- 13-0549-82 - Invitrogen Antibodies ICAM1 antibody

Submitted references Pomalidomide restores immune recognition of primary effusion lymphoma through upregulation of ICAM-1 and B7-2.

Shrestha P, Davis DA, Jaeger HK, Stream A, Aisabor AI, Yarchoan R
PLoS pathogens 2021 Jan;17(1):e1009091

Preservation of microvascular barrier function requires CD31 receptor-induced metabolic reprogramming.

Cheung KCP, Fanti S, Mauro C, Wang G, Nair AS, Fu H, Angeletti S, Spoto S, Fogolari M, Romano F, Aksentijevic D, Liu W, Li B, Cheng L, Jiang L, Vuononvirta J, Poobalasingam TR, Smith DM, Ciccozzi M, Solito E, Marelli-Berg FM
Nature communications 2020 Jul 17;11(1):3595

CD54-NOTCH1 axis controls tumor initiation and cancer stem cell functions in human prostate cancer.

Li C, Liu S, Yan R, Han N, Wong KK, Li L
Theranostics 2017;7(1):67-80

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

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

Tubulation of endosomal structures in human dendritic cells by Toll-like receptor ligation and lymphocyte contact accompanies antigen cross-presentation.

Compeer EB, Flinsenberg TW, Boon L, Hoekstra ME, Boes M
The Journal of biological chemistry 2014 Jan 3;289(1):520-8

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

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

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

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

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

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Normal human peripheral blood cells were stained with Mouse IgG1 kappa Isotype Control, Biotin (Product # 13-4714-85) (blue histogram) or CD54 (ICAM-1) Monoclonal Antibody, Biotin (purple histogram) followed by Streptavidin PE (Product # 12-4317-87). Cells in the lymphocyte gate were used for analysis.
Conjugate: Biotin

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL
Conjugate: Biotin

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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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
Conjugate: Biotin

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 8 GATA2 SUMOylation inhibits its DNA binding activity. ( a ) SUMO conjugation reduces GATA2 DNA binding activity. GATA2-WT, GATA2-2KR, SUMO-GATA2 or control constructs were transfected into 293 T cells, and nuclear extracts were processed with EMSA using a GATA2-specific oligonucleotide probe (top). Input of GATA2 was detected by western blotting with anti-Flag antibody (bottom). ( b ) Overexpression of catalytic inactive form of SENP1 (SENP1-Mut) inhibits recruitment of GATA2 to the promoter of ICAM-1, VCAM-1 and E-selectin. HUVECs were infected by Ad-SENP1-Mut or Ad-LacZ and then treated with TNF. Nuclear extracts were then subjected to ChIP assay with the anti-GATA2 antibody followed by quantitative real-time PCR for the promoter sequences of ICAM-1, VCAM-1 and E-selectin containing a GATA2 binding site. Quantitative results are shown as the ratio of ChIP to input values. Data are presented as the mean+-s.e.m. from three independent experiments. * P
Conjugate: Biotin

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 9 The critical role of GATA2 SUMOylation in EC activation. ( a ) GATA2 SUMOylation regulates the expression of endothelial adhesion molecules. HUVECs were transfected by GATA2 siRNA or control siRNA for 48 h followed by infection with Ad-GATA2-WT, Ad-GATA2-KR, Ad-SUMO-GATA2 or their vector control (GFP) as indicated. HUVECs were treated with TNF or vehicle control for 24 h, and the cell lysates were then subjected to western blotting with anti-ICAM-1, anti-VCAM-1, anti-E-selectin or anti-GATA2 antibodies. Actin was used as a loading control. ( b ) GATA2 SUMOylation site mutation increases endothelial adhesion molecule induction by TNF at the early phase. The expression of endothelial adhesion molecules was determined by quantitative real-time PCR in HUVECs with GATA2-WT or GATA2-2KR reconstitution as described in ( a ). Data are presented as the mean+-s.e.m. from at least three independent experiments. * P
Conjugate: Biotin

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 1 CD31 interactions promote the recovery of endothelial integrity following endothelial contraction induced by MHC molecule triggering. a - d Following MHC or ICAM-1 and/or CD31 antibody-mediated co-ligation for 30 min, EC were fixed and stained with rhodamine-phalloidin. Images taken on EC monolayers seeded at identical density are shown in ( a , b ). The average F-actin intensity per cell of three independent experiments is shown in ( c , d ). Scale bar, 20 mum. ( n = 3 biologically independent samples, N = 3 independent experiments, data are mean +- SD). One-way Anova with Tuckey post-hoc test. MHC vs all **** p < 0.0001, MHC + CD31 vs Isc **** p < 0.0001, MHC + CD31 vs all ****p < 0.0001. e Western blot (WB) analysis of Erk activation by WT and cd31 -/- EC 30 min after MHC stimulation. The bar graph shows relative protein expression +- SEM. N = 3 independent experiments (data are mean +- SD). One-way Anova with Tuckey post-hoc test. cd31 -/- MHC vs cd31 -/- IsC *** p = 0.0002, cd31 -/- MHC vs all **** p < 0.0001. f Western blot (WB) analysis of RhoA activation by WT and cd31 -/- EC 30 min after MHC stimulation. The bar graph shows relative protein expression +- SEM. N = 3 independent experiments (data are mean +- SD). One-way Anova with Tuckey post-hoc test. cd31 -/- 15' vs all *** p = 0.0003, cd31 -/- 30' vs all **** p < 0.0001. g Immunoprecipitation of CD31 molecules from WT EC exposed to MHC/ICAM-1 stimulation for 30 min followed by immunoblotting with an anti-pho
Conjugate: Biotin

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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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
Conjugate: Biotin

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 2 Cancer Stem Cell Traits of Differential Populations of CD54 + and CD54 - Cells. ( a ) FACS histograms show separate gating for the isolation of CD54 + and CD54 - PC3 and LNCaP cells. ( b ) Representative light micrograph fields and comparative quantification of the sphere-forming capacity of CD54 + and CD54 - LNCaP and PC3 cells. ( c ) Representative microscope fields from colony formation assays for CD54 + and CD54 - PC3 cells. ( d ) The cisplatin (DDP) IC 50 of CD54 + and CD54 - cells from the PC3, LNCaP, DU145, and 22RV1 prostate cancer cell lines. ( e ) q-PCR analysis of the expression of Hedgehog, Notch, and Wnt signaling pathway genes as well as genes involved in stem cell self-renewal in CD54 + and CD54 - PC3 cells. ( f ) Representative micrographs of in situ protein expression of the key signaling pathway components HES1 and CD54 in DAPI-stained LNCaP and PC3 cells. ** P < 0.01.
Conjugate: Biotin

13-0549-82

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