage infiltration into tumor in bevacizumab-treated mice ( A ) and ( B ) Immunofluorescence staining with F4/80 (red) (A) and the bar graph of F4/80 positive cells in each high powered microscopic field (B) revealed that shRNA ICAM-1generated tumor had less F4/80 positive macrophage infiltration compared with GSC11GFP generated tumor. Representative photomicrographic images are shown (magnification ×200). ( C ) Immunofluorescence staining for Nestin (green) and F4/80 revealed that blocking ICAM-1 by treatment with ICAM-1 antibody 10 µg/ml or 20 µg/ml in GSC11 cells reduced GSC11 binding to macrophages. ( D ) The bar graph represents the ratio of Nestin positive to F4/80 positive. Data showed that blocking ICAM-1 decreased GSC capacity of binding to macrophages.

    Journal: Oncotarget

    Article Title: Targeting intercellular adhesion molecule-1 prolongs survival in mice bearing bevacizumab-resistant glioblastoma

    doi: 10.18632/oncotarget.18859

    Figure Lengend Snippet: ICAM-1 knockdown inhibits macrophage infiltration into tumor in bevacizumab-treated mice ( A ) and ( B ) Immunofluorescence staining with F4/80 (red) (A) and the bar graph of F4/80 positive cells in each high powered microscopic field (B) revealed that shRNA ICAM-1generated tumor had less F4/80 positive macrophage infiltration compared with GSC11GFP generated tumor. Representative photomicrographic images are shown (magnification ×200). ( C ) Immunofluorescence staining for Nestin (green) and F4/80 revealed that blocking ICAM-1 by treatment with ICAM-1 antibody 10 µg/ml or 20 µg/ml in GSC11 cells reduced GSC11 binding to macrophages. ( D ) The bar graph represents the ratio of Nestin positive to F4/80 positive. Data showed that blocking ICAM-1 decreased GSC capacity of binding to macrophages.

    Article Snippet: Blots were incubated with the primary antibody against ICAM-1 (1:1000; Cell signaling Technology, Danvers, MA), GFP (1:1000, CST), p-STAT3 (1:1000, Cell signaling), Tubulin (1:3000; Sigma), p-AKT (1: 1000, Cell signaling Technology, Danvers, MA), AKT (1: 1000, Cell signaling).

    Techniques: Mouse Assay, Immunofluorescence, Staining, shRNA, Generated, Blocking Assay, Binding Assay

    ICAM-1 is overexpressed in bevacizumab-resistant GSC11 xenografts ( A ) Quantitative real-time PCR, in which GAPDH mRNA expression was used as internal control, revealed that the fold-change in the RNA expression level of ICAM-1 in xenografts from bevacizumab-treated mice was significantly higher than that in vehicle-treated control mice. ( B ) Immunohistochemical analysis revealed that GSC11 xenografts from mice treated with vehicle only (Control) had lower ICAM-1 expression than those from mice treated with bevacizumab (Bev) did. Representative images are shown; cell membranes expressing ICAM-1 are brown (indicated by red arrows; magnification × 400). ( C ) Western blotting revealed that ICAM-1 was expressed in the GSC11 xenografts regardless of whether mice were treated with vehicle (Control) or bevacizumab (Bev).

    Journal: Oncotarget

    Article Title: Targeting intercellular adhesion molecule-1 prolongs survival in mice bearing bevacizumab-resistant glioblastoma

    doi: 10.18632/oncotarget.18859

    Figure Lengend Snippet: ICAM-1 is overexpressed in bevacizumab-resistant GSC11 xenografts ( A ) Quantitative real-time PCR, in which GAPDH mRNA expression was used as internal control, revealed that the fold-change in the RNA expression level of ICAM-1 in xenografts from bevacizumab-treated mice was significantly higher than that in vehicle-treated control mice. ( B ) Immunohistochemical analysis revealed that GSC11 xenografts from mice treated with vehicle only (Control) had lower ICAM-1 expression than those from mice treated with bevacizumab (Bev) did. Representative images are shown; cell membranes expressing ICAM-1 are brown (indicated by red arrows; magnification × 400). ( C ) Western blotting revealed that ICAM-1 was expressed in the GSC11 xenografts regardless of whether mice were treated with vehicle (Control) or bevacizumab (Bev).

    Article Snippet: Blots were incubated with the primary antibody against ICAM-1 (1:1000; Cell signaling Technology, Danvers, MA), GFP (1:1000, CST), p-STAT3 (1:1000, Cell signaling), Tubulin (1:3000; Sigma), p-AKT (1: 1000, Cell signaling Technology, Danvers, MA), AKT (1: 1000, Cell signaling).

