VCAM1 Analysis Service

Are you currently facing long drug development cycles, difficulty in biomarker validation, or challenges in identifying actionable targets? Our vascular cell adhesion molecule-1 (VCAM1) analysis service helps you accelerate lead generation and validate high-sensitivity diagnostics through advanced immunoassay, molecular imaging, and cell-based adhesion platforms.

Introduction of VCAM1 Analysis

VCAM1 analysis centers on VCAM1, a key sialoglycoprotein on activated endothelium. It mediates the critical adhesion of immune cells and, aberrantly, tumor cells, such as melanoma, breast cancer, by binding its counterreceptor. VCAM1 expression is a validated marker for multiple pathologies, including atherosclerosis, autoimmune disorders, and cancer metastasis.

Schematic of VCAM-1 Ig-like domains' roles in immune disorders & cancer. (OA Literature)Fig.1 Schematic representation of the specific role of each vascular cell adhesion molecule-1
(VCAM-1) immunoglobulin (Ig)-like domain in immunological disorders and cancer.1

VCAM1 Related Pathways

NF-κB and Cytokine Signaling

The primary regulatory mechanism for VCAM1 expression is the activation and nuclear translocation of the NF-κB transcription factor. Pro-inflammatory cytokines like TNF-α and IL-1 beta drive this pathway, making it a critical checkpoint for screening anti-inflammatory compounds. Our assays confirm compound efficacy by quantifying NF-κB-dependent VCAM1 transcriptional suppression.

PI3K/Akt Pathway

In cancer metastasis, the functional engagement of tumor-expressed VCAM1 with the α4 integrin on macrophages initiates a juxtacrine signal. This signal recruits the adaptor protein Ezrin, which subsequently activates the PI3K/Akt prosurvival pathway inside the cancer cell.

ROS and MAPK Cascades

Cellular stressors, including Reactive Oxygen Species (ROS) and mechanical shear stress, amplify VCAM1 expression through activated p38 MAPK and JNK pathways. This mechanistic link is leveraged by our high-sensitivity assays to model acute endothelial injury and screen compounds that modulate oxidative stress, essential for cardiovascular and diving medicine research applications.

Our Offerings

ELISA

ELISA remains the most widely used method for soluble VCAM1 detection in serum, plasma, and cell culture supernatants. Our sandwich ELISA kits employ high-affinity monoclonal antibodies against human, mouse, or rat VCAM1, ensuring species-specific accuracy.

Flow Cytometry

For cell-surface VCAM1 detection, flow cytometry offers cell resolution. We use fluorochrome-conjugated anti-VCAM1 antibodies, such as PE- or FITC-labeled, to analyze endothelial cells, macrophages, or tumor-associated fibroblasts.

Multiplex Immunoassays

To contextualize VCAM1 within inflammatory networks, we offer Luminex-based multiplex platforms. These assays simultaneously measure VCAM1 alongside cytokines, chemokines, and adhesion molecules.

Western Blotting

Western blotting provides semi-quantitative insights into VCAM1 protein expression in tissue lysates or cell extracts.

Applications

Prognostic Marker Validation

Utilize sVCAM1 quantification to establish correlation with disease severity and predict outcomes in cohorts suffering from lupus nephritis, rheumatoid arthritis, and diabetic kidney disease.

Atherosclerosis Risk Assessment

Measure VCAM1 expression as a high-sensitivity indicator of endothelial dysfunction and plaque instability, guiding risk stratification and monitoring in cardiovascular studies.

Multi-Analyte Panel Integration

Incorporate VCAM1 as a robust, acute inflammatory endpoint in broader diagnostic panels for sepsis, acute respiratory distress, and other systemic inflammatory syndromes.

Anti-Metastasis Drug Validation

Use tumor-stromal co-culture models to test leads that suppress the VCAM1-driven PI3K/Akt prosurvival signal, a critical step in lung and bone colonization by cancer cells.

FAQs

  1. Which biological samples can be analyzed for VCAM1 levels using your service?

    We routinely validate our assays across various human matrices, including serum, plasma, urine, cell lysates, and tissue homogenates. Our expertise allows us to recommend the optimal sample type for your specific research focus, whether it's sVCAM1 quantification or total VCAM1 expression.

  2. How does your VCAM1 analysis assist in therapeutic development for cancer metastasis?

    We provide specialized cell-adhesion assays to model the crucial VCAM1 interaction. This directly validates whether your therapeutic lead can disrupt the adhesion and subsequent prosurvival PI3K-Akt signaling that fuels lung and bone metastasis in cancer cells.

  3. What is the primary advantage of targeting VCAM1 over general adhesion molecules?

    VCAM1 is uniquely responsive to both cytokine (TNF-α) and oxidative stress (ROS), giving it superior sensitivity over many general markers. Furthermore, its crucial role in osteoclast progenitor maturation during bone metastasis makes it a uniquely valuable, multi-functional target.

Related Services

Adhesion Molecule Screening Panel

Broader analysis covering related endothelial markers, including ICAM-1, E-Selectin, and P-Selectin, to map the complete inflammatory profile.

Targeted Antibody Development

Custom services for the generation and engineering of high-affinity antibodies specifically targeting VCAM1 isoforms for therapeutic or in vivo imaging applications.

Biomarker Discovery & Validation Platform

Comprehensive proteomic and genomic services to identify novel biomarkers that regulate or are regulated by VCAM1 expression.

Creative Biolabs is your trusted partner for VCAM1 analysis, delivering precise data to validate your diagnostic tools and accelerate your therapeutic leads against inflammation and metastatic disease. Contact us to discuss your specific project requirements.

Reference

  1. Kong, Deok-Hoon, et al. "Emerging roles of vascular cell adhesion molecule-1 (VCAM-1) in immunological disorders and cancer." International journal of molecular sciences 19.4 (2018): 1057. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.3390/ijms19041057

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