Human ICAM-1/CD54 Antibody

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BBA17

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Detection of Human ICAM‑1/CD54 by Western Blot.
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Product Details
Citations (18)
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Human ICAM-1/CD54 Antibody Summary

Species Reactivity
Human
Specificity
Detects human ICAM‑1/CD54 in direct ELISAs and Western blots. ICAM‑1/CD54 has been screened using CHO cells transfected with cDNAs for ICAM-1, VCAM-1, and E-Selectin. ICAM‑1/CD54 was shown to be only reactive with ICAM-1.
Source
Polyclonal Goat Serum
Purification
N/A
Immunogen
Chinese hamster ovary cell line CHO-derived recombinant human ICAM‑1/CD54
Extracellular domain
Formulation
Lyophilized from a 0.2 μm filtered solution in Serum.
Label
Unconjugated

Applications

Recommended Concentration
Sample
Western Blot
1:1000 dilution
Ramos human Burkitt's lymphoma cell line and Raji human Burkitt's lymphoma cell line
Immunohistochemistry
1:300 dilution
Immersion fixed paraffin-embedded sections of human kidney
Immunocytochemistry
1-25 µg/mL
See below
Knockout Validated
ICAM‑1/CD54 is specifically detected in the parental Ramos human Burkitt's lymphoma cell line but is not detectable in knockout Ramos human Burkitt's lymphoma cell line.
 

Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.

Scientific Data

Western Blot View Larger

Detection of Human ICAM‑1/CD54 by Western Blot. Western blot shows lysates of Ramos human Burkitt's lymphoma cell line and Raji human Burkitt's lymphoma cell line. PVDF membrane was probed with 1:1000 µg/mL of Goat Anti-Human ICAM‑1/CD54 Polyclonal Antibody (Catalog # BBA17) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (HAF017). A specific band was detected for ICAM‑1/CD54 at approximately 90 kDa (as indicated). This experiment was conducted under reducing conditions and using Western Blot Buffer Group 1.

Immunocytochemistry ICAM‑1/CD54 antibody in A431 Human Cell Line by Immunocytochemistry (ICC). View Larger

ICAM‑1/CD54 in A431 Human Cell Line. ICAM-1/CD54 was detected in immersion fixed A431 human epithelial carcinoma cell line using Goat Anti-Human ICAM-1/CD54 Polyclonal Antibody (Catalog # BBA17) at 1.7 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Goat IgG Secondary Antibody (red; Catalog # NL001) and counterstained with DAPI (blue). Specific staining was localized to plasma membrane. View our protocol for Fluorescent ICC Staining of Cells on Coverslips.

Knockout Validated View Larger

Western Blot Shows Human ICAM‑1/CD54 Specificity by Using Knockout Cell Line. Western blot shows lysates of Ramos human Burkitt's lymphoma cell line and human ICAM-1/CD54 Ramos human Burkitt's lymphoma cell line (KO). PVDF membrane was probed with 1:1000 µg/mL of Goat Anti-Human ICAM‑1/CD54 Polyclonal Antibody (Catalog # BBA17) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (HAF017). A specific band was detected for ICAM‑1/CD54 at approximately 90 kDa (as indicated) in the parental Ramos human Burkitt's lymphoma cell line, but is not detectable in knockout Ramos human Burkitt's lymphoma cell line. GAPDH (AF5718) is shown as a loading control. This experiment was conducted under reducing conditions and using Western Blot Buffer Group 1.

Immunocytochemistry/ Immunofluorescence Detection of Human ICAM-1/CD54 by Immunocytochemistry/Immunofluorescence View Larger

