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Flow cytometryAntibody data
- Antibody Data
- Antigen structure
- References [10]
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- Validations
- Flow cytometry [1]
- Other assay [3]
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- Product number
- 17-0549-41 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- CD54 (ICAM-1) Monoclonal Antibody (HA58), APC, eBioscience™
- Antibody type
- Monoclonal
- Antigen
- Other
- Description
- Description: The HA58 monoclonal antibody reacts with human CD54 (InterCellular Adhesion Molecule-1, ICAM-1), a 90-110 kDa transmembrane glycoprotein expressed by monocytes, lymphocytes and endothelial cells. Expression of CD54 is upregulated on activated lymphocytes. Interaction of CD54 with its ligand CD11a is important in the inflammatory response. Applications Reported: This HA58 antibody has been reported for use in flow cytometric analysis. Applications Tested: This HA58 antibody has been pre-titrated and tested by flow cytometric analysis of normal human peripheral blood cells. This can be used at 5 µL (0.5 µg) per test. A test is defined as the amount (µg) of antibody that will stain a cell sample in a final volume of 100 µL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. Excitation: 633-647 nm; Emission: 660 nm; Laser: Red Laser. Filtration: 0.2 µm post-manufacturing filtered.
- Reactivity
- Human
- Host
- Mouse
- Isotype
- IgG
- Antibody clone number
- HA58
- Vial size
- 25 Tests
- Concentration
- 5 µL/Test
- Storage
- 4° C, store in dark, DO NOT FREEZE!
Submitted references Pomalidomide restores immune recognition of primary effusion lymphoma through upregulation of ICAM-1 and B7-2.
EWS-FLI1 low Ewing sarcoma cells demonstrate decreased susceptibility to T-cell-mediated tumor cell apoptosis.
The critical role of SENP1-mediated GATA2 deSUMOylation in promoting endothelial activation in graft arteriosclerosis.
Mesenchymal stem cells augment the anti-bacterial activity of neutrophil granulocytes.
Effect of nicotine and porphyromonas gingivalis lipopolysaccharide on endothelial cells in vitro.
Expression of intercellular adhesion molecule 1 by hepatocellular carcinoma stem cells and circulating tumor cells.
Requirements for ICAM-1 immunogene therapy of lymphoma.
PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated I kappa B alpha degradation.
PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated I kappa B alpha degradation.
The human natural killer cell immune synapse.
Shrestha P, Davis DA, Jaeger HK, Stream A, Aisabor AI, Yarchoan R
PLoS pathogens 2021 Jan;17(1):e1009091
PLoS pathogens 2021 Jan;17(1):e1009091
EWS-FLI1 low Ewing sarcoma cells demonstrate decreased susceptibility to T-cell-mediated tumor cell apoptosis.
Bailey KM, Julian CM, Klinghoffer AN, Bernard H, Lucas PC, McAllister-Lucas LM
Oncotarget 2019 May 21;10(36):3385-3399
Oncotarget 2019 May 21;10(36):3385-3399
The critical role of SENP1-mediated GATA2 deSUMOylation in promoting endothelial activation in graft arteriosclerosis.
Qiu C, Wang Y, Zhao H, Qin L, Shi Y, Zhu X, Song L, Zhou X, Chen J, Zhou H, Zhang H, Tellides G, Min W, Yu L
Nature communications 2017 Jun 1;8:15426
Nature communications 2017 Jun 1;8:15426
Mesenchymal stem cells augment the anti-bacterial activity of neutrophil granulocytes.
Brandau S, Jakob M, Bruderek K, Bootz F, Giebel B, Radtke S, Mauel K, Jäger M, Flohé SB, Lang S
PloS one 2014;9(9):e106903
PloS one 2014;9(9):e106903
Effect of nicotine and porphyromonas gingivalis lipopolysaccharide on endothelial cells in vitro.
An N, Andrukhov O, Tang Y, Falkensammer F, Bantleon HP, Ouyang X, Rausch-Fan X
PloS one 2014;9(5):e96942
PloS one 2014;9(5):e96942
Expression of intercellular adhesion molecule 1 by hepatocellular carcinoma stem cells and circulating tumor cells.
