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anti-Human S100A8 Anticorps:
anti-Rat (Rattus) S100A8 Anticorps:
anti-Mouse (Murine) S100A8 Anticorps:
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Human Monoclonal S100A8 Primary Antibody pour EIA, IHC (fro) - ABIN111891
Odink, Cerletti, Brüggen, Clerc, Tarcsay, Zwadlo, Gerhards, Schlegel, Sorg: Two calcium-binding proteins in infiltrate macrophages of rheumatoid arthritis. dans Nature 1987
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Human Monoclonal S100A8 Primary Antibody pour EIA, IHC (fro) - ABIN111890
Brandtzaeg, Jones, Flavell, Fagerhol: Mac 387 antibody and detection of formalin resistant myelomonocytic L1 antigen. dans Journal of clinical pathology 1989
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Human Monoclonal S100A8 Primary Antibody pour 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. dans The Journal of biological chemistry 2002
Mouse (Murine) Polyclonal S100A8 Primary Antibody pour IF (p), IHC (p) - ABIN749273
Nguyen, Fentress, Qiu, Yun, Cox, Chawla: Circadian gene Bmal1 regulates diurnal oscillations of Ly6C(hi) inflammatory monocytes. dans Science (New York, N.Y.) 2013
Human Polyclonal S100A8 Primary Antibody pour ELISA, WB - ABIN4242803
Eggers, Sikora, Lorenz, Taubert, Moobed, Baumann, Stangl, Stangl: RAGE-dependent regulation of calcium-binding proteins S100A8 and S100A9 in human THP-1. dans Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association 2011
Human Polyclonal S100A8 Primary Antibody pour 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. dans Infection and immunity 2015
Report role of fecal calprotectin assay in the diagnosis and management of inflammatory bowel disease.
S100A8 and S100A9 (Montrer S100A9 Anticorps) aggravate Coxsackievirus B3-induced myocarditis and might serve as therapeutic targets in inflammatory cardiomyopathies.
Data suggest that fecal calprotectin may be a potential biomarker to identify patients with ankylosing spondylitis (AS) at risk of developing inflammatory bowel disease (IBD).
Elevated S100A8 and S100A9 (Montrer S100A9 Anticorps) gene expression in SP-infected HMEECs and in the middle ear mucosa of OM, minor co-localized with neutrophil markers suggests that middle ear epithelial cell secretion of S100A8 and S100A9 (Montrer S100A9 Anticorps) may play a role in the pathogenesis of recurrent and chronic OM
results of this study support an additional role of calprotectin in assessing inflammatory activity in patients with RA
Data show that E3 ubiquitin ligase (Montrer MUL1 Anticorps) HRD1 (HRD1 (Montrer SYVN1 Anticorps)) decreased the protein level of S100A8 through ubiquitination.
High S100A8 expression is associated with glioblastoma.
This study implicates S100A8 and S100A9 (Montrer S100A9 Anticorps) as important mediators of tumor cell aggressiveness, and highlights the therapeutic potential of S100A8 and S100A9 (Montrer S100A9 Anticorps) for interference of metastasis.
Data indicate a statistical correlation between fecal calprotectin (FC) and gastrointestinal graft-versus-host disease (GvHD).
Perinatal alarmins S100A8 and S100A9 (Montrer S100A9 Anticorps) specifically altered MyD88 (Montrer MYD88 Anticorps)-dependent proinflammatory gene programs. S100 programming prevented hyperinflammatory responses without impairing pathogen defense. TRIF (Montrer TRIM69 Anticorps)-adaptor-dependent regulatory genes remained unaffected by perinatal S100 programming and responded strongly to lipopolysaccharide, but were barely expressed.
Data suggest that up-regulation of S100A8 and S100A9 (Montrer S100A9 Anticorps) 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.
Neutrophil-derived S100A8/A9 promotes thrombocytosis in diabetic mice
Perinatal alarmins S100A8 and S100A9 (Montrer S100A9 Anticorps) specifically altered MyD88 (Montrer MYD88 Anticorps)-dependent proinflammatory gene programs. S100 programming prevented hyperinflammatory responses without impairing pathogen defense. TRIF (Montrer RNF138 Anticorps)-adaptor-dependent regulatory genes remained unaffected by perinatal S100 programming and responded strongly to lipopolysaccharide, but were barely expressed.
S100a8 upregulation triggers NF-kappaB (Montrer NFKB1 Anticorps) signal pathway through RAGE (Montrer AGER Anticorps) and TLR4 (Montrer TLR4 Anticorps), 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 (Montrer DST Anticorps).
TLR4 (Montrer TLR4 Anticorps), TLR2 (Montrer TLR2 Anticorps) also contributed to Mrp8-induced inflammatory response and tolerance.
S100A8 appears to play a crucial role in the activation of the TLR4 (Montrer TLR4 Anticorps)/MD-2 (Montrer LY96 Anticorps) pathway and the promotion of a tumor growth-enhancing immune microenvironment.
Rps14 (Montrer RPS14 Anticorps) haploinsufficiency in del(5q) myelodysplastic syndrome is linked to activation of the innate immune system and induction of S100A8-S100A9 (Montrer S100A9 Anticorps) expression, leading to a p53 (Montrer TP53 Anticorps)-dependent erythroid differentiation defect.
S100A8 is primarily produced from CXCR2 (Montrer CXCR2 Anticorps)-expressing CD11b (Montrer ITGAM Anticorps)(+)Gr-1 (Montrer GSR Anticorps)(high) cells, and it upregulates TNF-alpha (Montrer TNF Anticorps) production in CD11b (Montrer ITGAM Anticorps)(+)F4/80(+) cells through cellular cross-talk, which is an important mechanism in the development of Nonalcoholic fatty liver disease
Alarmins S100A8/S100A9 (Montrer S100A9 Anticorps) aggravate osteophyte formation in experimental osteoarthritis and predict osteophyte progression in early human symptomatic osteoarthritis.
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