    Techniques: Real-time Polymerase Chain Reaction, Expressing, RNA Expression, Mouse Assay, Immunohistochemistry, Western Blot

    ICAM-1 knockdown prolongs survival in mice with bevacizumab-resistant glioblastoma ( A ) Kaplan-Meier survival analysis revealed that when mice bearing shRNA ICAM-1 #4 xenografts prolonger survival compared with the mice bearing GSC11 GFP after treatment with bevacizumab. H E staining analysis ( B ) and the bar graph of tumor volume ( C ) revealed that the size of the tumor which from mice bearing shRNA ICAM-1 #4 xenografts significantly decreased compared with the tumor from the mice bearing GSC11 GFP after with or without treatment of bevacizumab for 5 weeks. Representative images are shown ( D ) for the immunofluorescence staining of ICAM-1 (green) revealing that ICAM-1 expression was significantly lower in tumor from mice bearing shRNA ICAM-1 xenografts compared with tumor from mice bearing GSC11GFP after treatment with or without bevacizumab. Representative photomicrograph images are shown (magnification × 200). ( E ) The bar graph from the percentage of ICAM-1 staining in tumor area (D) revealed that ICAM-1 expression was blocked in tumor from mice bearing shRNA ICAM-1#4 compared with tumor from the mice bearing GSC11 GFP ( * P

    Journal: Oncotarget

    Article Title: Targeting intercellular adhesion molecule-1 prolongs survival in mice bearing bevacizumab-resistant glioblastoma

    doi: 10.18632/oncotarget.18859

    Figure Lengend Snippet: ICAM-1 knockdown prolongs survival in mice with bevacizumab-resistant glioblastoma ( A ) Kaplan-Meier survival analysis revealed that when mice bearing shRNA ICAM-1 #4 xenografts prolonger survival compared with the mice bearing GSC11 GFP after treatment with bevacizumab. H E staining analysis ( B ) and the bar graph of tumor volume ( C ) revealed that the size of the tumor which from mice bearing shRNA ICAM-1 #4 xenografts significantly decreased compared with the tumor from the mice bearing GSC11 GFP after with or without treatment of bevacizumab for 5 weeks. Representative images are shown ( D ) for the immunofluorescence staining of ICAM-1 (green) revealing that ICAM-1 expression was significantly lower in tumor from mice bearing shRNA ICAM-1 xenografts compared with tumor from mice bearing GSC11GFP after treatment with or without bevacizumab. Representative photomicrograph images are shown (magnification × 200). ( E ) The bar graph from the percentage of ICAM-1 staining in tumor area (D) revealed that ICAM-1 expression was blocked in tumor from mice bearing shRNA ICAM-1#4 compared with tumor from the mice bearing GSC11 GFP ( * P

    Article Snippet: Blots were incubated with the primary antibody against ICAM-1 (1:1000; Cell signaling Technology, Danvers, MA), GFP (1:1000, CST), p-STAT3 (1:1000, Cell signaling), Tubulin (1:3000; Sigma), p-AKT (1: 1000, Cell signaling Technology, Danvers, MA), AKT (1: 1000, Cell signaling).

    Techniques: Mouse Assay, shRNA, Staining, Immunofluorescence, Expressing

    ICAM-1 knockdown suppresses cell invasion in vitro and in vivo ( A ) and ( B ) GSC11GFP control and shRNA ICAM-1#4 cells treated with or without bevacizumab were subjected to a transwell migration assay. Photomicrographs of representative samples from the assay (A) and the bar graph of quantitative absorbance (590 nm) (B) revealed that shRNA ICAM-1#2 and shRNA ICAM-1 #4 cells significantly were less invaded compared with GSC GFP after cells treated with or without bevacizumab. Representative photomicrographs from three independent experiments are shown (magnification ×200) ( * P

    Journal: Oncotarget

    Article Title: Targeting intercellular adhesion molecule-1 prolongs survival in mice bearing bevacizumab-resistant glioblastoma

    doi: 10.18632/oncotarget.18859

    Figure Lengend Snippet: ICAM-1 knockdown suppresses cell invasion in vitro and in vivo ( A ) and ( B ) GSC11GFP control and shRNA ICAM-1#4 cells treated with or without bevacizumab were subjected to a transwell migration assay. Photomicrographs of representative samples from the assay (A) and the bar graph of quantitative absorbance (590 nm) (B) revealed that shRNA ICAM-1#2 and shRNA ICAM-1 #4 cells significantly were less invaded compared with GSC GFP after cells treated with or without bevacizumab. Representative photomicrographs from three independent experiments are shown (magnification ×200) ( * P

    Article Snippet: Blots were incubated with the primary antibody against ICAM-1 (1:1000; Cell signaling Technology, Danvers, MA), GFP (1:1000, CST), p-STAT3 (1:1000, Cell signaling), Tubulin (1:3000; Sigma), p-AKT (1: 1000, Cell signaling Technology, Danvers, MA), AKT (1: 1000, Cell signaling).

