anti-S100A9 (S100A9) Antikörper

Human S100 Calcium Binding Protein A9 (S100A9) Interaktionspartner

1. considering erythrocyte sedimentation rate, CRP and albumin as additional markers to fecal calprotectin significantly improved diagnostic performance

2. Extracellular S100A8/A9 induced by cancer-associated inflammation in the lung plays a pivotal role in lung cancer progression through anchorage-independent growth, migration and invasion. The S100A8/A9 signal use cell surface NPTNbeta which is highly elevated at mRNA and protein levels. Data indicate that S100A8/A9-NPTNbeta plays a pivotal role in lung cancer progression with dissemination through TRAF2-NFIA/NFIB signa...

3. S100A9, which is instrumental in the pathogenesis of MDS, plays a critical role in the induction of PD-1/PD-L1 surface receptor expression on hematopoietic stem and progenitor cells (HSPCs) and myeloid-derived suppressor cells (MDSCs).

4. S100A8/A9 induced the activation of NF-kappaB and expression of MMP-9 protein through facilitating secretion of TNFalpha from macrophages, which may play a role in triggering extracellular matrix degradation and cardiac rupture.

5. There is a log-linear association of calprotectin concentration with risk of cardiovascular disease, which may be partly dependent on hsCRP.

6. Data show that calprotectin serum levels were significantly associated with disease relapse.

7. The expression of S100A9 in osteosarcoma can serve as a diagnostic marker and a therapeutic target.

8. s100a9 has shown to play an important role in vascular inflammation and may serve as a biomarker and potential therapeutic target for intracranial aneurysms

9. Calgranulin B and KL-6 in BAL proved to be reliable biomarkers of diopathic pulmonary fibrosis (IPF) and non-specific interstitial pneumonia (NSIP) and to have prognostic meaning, discriminating severe and advanced patients. The combination of the two biomarkers can facilitate the stratification of severity.

10. During the anti-TNF therapy, the serum fibulin-3 level decreased in RA[rheumatoid arthritis] patients. Serum MRP8/14 concentration also decreased. No correlation between fibulin-3 and MRP8/14 was observed in the study group before and after the treatment. We found a poor correlation between serum fibulin-3 and other cartilage metabolism biomarkers after anti-TNF therapy.

11. this study demonstrates that S100A8/A9 mediates renal damage and fibrosis, presumably through loss of tubular epithelial cell contacts and irreversible damage

12. Hepatitis b virus infection may enhance S100A9 expression.

13. Calprotectin is found in various body fluids in proportion to the degree of any existing inflammation and its concentration in feces is about six times that of plasma. Measurement of fecal calprotectin is a useful surrogate marker of gastrointestinal inflammation. [review]

14. this study shows fecal calprotectin rise in chronic granulomatous disease-associated colitis

15. Calprotectin during remission in ANCA vasculitis may be useful to identify subclinical inflammation and worse renal prognosis patients.

16. 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). This analysis reveals conformational changes associated with coordination of Ca(II) to the EF-hands of S100A9.

17. 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.

18. 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.

19. 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.

20. Infliximab (IFX) levels (at week 14) and baseline fecal calprotectin levels could predict primary nonresponse after induction IFX therapy in patients with Crohn's disease.

Cow (Bovine) S100 Calcium Binding Protein A9 (S100A9) Interaktionspartner

1. study of nonsynonymous DNA variation in the functional domain of the S100A7, -A8, -A9 genes in taurine cattle and yak

2. 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.

Pig (Porcine) S100 Calcium Binding Protein A9 (S100A9) Interaktionspartner

1. Study verified porcine calprotectin (S100A8/A9) expression at the protein level in multiple Haemophilus parasuis infected tissues and explored their molecular characterization.

Rabbit S100 Calcium Binding Protein A9 (S100A9) Interaktionspartner

1. this study shows that S100A9 inhibits B lymphopoiesis by acting on myeloid cells and promoting the release of inflammatory molecules, including IL-1beta

Mouse (Murine) S100 Calcium Binding Protein A9 (S100A9) Interaktionspartner

1. S100A9, which is instrumental in the pathogenesis of MDS, plays a critical role in the induction of PD-1/PD-L1 surface receptor expression on hematopoietic stem and progenitor cells (HSPCs) and myeloid-derived suppressor cells (MDSCs).

2. The results indicated that S100A9 gene silencing suppressed the release of pro-inflammatory cytokines through blocking of the IL-17 pathway in acute pancreatitis (AP).

3. S100A9 promotes MDSC expansion and immunosuppression in late/chronic sepsis by inducing the expression of miR-21 and miR-181b.

4. Increased VEGF165b expression in macrophages induces an antiangiogenic M1-like phenotype that directly impairs angiogenesis. VEGFR1 inhibition by VEGF165b results in S100A8/S100A9-mediated calcium influx to induce an M1-like phenotype that impairs ischemic muscle revascularization and perfusion recovery.

5. Autoinhibitory regulation of S100A8/S100A9 alarmin activity locally restricts sterile inflammation.

6. Both IL-6 and IL-10 can activate S100A9 expression.

7. this study shows that neutrophil-derived MRP14 supports plasma cell commitment and protects myeloma cells from apoptosis

8. this study shows that MRP14 does not contribute to dissemination or inflammation in a murine model of Lyme borreliosis

9. this study demonstrates that S100A8/A9 mediates renal damage and fibrosis, presumably through loss of tubular epithelial cell contacts and irreversible damage

10. emphasized the pathogenic nature of S100A9 fibrillar aggregates in causing spatial memory amnesia associated with enhanced hippocampal glutamate release

11. Fc gammaRIV (FcgammaRIV) mediates bone erosion in antigen-induced arthritis (AIA) by inducing the influx of S100A8/A9-producing neutrophils into the arthritic joint.

12. 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

13. MRP14 is a one of key molecules for liver inflammation during rodent malaria

14. These results suggest that immunological functions of MRP14, and possibly also the associated molecule MRP8, are different between BALB/c and C57BL/6 mice, at least in the response to LPS.

15. the biologically potent dimeric form of S100A9 is induced in vivo in situations of tumor burden or inflammatory challenge.

16. 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

17. Chronic Pseudomonas aeruginosa biofilm infection reduces murine S100A8/ S100A9 expression and delays species-specific burn wound closure.

18. 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.

19. Like S100A8, S100A9 and S100A8/A9 reduced neutrophil influx in acute lung injury provoked by lipopolysaccharide (LPS) challenge.

20. 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

Horse (Equine) S100 Calcium Binding Protein A9 (S100A9) Interaktionspartner

1. Calprotectin expression in laminar epidermis occurs after extravasation of leukocytes indicating that leukocyte emigration may be an initiating factor in laminar epithelial stress and inflammation in black walnut extract-induced laminitis.