Anti-Human ICAM-1 (CD54) (Clone R6-5-D6) – Biotin

EBV transformed lymphoblast cell line

This Biotinylated antibody is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.4, 1% BSA and 0.09% sodium azide as a preservative.

Liquid

This biotinylated antibody is stable when stored at 2-8°C. Do not freeze.

Research Use Only

2 – 8° C Wet Ice

R6-5-D6 activity is directed against human ICAM-1 (CD54)

ICAM-1 or CD54 is a glycoprotein found on the surface of endothelial and epithelial cells during inflammation. It plays a significant role in the interactions between cells and immune responses. ICAM-1 helps in the adhesion and movement of leukocytes expressing activated LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18)¹.

Studies suggest that sICAM-1 (soluble ICAM-1) can bind to various non-integrin ligands, such as CD43/sialophorin, fibrinogen, hyaluronan, rhinoviruses, and Plasmodium falciparum-infected erythrocytes. In addition, sICAM-1 can be used as an indicator of vascular endothelial cell activation or damage by promoting angiogenesis².

Increased levels of sICAM-1 are associated with various diseases such as chronic coronary heart disease, type 2 diabetes, organ transplant dysfunction, oxidant stress, and certain malignancies^3-5.

Clone R6-5-D6, is a monoclonal antibody that has been used in research to study the expression and function of ICAM-1 in different contexts, such as viral infections, solid tumors, and graft-versus-host disease. The antibody has shown efficacy in inhibiting infection, characterizing ICAM-1 expression, and enhancing immune responses^6-9. It also inhibits CD54 interaction with leukocytes, thereby reducing inflammation^10,11.

CD54 is typically expressed on non-hematopoietic cells such as endothelial cells, thymic epithelial cells, fibroblasts, macrophages, T-lymphoblasts, germinal center B cells and dendritic cells.

CD40

1. Bullard DC, Hu X, Crawford D, McDonald K, Ramos TN, Barnum SR. Eur J Immunol. 2014;44(4):1194-1199.
2. Gho YS, Kleinman HK, Sosne G. Cancer Res. 1999;59(20):5128-5132.
3. Haim M, Tanne D, Boyko V, et al. J Am Coll Cardiol. 2002;39(7):1133-1138.
4. Al-Heety QQ, Kasabri V, Akour A, Naffa R, Abu Rkhaya S. Ther Adv Endocrinol Metab. 2018;9(10):303-310.
5. Hoogeveen RC, Ballantyne CM, Bang H, et al. Diabetologia. 2007;50(1):36-42.
6. Chen Y, Zhao C, Liu G, et al. Sheng Wu Gong Cheng Xue Bao. 2018;34(12):2016-2024.
7. Kobayashi H, Miyano T, Yamataka A, et al. Cardiovasc Surg. 1993;1(5):577-582.
8. Lawson C, Holder AL, Stanford RE, Smith J, Rose ML. Transplantation. 2005;80(2):264-271.
9. Gerbitz A, Ewing P, Olkiewicz K, et al. Transplantation. 2005;79(5):536-542.
10. Gudemez E, Turegun M, Carnevale K, Zins J, Siemionow M. Plast Reconstr Surg. 1999;104(1):161-170.
11. Steidl U, Haas R, Kronenwett R. Ann Hematol. 2000;79(8):414-423.
12. Williams KM, Dotson AL, Otto AR, Kohlmeier JE, Benedict SH. Cell Immunol. 2011;271(2):418-427.
13. Vestweber D, Zeuschner D, Rottner K, Schnoor M. Tissue Barriers. 2013;1(1):e23862.
14. Schnoor M, Lai FPL, Zarbock A, et al. J Exp Med. 2011;208(8):1721-1735.