BMS108

antibody from Invitrogen Antibodies

Targeting: ICAM1 BB2, CD54

Other assay (Supportive data in Antibodypedia)

Antibody Data

Product number

BMS108

Provider

Invitrogen Antibodies

Product name

CD54 (ICAM-1) Monoclonal Antibody (RR1/1), eBioscience™

Antibody type

Monoclonal

Antigen

Other

Description

Description: Recognizes the D1 domain of human CD54.

Antibody clone number

RR1/1

Concentration

0.5 mg/mL

References

Submitted references

Assessment of ICAM-1 N-glycoforms in mouse and human models of endothelial dysfunction.

Regal-McDonald K, Somarathna M, Lee T, Litovsky SH, Barnes J, Peretik JM, Traylor JG Jr, Orr AW, Patel RP
PloS one 2020;15(3):e0230358

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Hydrogen peroxide regulates endothelial surface N-glycoforms to control inflammatory monocyte rolling and adhesion.

McDonald KR, Hernandez-Nichols AL, Barnes JW, Patel RP
Redox biology 2020 Jul;34:101498

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Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures.

Sabry M, Zubiak A, Hood SP, Simmonds P, Arellano-Ballestero H, Cournoyer E, Mashar M, Pockley AG, Lowdell MW
PloS one 2019;14(6):e0218674

Other assay

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Fig 2 HM epitopes co-localize with ICAM-1 in high fat-induced mouse atherosclerosis. Total, HM / hybrid, alpha-2,6-sialylated, and alpha-2,3-sialylated ICAM-1 were measured in the innominate and left carotid arteries from ApoE-/- mice fed a normal or high fat diet. A) Shown are representative images of innominate arteries from paired lesion and non-lesion areas of the same vessel section. Red staining represents total ICAM-1, red puncta represent positive PLA staining for specific ICAM-1 N-glycoforms (indicated by arrows), and blue staining represents DAPI. # indicates the lumen of each vessel. Panels B and C show PLA staining of lesion areas when the anti-ICAM-1 antibody or avidin were excluded. Panel D shows total ICAM-1 staining in lesion versus non-lesion areas. *p

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Fig 5 HM / hybrid ICAM-1 is increased in human atherosclerosis. Panel A shows representative images of total ICAM-1 (red staining) and specified N-glycoforms in human vessels with lesions spanning types 1-5. Red puncta represent positive PLA staining (as indicated by arrows). Panel B shows the quantification of total ICAM-1 in early (1-2) and late (3-5) disease stages. Each symbol represents a different patient, with same symbol representing multiple vessels from the same patient. Data are mean +- SEM, n = 7-10. * p

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Fig 7 HM / hybrid, HM, alpha-2,6-sialylated, ICAM-1 are increased CKD patients with failed arteriovenous fistulas. Panel A shows total ICAM-1 (red staining) and specified N-glycoforms in vessels from CKD patients with failed or successful AVF creation. Red puncta represent positive PLA staining (as indicated by arrows). B) Quantification of total ICAM-1 signal in failed and successful AVF samples (n = 4 each). Error bars are mean +- SEM; * p

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Fig. 4 TNFalpha-induced HM-ICAM-1 formation and alpha-mannosidase activity inhibition can be reversed with PEG-Catalase. A. HUVECs treated with 100 units of PEG-catalase 30 min prior to TNFalpha treatment and lectin staining with ConA, HHL, SNA, and MAL-II was performed. * = p

Supportive validation

Submitted by

Invitrogen Antibodies (provider)

Main image

Experimental details

Fig. 5 ERO1-alpha inhibition abrogates TNFalpha-inhibition of alpha mannosidase activity and HM N-glycan formation. A. HUVECs were pretreated with either 10 muM GKT137831 or 5 muM EN460 to inhibit NOX4, ERO1-alpha, respectively, prior to TNFalpha treatment and alpha-mannosidase activity measured. * = p