Detection of Human ICAM-1/CD54 by Immunocytochemistry/Immunofluorescence Requirement of NF-kappa B activation for cytokine-mediated reductions in TEER.A: Concentration-dependent inhibition of induction of ICAM-1 expression by I kappa K-beta -inhibitor Bay11, confirming the effect of Bay11 on TNF induction of NF-kappa B-dependent genes. Conditions are lane 1, DMSO Control; lanes, 2, 3, 4 and 5, Bay11 at 0.375, 0.75, 1.5 and 3.0 μM, respectively all after 0.8 ng/ml TNF for 16 hours. B: Effect of Bay11 concentration on the TNF-induced TEER decrease. ECIS analysis. X-axis: Duration of 0.8 ng/ml TNF treatment. Y-axis: TEER (ohms) normalized to basal barrier level prior to addition of TNF. TEER levels were not affected by these concentrations of Bay11 in the absence of TNF (not shown). The corrected basal TEER for this experiment was 69.9 ± 1.3 Ω·cm2. n = 6,6,6,6. C: Effects of SR-I kappa B dominant negative overexpression on HDMEC barrier responses. Upper panel: A time course of TNF treatment (1 ng/ml for 12 h) in control-transduced (black trace) and SR-I kappa B-transduced (red trace) HDMEC. n = 4,4. Lower panel: A time course of thrombin (1 U/ml for 12 h) in control-transduced (black trace) and SR-I kappa B-transduced (red trace) HDMEC. The corrected basal TEER for this experiment was 72.4 ± 0.9 Ω·cm2 for SR-I kappa B-transduced HDMEC and 80.0 ± 0.7 Ω·cm2 for vector control-transduced HDMEC. n = 3,3. Note that the phase 1 and phase 2 decreases initiated by TNF are markedly inhibited in SR-I kappa B-relative to control-transduced HDMEC but that thrombin-induced TEER decreases are similar in the same control- and SR-I kappa B-transduced HDMEC lines. D: Effects of Bay11 (used at 1 or 3 μM as labeled) on disruption of CL5 staining by 6 hours of TNF at 10 ng/ml. Morphometric measurements of TNF-induced disruption of CL5 junctional staining as described in the Methods (left). Immunofluorescence images representative of those used to assess the extent of disruption (right). Anti-CL5 (green), and anti-ICAM (red). Scale bar, 15 μm. E: Effects of SR-I kappa B transduction on disruption of CL5 staining by 6 hours of TNF at 10 ng/ml. Morphometric measurements (left) and representative immunofluorescence (right) images as in (D). Anti-CL5 (green), and anti-ICAM (red). Scale bar, 15 μm. Note that Bay 11 and SR-I kappa B each prevented the induction of ICAM-1 as well as the induction of a disrupted pattern of anti-CL5 immunofluorescence staining (arrows in D and E) by TNF. F: Effects of SR-I kappa B dominant negative overexpression on IL-1 beta -leak (ECIS). Note that IL-1 beta over a 12 hour time course was ineffective at decreasing TEER in SR-I kappa B-transduced HDMEC. The corrected basal TEER for this experiment was 64.5 ± 2.8 Ω·cm2 for SR-I kappa B-transduced HDMEC and 59.6 ± 1.1 Ω·cm2 for vector control-transduced HDMEC. n = 3,3. Representative of 3 (A, B and C) or 2 (D, E and F) independent experiments with similar results. Image collected and cropped by CiteAb from the following publication (https://dx.plos.org/10.1371/journal.pone.0120075), licensed under a CC-BY license. Not internally tested by R&D Systems.

Immunocytochemistry/ Immunofluorescence Detection of Human ICAM-1/CD54 by Immunocytochemistry/Immunofluorescence View Larger

