2024年12月25日 · ICAM2 (Intercellular Adhesion Molecule 2) is a Protein Coding gene. Diseases associated with ICAM2 include Colon Carcinoma In Situ and Intestine Carcinoma In Situ . Among its related pathways are Innate Immune System and CLEC7A (Dectin-1) signaling .

Endothelial ICAM-1 or ICAM-2 is involved in neutrophil-mediated plasma leakage. ICAM-1 on pericytes assists the final step of neutrophil extravasation. Epithelial ICAM-1 rather indirectly promotes neutrophil migration to peri-epithelial sites.

ICAM2 encodes a type I transmembrane glycoprotein that is a member of the ICAM family of adhesion proteins. ICAM2 is expressed in vascular endothelial cells and blood cells, and plays an important role in neutrophil migration into the tissue and cell-cell interactions during humoral immunity [14, 20]. Several reports state that ICAM2 functions ...

1998年5月8日 · Here we describe the in vitro characterization of this region. The ICAM-2 promoter is TATA-less, and transcription in endothelial cells initiates at four sites.

ICAM proteins are ligands for the leukocyte adhesion protein LFA-1 (integrin alpha-L/beta-2). ICAM2 may play a role in l ymphocyte recirculation by blocking LFA-1-dependent cell adhesion.

2005年9月1日 · Using ICAM-2–deficient mice and ICAM-2–deficient endothelial cells, we show that the lack of ICAM-2 expression results in impaired angiogenesis both in vitro and in vivo. We show that ICAM-2 supports homophilic interaction, and that this may be …

Intercellular adhesion molecule 2 as a novel prospective tumor suppressor induced by ERG promotes ubiquitination-mediated radixin degradation to inhibit gastric cancer tumorigenicity and metastasis.

ICAMs are important cell adhesion proteins involved in cell movement. Based on our results, we conclude that ICAM1 and sICAM1 have opposing roles in the seminiferous epithelium, with ICAM1 and sICAM1 improving and worsening BTB function, respectively.

2021年8月15日 · We found that human and murine alveolar epithelium expressed ICAM-1, whilst the bronchial epithelium expressed ICAM-2, and both were up-regulated during inflammatory stimulation in vitro and in inflammatory lung diseases such as cystic fibrosis.

We demonstrate that the ICAM-2 promoter is endothelial cell-specific in vitro and identify four elements, an Sp1 site, two GATA sites, and an 8-bp palindromic sequence also present in the tie2 enhancer, that are necessary for full promoter activity.