ICAM1 Antibodies

Structure of ICAM1

ICAM1 is a transmembrane glycoprotein with a molecular weight of approximately 55-90 kDa, and its differences mainly stem from the varying degrees of glycosylation modification.

This protein is composed of 574 amino acids, and its extracellular segment contains five immunoglobulin-like domains (D1-D5). Among them, the D1 domain contains epitopes bound to the LFA-1 integrin, the D2 domain is involved in conformational stability, and the D3-D5 domain mediates the localization of the proximal and distal ends of the membrane. The transmembrane region is composed of 24 hydrophobic amino acids, and the intracellular segment contains 28 amino acid residues, which are connected to the actin cytoskeleton through ERM proteins. This multi-domain structure enables ICAM1 to undergo conformational changes in response to inflammatory stimuli, effectively regulating the leukocyte adhesion cascade reaction.

Fig. 1 Domain diagram of ICAM-1 and PfEMP1.¹

Key structural properties of ICAM1:

• Extracellular section contains five immunoglobulin sample structure domain (D1 - D5)
• Highly glycosylated rod-shaped transmembrane structure
• Integrin binding site of D1 domain (LFA-1/MAC-1)
• Intracellular segments are connected to the cytoskeleton through anchoring proteins

Functions of ICAM1

The main function of ICAM1 is to mediate the adhesion of white blood cells to vascular endothelium and signal transduction. In addition, it is also involved in various physiological and pathological processes such as the initiation of immune responses and the regulation of inflammation.

The binding affinity of ICAM1 to ligands is regulated by inflammatory factors. It is expressed at a low level in the resting state, but can be rapidly upregulated under the stimulation of TNF-α, IL-1, etc. This dynamic regulatory characteristic makes it a key control node in the immune inflammatory process.

Applications of ICAM1 and ICAM1 Antibody in Literature

1. Taftaf, Rokana, et al. "ICAM1 initiates CTC cluster formation and trans-endothelial migration in lung metastasis of breast cancer." Nature communications 12.1 (2021): 4867. https://doi.org/10.1038/s41467-021-25189-z

This study reveals that in triple-negative breast cancer, the ICAM1 protein is significantly upregulated in lung metastases. It promotes metastasis by mediating the aggregation between tumor cells (forming circulating tumor cell clusters) and tumor-endothelial cell adhesion. Targeting ICAM1 can effectively inhibit metastasis initiation, indicating that it can serve as a potential therapeutic target.

2. Zhang, Ying, et al. "Fusobacterium nucleatum promotes colorectal cancer cells adhesion to endothelial cells and facilitates extravasation and metastasis by inducing ALPK1/NF-κB/ICAM1 axis." Gut Microbes 14.1 (2022): 2038852. https://doi.org/10.1080/19490976.2022.2038852

Research has found that Fusobacterium nucleatum upregulates the expression of ICAM1 in colorectal cancer cells by inducing the ALPK1/NF-κB signaling pathway. This enhances the adhesion between cancer cells and endothelial cells, promoting tumor extravasation and distant metastasis. High expression of ICAM1 indicates a poor prognosis for patients, revealing a new mechanism by which the gut microbiota promotes metastasis.

3. Tinajero-Rodríguez, José Manuel, et al. "ICAM1 (CD54) Contributes to the Metastatic Capacity of Gastric Cancer Stem Cells." International Journal of Molecular Sciences 25.16 (2024): 8865. https://doi.org/10.3390/ijms25168865

Research has found that in gastric cancer stem cells, ICAM1 regulates their migration, invasion and metastasis abilities by activating STAT3 signaling. After knockout of ICAM1, although cancer cells' resistance to cisplatin increased, their migration and metastasis abilities were significantly lost. This indicates that ICAM1 is a key molecule regulating the metastasis of gastric cancer stem cells.

4. Tinajero-Rodríguez, José Manuel, et al. "ICAM1 (CD54) Contributes to the Metastatic Capacity of Gastric Cancer Stem Cells." International Journal of Molecular Sciences 25.16 (2024): 8865. https://doi.org/10.3389/fimmu.2024.1484483

Research has found that in periodontitis, ICAM1 marks a subpopulation of fibroblasts with inflammatory characteristics. This cell produces factors such as CCL2 through the NF-κB pathway, which in turn recruits macrophages and eliminates neutrophils, exerting a protective effect in the early stage of the disease and inhibiting bone resorption.

5. Zhou, Qin, et al. "Role of ICAM1 in tumor immunity and prognosis of triple-negative breast cancer." Frontiers in Immunology 14 (2023): 1176647. https://doi.org/10.3389/fimmu.2023.1176647

Research has found that in triple-negative breast cancer, low expression of ICAM1 is associated with a poor prognosis for patients. The mechanism might be that the low expression of ICAM1 leads to immunosuppression, such as promoting the polarization of M2 macrophages and T cell exhaustion, thereby weakening anti-tumor immunity and possibly affecting the efficacy of immunotherapy.

Creative Biolabs: ICAM1 Antibodies for Research

Creative Biolabs specializes in the production of high-quality ICAM1 antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom ICAM1 Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our ICAM1 antibodies, custom preparations, or technical support, contact us at email.