Detection of Human ICAM-1/CD54 by Immunocytochemistry/Immunofluorescence Requirement of NF-kappa B activation for cytokine-mediated reductions in TEER.A: Concentration-dependent inhibition of induction of ICAM-1 expression by I kappa K-beta -inhibitor Bay11, confirming the effect of Bay11 on TNF induction of NF-kappa B-dependent genes. Conditions are lane 1, DMSO Control; lanes, 2, 3, 4 and 5, Bay11 at 0.375, 0.75, 1.5 and 3.0 μM, respectively all after 0.8 ng/ml TNF for 16 hours. B: Effect of Bay11 concentration on the TNF-induced TEER decrease. ECIS analysis. X-axis: Duration of 0.8 ng/ml TNF treatment. Y-axis: TEER (ohms) normalized to basal barrier level prior to addition of TNF. TEER levels were not affected by these concentrations of Bay11 in the absence of TNF (not shown). The corrected basal TEER for this experiment was 69.9 ± 1.3 Ω·cm2. n = 6,6,6,6. C: Effects of SR-I kappa B dominant negative overexpression on HDMEC barrier responses. Upper panel: A time course of TNF treatment (1 ng/ml for 12 h) in control-transduced (black trace) and SR-I kappa B-transduced (red trace) HDMEC. n = 4,4. Lower panel: A time course of thrombin (1 U/ml for 12 h) in control-transduced (black trace) and SR-I kappa B-transduced (red trace) HDMEC. The corrected basal TEER for this experiment was 72.4 ± 0.9 Ω·cm2 for SR-I kappa B-transduced HDMEC and 80.0 ± 0.7 Ω·cm2 for vector control-transduced HDMEC. n = 3,3. Note that the phase 1 and phase 2 decreases initiated by TNF are markedly inhibited in SR-I kappa B-relative to control-transduced HDMEC but that thrombin-induced TEER decreases are similar in the same control- and SR-I kappa B-transduced HDMEC lines. D: Effects of Bay11 (used at 1 or 3 μM as labeled) on disruption of CL5 staining by 6 hours of TNF at 10 ng/ml. Morphometric measurements of TNF-induced disruption of CL5 junctional staining as described in the Methods (left). Immunofluorescence images representative of those used to assess the extent of disruption (right). Anti-CL5 (green), and anti-ICAM (red). Scale bar, 15 μm. E: Effects of SR-I kappa B transduction on disruption of CL5 staining by 6 hours of TNF at 10 ng/ml. Morphometric measurements (left) and representative immunofluorescence (right) images as in (D). Anti-CL5 (green), and anti-ICAM (red). Scale bar, 15 μm. Note that Bay 11 and SR-I kappa B each prevented the induction of ICAM-1 as well as the induction of a disrupted pattern of anti-CL5 immunofluorescence staining (arrows in D and E) by TNF. F: Effects of SR-I kappa B dominant negative overexpression on IL-1 beta -leak (ECIS). Note that IL-1 beta over a 12 hour time course was ineffective at decreasing TEER in SR-I kappa B-transduced HDMEC. The corrected basal TEER for this experiment was 64.5 ± 2.8 Ω·cm2 for SR-I kappa B-transduced HDMEC and 59.6 ± 1.1 Ω·cm2 for vector control-transduced HDMEC. n = 3,3. Representative of 3 (A, B and C) or 2 (D, E and F) independent experiments with similar results. Image collected and cropped by CiteAb from the following publication (https://dx.plos.org/10.1371/journal.pone.0120075), licensed under a CC-BY license. Not internally tested by R&D Systems.

Western Blot Detection of Human ICAM-1/CD54 by Western Blot View Larger

Detection of Human ICAM-1/CD54 by Western Blot Kinetics and dose response of distinct changes to HDMEC barriers induced by TNF and IL-beta.A: Relationship of the early TNF-induced TEER increase to basal TEER levels. A plot of the percent increase over basal TEER values (measured at the peak of the TNF-induced TEER increase, mean 0.7±0.01 hours; y-axis) vs. basal TEER (reported in ohms and read on a 96W20idf ECIS array; x-axis). TNF concentration was 20 ng/ml. The inverse correlation of basal TEER to the early TEER increase is statistically significant by a two-tailed Pearson analysis (p = 0.021 in 10 independent experiments). B: TNF induction of an early TEER rise and a bi-phasic TEER decrease. Labels indicate the peak of the early TEER increase and two distinct phases of TEER decrease (as nadirs to phases 1 and 2). X-axis, duration of incubation in 20 ng/ml TNF (units, hours); y-axis, in units of normalized TEER calculated as a ratio of TEER measurements taken post-TNF to the basal TEER level read before adding TNF, which is set at 1.0 (for a further explanation, please see Methods). The corrected basal TEER for this experiment was 63.7±1.2 Ω·cm2. n = 4,8 for vehicle, TNF. C: Relationship of TNF concentration to the decrease in TEER measured at the observed nadirs to phase 1 and phase 2. Example of data used to calculate EC50 values. Goodness of the non-linear regression curve fits are expressed as R-squared values. The corrected basal TEER for this experiment was 80.7± 0.8 Ω·cm2. D: Recovery of HDMEC barrier integrity relative to TNF concentration. TEER values show an inverse concentration-dependent recovery from phase 2 nadir levels (red trace) to pre-TNF basal levels in the continuous presence of TNF for 18 hours (black trace). The corrected basal TEER for this experiment was 57.5 ± 0.5 Ω·cm2. E: Effect of TNFR1 siRNA knockdown on TNF leak. Immunoblot analysis of siRNA silencing of TNFR1 expression confirmed by an inhibition of ICAM-1 expression (left) and ECIS analysis of the requirement for TNFR1 in TNF leak (right, y-axis TEER normalized to T0). The corrected basal TEER for this experiment was 75.6 ± 2.2 Ω·cm2 for TNFR1 siRNA-transfected HDMEC and 81.0 ± 1.2 Ω·cm2 for negative control siRNA-transfected HDMEC. Mean values are indicated by horizontal bars, n = 3,3) each at 10 hours of TNF at 0.8 ng/ml. MW, protein apparent molecular weight in kDa. F) Time course of discrete IL-beta -induced changes in TEER (ECIS plot). Note that like TNF, IL-beta (20 ng/ml) produced an initial small rise in TEER followed by two distinct phases of TEER decrease. The corrected basal TEER for this experiment was 72.0 ± 1.5 Ω·cm2. n = 3,3. Representative of 10 (A), 12 (B), 3 (C, D and F) or 2 (E) independent experiments with similar results. Image collected and cropped by CiteAb from the following publication (https://dx.plos.org/10.1371/journal.pone.0120075), licensed under a CC-BY license. Not internally tested by R&D Systems.