Liu S, Li N, Yu X, Xiao X, Cheng K, Hu J, Wang J, Zhang D, Cheng S, Liu S
Gastroenterology 2013 May;144(5):1031-1041.e10
Gastroenterology 2013 May;144(5):1031-1041.e10
Requirements for ICAM-1 immunogene therapy of lymphoma.
Kanwar JR, Berg RW, Yang Y, Kanwar RK, Ching LM, Sun X, Krissansen GW
Cancer gene therapy 2003 Jun;10(6):468-76
Cancer gene therapy 2003 Jun;10(6):468-76
PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated I kappa B alpha degradation.
Bao J, Sato K, Li M, Gao Y, Abid R, Aird W, Simons M, Post MJ
American journal of physiology. Heart and circulatory physiology 2001 Dec;281(6):H2612-8
American journal of physiology. Heart and circulatory physiology 2001 Dec;281(6):H2612-8
PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated I kappa B alpha degradation.
Bao J, Sato K, Li M, Gao Y, Abid R, Aird W, Simons M, Post MJ
American journal of physiology. Heart and circulatory physiology 2001 Dec;281(6):H2612-8
American journal of physiology. Heart and circulatory physiology 2001 Dec;281(6):H2612-8
The human natural killer cell immune synapse.
Davis DM, Chiu I, Fassett M, Cohen GB, Mandelboim O, Strominger JL
Proceedings of the National Academy of Sciences of the United States of America 1999 Dec 21;96(26):15062-7
Proceedings of the National Academy of Sciences of the United States of America 1999 Dec 21;96(26):15062-7
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Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Staining of normal human peripheral blood cells with Mouse IgG1 K Isotype Control APC (Product # 17-4714-81) (blue histogram) or Anti-Human CD54 (ICAM-1) APC (purple histogram). Cells in the lymphocyte gate were used for analysis.
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- NULL
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 3 Loss of endothelial SENP1 inhibits EC activation. ( a ) Grafts from WT or SENP1-ecKO mice were harvested 3 days post-transplantation. The induction of endothelial adhesion molecules was demonstrated by immunofluorescence staining of ICAM-1, VCAM-1, or P-selectin and PECAM-1 with DAPI labelling of the nuclei. Bar represents 50 mum. ( b - e ) Attenuated induction of adhesion molecules in SENP1-ecKO MAECs. Flow cytometry analysis of ICAM-1, VCAM-1 and P-selectin in MAECs isolated from WT or SENP1-ecKO mice after TNF or IL-1beta treatment. Representative histograms are shown in ( b ) with the quantification of mean intensity in ( c - e ). ( f - h ) Overexpression of the catalytically inactive form of SENP1 (SENP1-Mut) inhibits the induction of adhesion molecules in HUVECs. HUVECs were infected by Ad-SENP1-Mut or vector control (Ad-LacZ) for 24 h, treated with pro-inflammatory cytokines and analysed by flow cytometry in the same way as MAECs. Representative histograms of ICAM-1 and VCAM-1 are shown in ( f ) with the quantification of mean intensity in ( g , h ). Data are presented as the mean+-s.e.m. from at least three independent experiments. * P
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 5 Effect of nicotine on the P. gingivalis LPS-induced protein expression of pro-inflammatory mediators in HUVECs. HUVECs were stimulated by P. gingivalis LPS in the presence or absence of nicotine (10 uM-10 mM) for 4, 24, and 72 h. After stimulation, the surface expression levels of ICAM-1 (A), VCAM-1 (B), and E-selectin (C) were measured by flow cytometry, and the quantity of MCP-1 (D) and IL-8 (E) in conditioned media was measured by ELISA. Each value represents mean +-SD of three independent assays. Non-stimulated HUVECs were used as a control. The protein expression levels of pro-inflammatory mediators were not analyzed after stimulation with 10-mM nicotine for 24 and 72 h because the cells were not viable. * - significantly different between groups, p