    Techniques: In Vitro, In Vivo, shRNA, Transwell Migration Assay

    Effect of 9t18:1 and 11t18:1 on gene expression of ICAM-1, VCAM-1 and IL-6 of leptin/9c11t-CLA treated HUVECs. ( A ) The effect of 11t18:1 on expression of ICAM-1, VCAM-1 and IL-6 in leptin treated HUVECs. HUVECs were treated or without leptin (75 nmol/L) for 24 h and then cultured with 11t18:1(25, 50, 100 μmol/L) for 24 h. ( B ) The effect of 9t18:1 on expression of ICAM-1, VCAM-1 and IL-6 in 9c11tCLA treated HUVECs. HUVECs were treated or non-treated with 9c11tCLA (5, 25, 50 μmol/L) and then cultured with 9t18:1 (100 μmol/L) for 24 h. ( C ) The effect of 11t18:1 + leptin on expression of ICAM-1, VCAM-1 and IL-6 in 9c11tCLA treated HUVECs. HUVECs were treated or non-treated with 9c11tCLA (5, 25, 50 μmol/L) and then cultured with the group of 11t18:1 (100 μmol/L) + leptin (75 nmol/L) for 24 h. ( D ) The effect of 9t18:1 on expression of ICAM-1, VCAM-1 and IL-6 of leptin treated HUVECs. HUVECs were treated or non-treated with leptin (75 nmol/L) and then cultured with 9t18:1 (100 μmol/L) and 11t18:1 (100 μmol/L) for 24 h. a–g Data were presented as mean ± SD, values not sharing a common superscript denote significant difference ( P

    Journal: Scientific Reports

    Article Title: 9c11tCLA modulates 11t18:1 and 9t18:1 induced inflammations differently in human umbilical vein endothelial cells

    doi: 10.1038/s41598-018-19729-9

    Figure Lengend Snippet: Effect of 9t18:1 and 11t18:1 on gene expression of ICAM-1, VCAM-1 and IL-6 of leptin/9c11t-CLA treated HUVECs. ( A ) The effect of 11t18:1 on expression of ICAM-1, VCAM-1 and IL-6 in leptin treated HUVECs. HUVECs were treated or without leptin (75 nmol/L) for 24 h and then cultured with 11t18:1(25, 50, 100 μmol/L) for 24 h. ( B ) The effect of 9t18:1 on expression of ICAM-1, VCAM-1 and IL-6 in 9c11tCLA treated HUVECs. HUVECs were treated or non-treated with 9c11tCLA (5, 25, 50 μmol/L) and then cultured with 9t18:1 (100 μmol/L) for 24 h. ( C ) The effect of 11t18:1 + leptin on expression of ICAM-1, VCAM-1 and IL-6 in 9c11tCLA treated HUVECs. HUVECs were treated or non-treated with 9c11tCLA (5, 25, 50 μmol/L) and then cultured with the group of 11t18:1 (100 μmol/L) + leptin (75 nmol/L) for 24 h. ( D ) The effect of 9t18:1 on expression of ICAM-1, VCAM-1 and IL-6 of leptin treated HUVECs. HUVECs were treated or non-treated with leptin (75 nmol/L) and then cultured with 9t18:1 (100 μmol/L) and 11t18:1 (100 μmol/L) for 24 h. a–g Data were presented as mean ± SD, values not sharing a common superscript denote significant difference ( P

    Article Snippet: Anti-ICAM-1, anti-p38, anti-p-p38, anti-SAPK/JNK, anti-p-SAPK/JNK, anti-ERK 1/2, anti-p-ERK1/2, anti-TLR4 and anti-SCD-1 were purchased from Cell Signaling Technology (USA).

    Techniques: Expressing, Cell Culture

    Effect of TAK242 on MAPKs phosphorylation in HUVECs treated with 9t18:1 and 11t18:1. ( A ) Effect of TAK242 on ICAM-1 expression. HUVECs were treated with TAK242 (0.5, 1, 1.5 μmol/L) for 30 min and then cultured with 9t18:1 for 24 h. ( B ) Effect of TAK242 on MAPKs phosphorylation in HUVECs treated with 9t18:1 and 11t18:1. HUVECs were treated with TAK242 (1 μmol/L) for 30 min and then cultured with TFA for 24 h. Values labeled with different letters in each set indicate significant differences ( p

    Journal: Scientific Reports

    Article Title: 9c11tCLA modulates 11t18:1 and 9t18:1 induced inflammations differently in human umbilical vein endothelial cells

    doi: 10.1038/s41598-018-19729-9

    Figure Lengend Snippet: Effect of TAK242 on MAPKs phosphorylation in HUVECs treated with 9t18:1 and 11t18:1. ( A ) Effect of TAK242 on ICAM-1 expression. HUVECs were treated with TAK242 (0.5, 1, 1.5 μmol/L) for 30 min and then cultured with 9t18:1 for 24 h. ( B ) Effect of TAK242 on MAPKs phosphorylation in HUVECs treated with 9t18:1 and 11t18:1. HUVECs were treated with TAK242 (1 μmol/L) for 30 min and then cultured with TFA for 24 h. Values labeled with different letters in each set indicate significant differences ( p

    Article Snippet: Anti-ICAM-1, anti-p38, anti-p-p38, anti-SAPK/JNK, anti-p-SAPK/JNK, anti-ERK 1/2, anti-p-ERK1/2, anti-TLR4 and anti-SCD-1 were purchased from Cell Signaling Technology (USA).

    Techniques: Expressing, Cell Culture, Labeling