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findings suggest that CD11d/CD18 (show ITGB2 Proteins) upregulation on proinflammatory macrophages may represent a common mechanism for macrophage retention at inflammatory sites, thereby promoting chronic inflammation and disease development.
These results expand the potential for CD11d to regulate lymphocyte migration and tissue retention, and illuminate the possibility of a previously unconsidered role for CD11d in leukocyte biology and disease.
The effects of anti-CD11d treatment improves functional recovery in a rat model of repeated concussion.
the cross-talk between neutrophils and NK cells is mediated by ICAM-3 (show ICAM3 Proteins) and CD11d/CD18 (show ITGB2 Proteins), respectively.
CD11d expression increased in the subcutaneous white adipose tissue of obese adult women; this appears to be a common feature of obesity.
a longer isoform of gut (show GUSB Proteins)-enriched Kruppel-like factor 4 (show KLF4 Proteins) (GKLF (show KLF4 Proteins)) we term GKLFa interacts with the CD11d promoter
multiple CD11d domains play a role in controlling intracellular location and association with CD18 (show ITGB2 Proteins).
The results indicate that both Mac-1 (show ITGAM Proteins) and alphaDbeta2 support macrophage fusion with Mac-1 (show ITGAM Proteins) playing a dominant role
Relative white adipose tissue (WAT) expression of CD11d was massively induced by obesity to an extent greater than any other inflammatory marker (to >300-fold of controls in the 45 and 60% fat groups) and this induction was WAT specific.
Integrin alpha-D/beta-2 is a receptor for ICAM3 and VCAM1. May play a role in the atherosclerotic process such as clearing lipoproteins from plaques and in phagocytosis of blood- borne pathogens, particulate matter, and senescent erythrocytes from the blood.
CD11 antigen-like family member D
, integrin alpha-D
, leukointegrin alpha D
, integrin alpha X (Cd11c)