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Major acute phase reactant. De plus, nous expédions SAA3 Protéines (2) et beaucoup plus de produits pour cette protéine.
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Twenty four hours post E. coli stimulation, IL1b (Montrer IL1B Kits ELISA), IL6 (Montrer IL6 Kits ELISA), IL8 (Montrer IL8 Kits ELISA), TNF (Montrer TNF Kits ELISA) and LAP gene expression was decreased compared to 6h, whereas TAP and SAA3 expression was further increased to 209- and 3452-fold (P<0.05).
SAA3 serves an important tissue-specific function for the welfare of the mammary gland during both bacterial infection and tissue remodeling.
The induction of Saa3 by PTH (Montrer PTH Kits ELISA) may explain the suppression of bone formation when PTH (Montrer PTH Kits ELISA) is applied continuously and may be a new therapeutic target for osteoporosis.
results also suggest that Saa3 influences liver-specific SAA1 (Montrer SAA1 Kits ELISA)/2 expression, and that SAA3 could play a larger role in the acute phase response than previously thought
Expression of Saa3 in osteoblasts positively correlates with increased cellular maturation toward the osteocyte phenotype.
Serum amyloid A is a retinol binding protein that transports retinol during bacterial infection.
These results suggest that SAA3 plays a role in host innate immunity in the colon by up-regulating MUC2 (Montrer MUC2 Kits ELISA) mucin (Montrer SLC13A2 Kits ELISA) production, which builds a physiological barrier of colonic epithelia against bacterial invasion.
these data suggest a novel mechanism by which Mo MDSCs mediate inflammation through SAA3-TLR2 signaling and thus exacerbate cancer progression by a STAT3 (Montrer STAT3 Kits ELISA)-dependent mechanism.
Hypoxia leads to a substantial increase in SAA3 mRNA and protein level, apparently in a time-dependent manner (threefold in 48 h), in fully differentiated 3T3-L1, followed by reestablishment of gene expression to basal levels after 24 h of reoxygenation.
Using various synthetic peptide fragments, it was shown that SAA3 directly binds MD-2 and activates the MyD88-dependent TLR4/MD-2 pathway, induced IL-6 and TNF-alpha, and recruited CD11b(+)Gr-1(+) cells to the lung.
HSV-1 induces and activate TLR2 and TLR4 receptors directly through interaction of astrocytes with the pathogen and also indirectly by endogenous ligands produced locally, such as serum amyloid A, potentiating the neuroinflammatory response.
Saa3 is expressed in the lungs of mice exposed to several mixed T helper (Th) type 2/Th17-polarizing allergic sensitization regimen and is implicated in the pathogenesis of experimental allergic asthma.
Major acute phase reactant. Apolipoprotein of the HDL complex.
serum amyloid A-3 protein
, serum amyloid A