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findings suggest that CD11d/CD18 (zeige ITGB2 ELISA Kits) 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 (zeige ICAM3 ELISA Kits) and CD11d/CD18 (zeige ITGB2 ELISA Kits), 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 (zeige GUSB ELISA Kits)-enriched Kruppel-like factor 4 (zeige KLF4 ELISA Kits) (GKLF (zeige KLF4 ELISA Kits)) we term GKLFa interacts with the CD11d promoter
multiple CD11d domains play a role in controlling intracellular location and association with CD18 (zeige ITGB2 ELISA Kits).
The results indicate that both Mac-1 (zeige ITGAM ELISA Kits) and alphaDbeta2 support macrophage fusion with Mac-1 (zeige ITGAM ELISA Kits) 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)