Western Blot Detection of Human ICAM-1/CD54 by Western Blot View Larger

Detection of Human ICAM-1/CD54 by Western Blot Effects of TNF on the actin cytoskeleton and MLC phosphorylation.A) Analysis of the effects of TNF on actin/CL5 co-localization. Post-confluent HDMEC monolayers immunostained with anti-CL5 and phalloidin-stained for actin were imaged by fluorescence microscopy and analyzed for co-localization as described. Actin/CL5 co-localization was lost after TNF treatment for 8 hours at 0.8 ng/ml, resulting in a statistically significant difference in the Pearson correlation co-efficient (y-axis) by two-tailed t-test. B) Immunofluorescence microscopy representative of the data in Fig. 4. Co-localization of the cortical actin cytoskeleton with junctional CL5 in DMSO control HDMEC (arrow in left panel; phalloidin staining, red; anti-CL5, green) is dissociated by TNF (center panel), a change prevented by Bay11 (right panel). Scale bar, 15 μm. C) Time course of TNF-induced changes in MLC (Thr18/Ser19) phosphorylation and ICAM-1 levels measured by immunoblotting with controls for total MLC and for beta -actin. TNF treatment for the times indicated was at 10 ng/ml. D) Dose response of TNF-induced changes in phospho-MLC levels assessed by immunoblot analysis. HDMEC lysates were harvested at 6 hours of TNF. E) Effect of Bay11 on changes in P-MLC levels induced by TNF. Bay-11 was used at a 3 μM concentration. F) Effect of SR-I kappa B on changes in P-MLC levels induced by TNF. In E and F) TNF treatment was for 6 hours at 0.8 ng/ml. Note that Bay11 and SR-I kappa B each inhibit TNF-induced increases in ICAM-1 protein levels as well as MLC phosphorylation. Representative of 2 (B, E) or 3 (C, D, F) independent experiments with similar results. Image collected and cropped by CiteAb from the following publication (https://dx.plos.org/10.1371/journal.pone.0120075), licensed under a CC-BY license. Not internally tested by R&D Systems.

