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anti-Human S100A8 Antibodies:
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Human Monoclonal S100A8 Primary Antibody for EIA, IHC (fro) - ABIN111890
Brandtzaeg, Jones, Flavell, Fagerhol: Mac 387 antibody and detection of formalin resistant myelomonocytic L1 antigen. in Journal of clinical pathology 1989
Show all 11 Pubmed References
Human Monoclonal S100A8 Primary Antibody for EIA, IHC (fro) - ABIN111891
Odink, Cerletti, Brüggen, Clerc, Tarcsay, Zwadlo, Gerhards, Schlegel, Sorg: Two calcium-binding proteins in infiltrate macrophages of rheumatoid arthritis. in Nature 1987
Show all 10 Pubmed References
Mouse (Murine) Polyclonal S100A8 Primary Antibody for IF (p), IHC (p) - ABIN749273
Nguyen, Fentress, Qiu, Yun, Cox, Chawla: Circadian gene Bmal1 regulates diurnal oscillations of Ly6C(hi) inflammatory monocytes. in Science (New York, N.Y.) 2013
Human Monoclonal S100A8 Primary Antibody for IA, FACS - ABIN2192036
Robinson, Tessier, Poulsom, Hogg: The S100 family heterodimer, MRP-8/14, binds with high affinity to heparin and heparan sulfate glycosaminoglycans on endothelial cells. in The Journal of biological chemistry 2002
Human Polyclonal S100A8 Primary Antibody for IHC, IHC (p) - ABIN4351730
Ellis, LaRocque, Uddin, Krastins, Mayo-Smith, Sarracino, Karlsson, Rahman, Shirin, Bhuiyan, Chowdhury, Khan, Ryan, Calderwood, Qadri, Harris: Comparative proteomic analysis reveals activation of mucosal innate immune signaling pathways during cholera. in Infection and immunity 2015
Study found that that the co-stimulation with both advanced glycation end-products and Porphyromonas gingivalis LPS (show IRF6 Antibodies) increased S100A8 and S100A9 (show S100A9 Antibodies) mRNA expression in gingival epithelial cells. These results demonstrated that the upregulation of calprotectin in gingival epithelial cells may primarily function intracellularly in this tissue and may contribute to the pathological process of periodontitis.
Our results showed that S100A8/A9, absent or present at very low level in skin biopsies from healthy subjects, is dramatically upregulated in each epidermal layer from psoriatic patients.
The results suggest that the calcium-binding proteins S100A8 and S100A9 (show S100A9 Antibodies) in myeloid cells have an immune regulatory effect.
Median MRP8/14 levels were higher in patients with Takayasu arteritis.
S100A8 gene knockdown reduced cell proliferation in the HEC (show NDC80 Antibodies)-1A cells compared with control cells, induced cell apoptosis, inhibited the phosphorylation of protein kinase B (Akt (show AKT1 Antibodies)), and induced the expression of pro-apoptotic genes.
Wide intra- and interindividual differences in calprotectin concentrations in the meconium may reflect intestinal inflammation associated with the fetal adaptation to life outside the uterus.
Salivary calprotectin levels were significantly higher in RAS [Recurrent aphthous stomatitis] group (23.72 +/- 4.28 mg/L) compared to the HC [Healthy Controls] (21.59 +/- 4.27 mg/L) (P = 0.013). No significant relationship was found between calprotectin levels and age or gender in both groups (P >0.05).
the levels of S100A8 and S100A9 (show S100A9 Antibodies) in the sera, and calprotectin levels in the sera and urines of bladder cancer patients, were determined.
MRP-8/14 concentration increases in coronary artery blood in association with thrombus formation in acute coronary syndrome.
ANGPTL6, S100A8 and S100A9 (show S100A9 Antibodies) are overexpressed in skin of psoriasis patients versus zero expression in controls.
