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anti-Human S100A8 Antibodies:
anti-Rat (Rattus) S100A8 Antibodies:
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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 15 Pubmed References
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 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
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 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
this study provides evidence that S100A8/PhosphoS100A9 is inducing cytokine secretion through toll-like receptor 4 signaling
this study demonstrates that S100A8/A9 mediates renal damage and fibrosis, presumably through loss of tubular epithelial cell contacts and irreversible damage
these results suggested that the activation of the expression of S100A8 induced by IL1a in TR146 epithelial cells involves a mechanism by which the binding activity of C/EBPB to the specific site (113/109) of the S100A8 promoter is increased
High S100A8 expression may be associated with the poor prognosis of children with acute lymphoblastic leukemia (ALL) and is promising as a new marker for individualized precise treatment of children with ALL
By employing energy dispersive X-ray (EDX) spectroscopy, this study evaluate the metal content of Ni(II)-bound Calprotectin-Ser [oligomer of S100A8(C42S) and S100A9(C3S)] crystals obtained in the absence and presence of Ca(II). Whereas the His6 site has a thermodynamic preference for Ni(II) over Zn(II), the His3Asp site selects for Zn(II) over Ni(II), and relatively rapid metal exchange occurs at this site.
Results show that S100A8 and S100A9 proteins induce specific cytokine secretion from PDAC cells, which in turn enhances the expression of S100A8/A9. This paracrine crosstalk could have implications for pancreatic ductal adenocarcinoma invasiveness and metastatic potential.
Fecal but not serum calprotectin seems to be a useful non-invasive tool for assessing disease activity in Behcet's syndrome patients with gastrointestinal involvement.
100A8 and S100A9 positive expression in cancer tissues was significantly higher than in para-cancer tissues and was correlated with tumor differentiation, which may be a potential marker for poor prognosis.
High S100A8 expression is associated with metastatic melanomas.
When human islet cells were co-cultured with U937 human monocyte cells, the palmitate treatment up-regulated S100A8 expression. This S100A8-mediated interaction between islets and macrophages evoked beta-cell apoptosis, which was ameliorated by TLR4 inhibition in the macrophages or S100A8 neutralization in the pancreatic islets.
Study found that that the co-stimulation with both advanced glycation end-products and Porphyromonas gingivalis LPS increased S100A8 and S100A9 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 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-1A cells compared with control cells, induced cell apoptosis, inhibited the phosphorylation of protein kinase B (Akt), 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 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 are overexpressed in skin of psoriasis patients versus zero expression in controls.
The findings indicated that plasma concentrations of S100A7 and S100A8 did not change significantly during pregnancy in cows.
study of nonsynonymous DNA variation in the functional domain of the S100A7, -A8, -A9 genes in taurine cattle and yak
Data suggest that up-regulation of S100A8 and S100A9 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.
Fc gammaRIV (FcgammaRIV) mediates bone erosion in antigen-induced arthritis (AIA) by inducing the influx of S100A8/A9-producing neutrophils into the arthritic joint.
results indicate that S100A8/A9 contributes to several facets of neuroinflammation in sepsis survivor mice, including granulocyte recruitment and priming of microglial-reactive oxygen species and cytokine production
Co-cultivation of pancreatic islets with unstimulated peritoneal macrophages in the presence of palmitate (to induce lipotoxicity) and high glucose (to induce glucotoxicity) synergistically increased the expression and release of islet-produced S100A8 in a Toll-like receptor 4 (TLR4)-independent manner.
Specific NLRC4 activation in Mrp8 (+) cells (primarily neutrophil lineage) is sufficient to cause severe inflammatory disease.
We present the reconstitution, purification, and characterization of mCP as well as the cysteine-null variant mCP-Ser. Apo mCP is a mS100A8/mS100A9 heterodimer, and Ca(II) 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 expression and delays species-specific burn wound closure.
data suggest that S100A8/A9 acts directly on BV-2 microglial cells via binding to TLR4 and RAGE on the membrane and then stimulates the secretion of proinflammatory cytokines through ERK and JNK-mediated NF-kappaB activity in BV-2 microglial cells.
The results obtained in the present study demonstrate for the first time that S100A8 as well as MyD88 and NF-B are activated by T3 and that these molecules are directly involved in the thyroid hormone-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 and S100A8/A9 reduced neutrophil influx in acute lung injury provoked by lipopolysaccharide (LPS) 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 accumulation promotes age-related inflammation
S100A8 and S100A9 aggravate Coxsackievirus B3-induced myocarditis and might serve as therapeutic targets in inflammatory cardiomyopathies.
Neutrophil-derived S100A8/A9 promotes thrombocytosis in diabetic mice
Perinatal alarmins S100A8 and S100A9 specifically altered MyD88-dependent proinflammatory gene programs. S100 programming prevented hyperinflammatory responses without impairing pathogen defense. TRIF-adaptor-dependent regulatory genes remained unaffected by perinatal S100 programming and responded strongly to lipopolysaccharide, but were barely expressed.
S100a8 upregulation triggers NF-kappaB signal pathway through RAGE and TLR4, in response to laser-induced dermis wound healing.
Although MRP-8/-14 expression is highly increased in experimental, these proteins do not contribute to the pathogenesis in the effector phase of epidermolysis bullosa acquisita and bullous pemphigoid.
TLR4, TLR2 also contributed to Mrp8-induced inflammatory response and tolerance.
S100A8 appears to play a crucial role in the activation of the TLR4/MD-2 pathway and the promotion of a tumor growth-enhancing immune microenvironment.
Rps14 haploinsufficiency in del(5q) myelodysplastic syndrome is linked to activation of the innate immune system and induction of S100A8-S100A9 expression, leading to a p53-dependent erythroid differentiation defect.
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