Western Blot Detection of Human ICAM-1/CD54 by Western Blot View Larger

Detection of Human ICAM-1/CD54 by Western Blot Requirement of NF-kappa B activation for cytokine-mediated reductions in TEER.A: Concentration-dependent inhibition of induction of ICAM-1 expression by I kappa K-beta -inhibitor Bay11, confirming the effect of Bay11 on TNF induction of NF-kappa B-dependent genes. Conditions are lane 1, DMSO Control; lanes, 2, 3, 4 and 5, Bay11 at 0.375, 0.75, 1.5 and 3.0 μM, respectively all after 0.8 ng/ml TNF for 16 hours. B: Effect of Bay11 concentration on the TNF-induced TEER decrease. ECIS analysis. X-axis: Duration of 0.8 ng/ml TNF treatment. Y-axis: TEER (ohms) normalized to basal barrier level prior to addition of TNF. TEER levels were not affected by these concentrations of Bay11 in the absence of TNF (not shown). The corrected basal TEER for this experiment was 69.9 ± 1.3 Ω·cm2. n = 6,6,6,6. C: Effects of SR-I kappa B dominant negative overexpression on HDMEC barrier responses. Upper panel: A time course of TNF treatment (1 ng/ml for 12 h) in control-transduced (black trace) and SR-I kappa B-transduced (red trace) HDMEC. n = 4,4. Lower panel: A time course of thrombin (1 U/ml for 12 h) in control-transduced (black trace) and SR-I kappa B-transduced (red trace) HDMEC. The corrected basal TEER for this experiment was 72.4 ± 0.9 Ω·cm2 for SR-I kappa B-transduced HDMEC and 80.0 ± 0.7 Ω·cm2 for vector control-transduced HDMEC. n = 3,3. Note that the phase 1 and phase 2 decreases initiated by TNF are markedly inhibited in SR-I kappa B-relative to control-transduced HDMEC but that thrombin-induced TEER decreases are similar in the same control- and SR-I kappa B-transduced HDMEC lines. D: Effects of Bay11 (used at 1 or 3 μM as labeled) on disruption of CL5 staining by 6 hours of TNF at 10 ng/ml. Morphometric measurements of TNF-induced disruption of CL5 junctional staining as described in the Methods (left). Immunofluorescence images representative of those used to assess the extent of disruption (right). Anti-CL5 (green), and anti-ICAM (red). Scale bar, 15 μm. E: Effects of SR-I kappa B transduction on disruption of CL5 staining by 6 hours of TNF at 10 ng/ml. Morphometric measurements (left) and representative immunofluorescence (right) images as in (D). Anti-CL5 (green), and anti-ICAM (red). Scale bar, 15 μm. Note that Bay 11 and SR-I kappa B each prevented the induction of ICAM-1 as well as the induction of a disrupted pattern of anti-CL5 immunofluorescence staining (arrows in D and E) by TNF. F: Effects of SR-I kappa B dominant negative overexpression on IL-1 beta -leak (ECIS). Note that IL-1 beta over a 12 hour time course was ineffective at decreasing TEER in SR-I kappa B-transduced HDMEC. The corrected basal TEER for this experiment was 64.5 ± 2.8 Ω·cm2 for SR-I kappa B-transduced HDMEC and 59.6 ± 1.1 Ω·cm2 for vector control-transduced HDMEC. n = 3,3. Representative of 3 (A, B and C) or 2 (D, E and F) independent experiments with similar results. Image collected and cropped by CiteAb from the following publication (https://dx.plos.org/10.1371/journal.pone.0120075), licensed under a CC-BY license. Not internally tested by R&D Systems.

Western Blot Detection of Human ICAM-1/CD54 by Western Blot View Larger

Detection of Human ICAM-1/CD54 by Western Blot Effects of ROCK inhibitors H-1152 and Y-27632 on TNF-induced MLC phosphorylation, actin and CL5 reorganization and the fall in TEER.A) Immunoblot analysis of the effects of H-1152 (top) or Y-27632 (bottom) concentration on induction of MLC phosphorylation at 6 hours of 0.8 ng/ml TNF. B) Fluorescence microscopy analysis of the effects of H-1152 or Y-27632 (at 10 μM concentrations) on TNF-induced actin re-organization. Actin visualized by phalloidin staining. Note that changes to the peripheral pattern of cortical actin at 6 hours of 0.8 ng/ml TNF treatment are inhibited by H-1152 and by Y-27632 (arrows). Scale bar, 15 μm. C) Top: Morphometric analysis of the effects of H-1152 (at concentrations of 2 or 20 μM, triangles and inverted triangles, respectively), and Y-27632 (at concentrations of 1 or 10 μM, squares and diamonds) on disruption of CL5 junctional staining at 6 hours of 0.8 ng/ml TNF. Open symbols, no TNF, closed symbols, plus TNF. Below: Examples of the morphometrically assessed immunofluorescence microscopy images. Note that CL5 staining disorganized by TNF in vehicle control appears condensed and contiguous in the presence of both ROCK inhibitors (arrows). Scale bar, 15 μm. D) Effects of H-1152 and Y-27632 on the phase 1 and phase 2 TEER decreases induced by TNF. Starting at T0, HDMEC plated on ECIS 96-well arrays received a 1 hour pre-treatment with vehicle (top panel, n = 4, 4) or with a ROCK inhibitor, either H-1152 (at 1 or 10 μM, middle panel, n = 6, 6) or Y-27632 (at 1 or 10 μM, bottom panel, n = 6, 6). One hour later 0.8 ng/ml TNF or (top panel only) vehicle was added, indicated by the vertical dashed lines. The corrected basal TEER for this experiment was 67.8 ± 0.4 Ω·cm2. E) Immunoblot analysis of the effects of H-1152 and Y-27632 on TNF-induced ICAM expression. Protein lysates were from HDMEC pre-treated with H-1152 (1 or 10 μM) or Y-27632 (1 or 10 μM) then TNF, 0.8 ng/ml for 6 h. Representative of 4 (A), 3 (B, D, E) and 2 (C) independent experiments with similar results. Image collected and cropped by CiteAb from the following publication (https://dx.plos.org/10.1371/journal.pone.0120075), licensed under a CC-BY license. Not internally tested by R&D Systems.