The findings indicated that plasma concentrations of S100A7 (show S100A7 Antibodies) and S100A8 did not change significantly during pregnancy in cows.
study of nonsynonymous DNA variation in the functional domain of the S100A7 (show S100A7 Antibodies), -A8, -A9 genes in taurine cattle and yak
Data suggest that up-regulation of S100A8 and S100A9 (show S100A9 Antibodies) is a key component of early endometrial response to uterine involution in the post-partum period and to prevent chronic endometritis/uterine inflammation; up-regulation can be influenced by diet.
Study verified porcine calprotectin (S100A8/A9) expression at the protein level in multiple Haemophilus parasuis infected tissues and explored their molecular characterization.
Specific NLRC4 (show NLRC4 Antibodies) activation in Mrp8 (+) cells (primarily neutrophil lineage) is sufficient to cause severe inflammatory disease.
We present the reconstitution, purification, and characterization of mCP (show CR1L Antibodies) as well as the cysteine-null variant mCP (show CR1L Antibodies)-Ser (show SIGLEC1 Antibodies). Apo (show C9orf3 Antibodies) mCP (show CR1L Antibodies) is a mS100A8/mS100A9 heterodimer, and Ca(II (show CA2 Antibodies)) binding causes two heterodimers to self-associate and form a heterotetramer
S100A8 was required for laser-induced new collagen synthesis in skin cells.
Chronic Pseudomonas aeruginosa biofilm infection reduces murine S100A8/ S100A9 (show S100A9 Antibodies) expression and delays species-specific burn wound closure.
data suggest that S100A8/A9 acts directly on BV-2 microglial cells via binding to TLR4 (show TLR4 Antibodies) and RAGE (show AGER Antibodies) on the membrane and then stimulates the secretion of proinflammatory cytokines through ERK (show EPHB2 Antibodies) and JNK (show MAPK8 Antibodies)-mediated NF-kappaB (show NFKB1 Antibodies) activity in BV-2 microglial cells.
The results obtained in the present study demonstrate for the first time that S100A8 as well as MyD88 (show MYD88 Antibodies) and NF-B are activated by T3 and that these molecules are directly involved in the thyroid hormone (show PTH Antibodies)-induced cardiac hypertrophic response. These data suggest that one of the mechanisms underlying T3-dependent cardiac hypertrophy/failure may involve the activation of an inflammatory pathway.
Like S100A8, S100A9 (show S100A9 Antibodies) and S100A8/A9 reduced neutrophil influx in acute lung injury provoked by lipopolysaccharide (LPS (show TLR4 Antibodies)) challenge.
theses findings reveal unexpected gene expression differences between WT and KO mice at a young age (in the absence of physiological stress), and address the hypothesis that Mrp8 and Mrp14 (show S100A9 Antibodies) accumulation promotes age-related inflammation
S100A8 and S100A9 (show S100A9 Antibodies) aggravate Coxsackievirus B3-induced myocarditis and might serve as therapeutic targets in inflammatory cardiomyopathies.
Neutrophil-derived S100A8/A9 promotes thrombocytosis in diabetic mice
The protein encoded by this gene is a member of the S100 family of proteins containing 2 EF-hand calcium-binding motifs. S100 proteins are localized in the cytoplasm and/or nucleus of a wide range of cells, and involved in the regulation of a number of cellular processes such as cell cycle progression and differentiation. S100 genes include at least 13 members which are located as a cluster on chromosome 1q21. This protein may function in the inhibition of casein kinase and as a cytokine. Altered expression of this protein is associated with the disease cystic fibrosis.
, S100 calcium-binding protein A8 (calgranulin A)
, calgranulin A
, calprotectin L1L subunit
, cystic fibrosis antigen
, leukocyte L1 complex light chain
, migration inhibitory factor-related protein 8
, protein S100-A8
, urinary stone protein band A
, S100 calcium binding protein A8 (calgranulin A)
, S100 calcium binding protein A8
, S100 calcium-binding protein A8
, neutrophil cytosolic 7 kDa protein
, chemotactic S100 protein
, chemotactic cytokine CP-10
, pro-inflammatory S100 cytokine
, macrophage migration inhibitory factor-related protein-8