Vascular cell adhesion protein 1 also known asvascular cell adhesion molecule 1 (VCAM-1) orcluster of differentiation 106 (CD106) is aprotein that in humans is encoded by theVCAM1gene.[5] VCAM-1 functions as acell adhesion molecule.
VCAM-1 is a member of theimmunoglobulin superfamily, the superfamily of proteins includingantibodies andT-cell receptors. The VCAM-1 gene contains six or sevenimmunoglobulin domains, and is expressed on both large and smallblood vessels only after theendothelial cells are stimulated bycytokines. It isalternatively spliced into two knownRNAtranscripts that encode different isoforms in humans.[6] The gene product is a cell surfacesialoglycoprotein, a type I membrane protein that is a member of theIg superfamily.
The VCAM-1 protein mediates the adhesion oflymphocytes,monocytes,eosinophils, andbasophils to vascularendothelium. It also functions in leukocyte-endothelial cellsignal transduction, and it may play a role in the development ofatherosclerosis andrheumatoid arthritis.
Upregulation of VCAM-1 in endothelial cells by cytokines occurs as a result of increasedgene transcription (e.g., in response totumor necrosis factor-alpha (TNF-α) andinterleukin-1 (IL-1)) and through stabilization ofmessenger RNA (mRNA) (e.g.,Interleukin-4 (IL-4)). The promoter region of theVCAM1 gene contains functional tandemNF-κB (nuclear factor-kappa B) sites. The sustained expression of VCAM-1 lasts over 24 hours.
Primarily, the VCAM-1 protein is an endothelialligand forVLA-4 (Very Late Antigen-4 or integrin α4β1) of the β1 subfamily ofintegrins. VCAM-1 expression has also been observed in other cell types (e.g.,smooth muscle cells). It has also been shown tointeract withEZR[7] andMoesin.[7]
VCAM-1 is also upregulated if vWF (Von Willebrand Factor) is given in knock-out (KO) ADMATS13 mice but not on mice without KO.[8]
CD106 also exists on the surface of some subpopulations ofmesenchymal stem cells (MSC).[9]
Certainmelanoma cells can use VCAM-1 to adhere to the endothelium,[10] VCAM-1 may participate in monocyte recruitment to atherosclerotic sites, and it is highly overexpressed in the inflamed brain.[11] As a result, VCAM-1 is a potentialdrug target.
{{cite journal}}: CS1 maint: DOI inactive as of July 2025 (link)