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Background: ICAM-1/CD54

Intercellular Adhesion Molecule-1 (ICAM-1, CD54) binds the leukocyte integrins LFA-1 and Mac-1. ICAM-1 expression is weak on leukocytes, epithelial and resting endothelial cells, as well as some other cell types, but expression can be stimulated by IFN-gamma, TNF-alpha, IL-1 beta and LPS.

Soluble ICAM-1 is found in a biologically active form in serum, probably as a result of proteolytic cleavage from the cell surface, and is elevated in patients with various inflammatory syndromes such as septic shock, LAD, cancer and transplantation.

References
  1. Pigott, R. and C. Power, 1993, The Adhesion Molecule Facts Book, pp. 74. Academic Press.
Long Name
Intercellular Adhesion Molecule 1
Entrez Gene IDs
3383 (Human); 15894 (Mouse); 25464 (Rat)
Alternate Names
BB2; CD54 antigen; CD54; cell surface glycoprotein P3.58; human rhinovirus receptor; ICAM1; ICAM-1; intercellular adhesion molecule 1 (CD54), human rhinovirus receptor; intercellular adhesion molecule 1; Major group rhinovirus receptor; P3.58

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Citations for Human ICAM-1/CD54 Antibody

R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.

18 Citations: Showing 1 - 10
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  1. Is later-life depression a risk factor for Alzheimer's disease or a prodromal symptom: a study using post-mortem human brain tissue?
    Authors: Lindsey I. Sinclair, Asher Mohr, Mizuki Morisaki, Martin Edmondson, Selina Chan, A. Bone-Connaughton et al.
    Alzheimers Res Ther
  2. Coronavirus Disease 2019 (COVID-19) Coronary Vascular Thrombosis: Correlation with Neutrophil but Not Endothelial Activation
    Authors: Justin E. Johnson, Declan McGuone, Mina L. Xu, Dan Jane-Wit, Richard N. Mitchell, Peter Libby et al.
    The American Journal of Pathology
  3. Transforming growth factor (TGF)-beta1 and interferon (IFN)-gamma differentially regulate ICAM-1 expression and adhesion of Toxoplasma gondii to human trophoblast (BeWo) and uterine cervical (HeLa) cells
    Authors: SC Teixeira, RJ Silva, JB Lopes-Mari, AO Gomes, MB Angeloni, ML Fermino, MC Roque-Barr, NM Silva, DAO Silva, JR Mineo, EAV Ferro, BF Barbosa
    Acta tropica, 2021-08-25;0(0):106111.
    Species: Human
    Sample Types: Cell Lysates, Whole Cells
    Applications: ICC, Western Blot
  4. Quantitative proteomic analysis of trypsin‐treated extracellular vesicles to identify the real‐vesicular proteins
    Authors: Dongsic Choi, Gyeongyun Go, Dae‐Kyum Kim, Jaewook Lee, Seon‐Min Park, Dolores Di Vizio et al.
    Journal of Extracellular Vesicles
  5. Inflammatory responses induced by Helicobacter pylori on the carcinogenesis of gastric epithelial GES‑1 cells
    Authors: Jianjun Wang, Yongliang Yao, Qinghui Zhang, Shasha Li, Lijun Tang
    International Journal of Oncology
  6. Amyloid-beta 1-40 is associated with alterations in NG2+ pericyte population ex�vivo and in�vitro
    Authors: N Schultz, K Brännström, E Byman, S Moussaud, HM Nielsen, A Olofsson, M Wennström
    Aging Cell, 2018-02-17;0(0):.
    Species: Human
    Sample Types: Whole Tissue
    Applications: IHC
  7. Engineered Microvasculature in PDMS Networks Using Endothelial Cells Derived from Human Induced Pluripotent Stem Cells
    Authors: Amogh Sivarapatna, Mahboobe Ghaedi, Yang Xiao, Edward Han, Binod Aryal, Jing Zhou et al.
    Cell Transplantation
  8. HIV-1 Vpu Downmodulates ICAM-1 Expression, Resulting in Decreased Killing of Infected CD4 + T Cells by NK Cells
    Authors: Scott M. Sugden, Tram N. Q. Pham, Éric A. Cohen
    Journal of Virology
  9. Changes in CD200 and intercellular adhesion molecule-1 (ICAM-1) levels in brains of Lewy body disorder cases are associated with amounts of Alzheimer's pathology not ?-synuclein pathology.
    Authors: Douglas G Walker, Lih-Fen Lue, Tiffany M Tang, Charles H Adler, John N Caviness, Marwan N Sabbagh, Geidy E Serrano, Lucia I Sue, Thomas G Beach
    Neurobiology of Aging, 2017-03-16;0(0):1558-1497.
    Species: Human
    Sample Types: Tissue Homogenates
    Applications: Western Blot
  10. Monomeric C-reactive protein and inflammation in age-related macular degeneration
    Authors: Kathleen R Chirco, S Scott Whitmore, Kai Wang, Lawrence A Potempa, Jennifer A Halder, Edwin M Stone et al.
    The Journal of Pathology
  11. Tumor necrosis factor disrupts claudin-5 endothelial tight junction barriers in two distinct NF-kappaB-dependent phases.
    Authors: Clark P, Kim R, Pober J, Kluger M
    PLoS ONE, 2015-03-27;10(3):e0120075.
    Species: Human
    Sample Types: Cell Lysates, Whole Cells
    Applications: IHC, Western Blot
  12. Plasticity-related gene 5 promotes spine formation in murine hippocampal neurons.
    Authors: Coiro P, Stoenica L, Strauss U, Brauer A
    J Biol Chem, 2014-07-29;289(36):24956-70.
  13. Outer membrane vesicles derived from Escherichia coli up-regulate expression of endothelial cell adhesion molecules in vitro and in vivo.
    Authors: Kim J, Yoon Y, Lee J, Choi E, Yi N, Park K, Park J, Lotvall J, Kim Y, Gho Y
    PLoS ONE, 2013-03-14;8(3):e59276.
    Species: Human
    Sample Types: Cell Lysates
    Applications: Western Blot
  14. Inflammatory cytokines stimulate the adhesion of colon carcinoma cells to mesothelial monolayers.
    Authors: van Grevenstein WM, Hofland LJ, van Rossen ME, van Koetsveld PM, Jeekel J, van Eijck CH
    Dig. Dis. Sci., 2007-03-30;52(10):2775-83.
    Species: Human
    Sample Types: Whole Cells
    Applications: ICC
  15. Endothelial adhesion molecule expression is unaltered in the peripheral nerve from patients with AIDS and distal sensory polyneuropathy.
    Authors: Fenzi F, Rossi F, Rava M, Cavallaro T, Ferrari S, Rizzuto N
    J. Neuroimmunol., 2006-07-20;178(1):111-6.
    Species: Human
    Sample Types: Whole Tissue
    Applications: IHC-P
  16. Requirement for intercellular adhesion molecule 1 and caveolae in invasion of human oral epithelial cells by Porphyromonas gingivalis.
    Authors: Tamai R, Asai Y, Ogawa T
    Infect. Immun., 2005-10-01;73(10):6290-8.
    Species: Human
    Sample Types: Whole Cells
    Applications: Neutralization
  17. TNFalpha increases the inflammatory response to vascular balloon injury without accelerating neointimal formation.
    Authors: Miller AM, McPhaden AR, Preston A, Wadsworth RM, Wainwright CL
    Atherosclerosis, 2004-12-23;179(1):51-9.
    Species: Rabbit
    Sample Types: Whole Tissue
    Applications: IHC-P
  18. E-selectin and ICAM-1 are incorporated into detergent-insoluble membrane domains following clustering in endothelial cells.
    Authors: Tilghman RW, 2019, Hoover RL
    eaav5562, 2002-08-14;525(1):83-7.
    Species: Human
    Sample Types: Cell Lysates
    Applications: Western Blot

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