Sheep Serum amyloid A 3 ELISA , SAA3
- Known as:
- Sheep Serum amyloid A 3 Enzyme-linked immunosorbent assay test , SAA3
- Catalog number:
- E14S0229
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Sheep Serum amyloid 3 ELISA SAA3
Related genes to: Sheep Serum amyloid A 3 ELISA , SAA3
- Gene:
- SAA3P NIH gene
- Name:
- serum amyloid A3, pseudogene
- Previous symbol:
- SAA3
- Synonyms:
- -
- Chromosome:
- 11p15.1
- Locus Type:
- pseudogene
- Date approved:
- 1992-06-12
- Date modifiied:
- 2018-01-12
Related products to: Sheep Serum amyloid A 3 ELISA , SAA3
Related articles to: Sheep Serum amyloid A 3 ELISA , SAA3
- Pancreatic ductal adenocarcinoma (PDAC) is characterized by the presence of abundant desmoplastic stroma primarily composed of cancer-associated fibroblasts (CAFs). It is generally accepted that CAFs stimulate tumor progression and might be implicated in drug resistance and immunosuppression. Here, we have compared the transcriptional profile of PDGFRα CAFs isolated from genetically engineered mouse PDAC tumors with that of normal pancreatic fibroblasts to identify genes potentially implicated in their protumorigenic properties. We report that the most differentially expressed gene, , a member of the serum amyloid A (SAA) apolipoprotein family, is a key mediator of the protumorigenic activity of PDGFRα CAFs. Whereas -competent CAFs stimulate the growth of tumor cells in an orthotopic model, -null CAFs inhibit tumor growth. Saa3 also plays a role in the cross talk between CAFs and tumor cells. Ablation of in pancreatic tumor cells makes them insensitive to the inhibitory effect of -null CAFs. As a consequence, germline ablation of does not prevent PDAC development in mice. The protumorigenic activity of Saa3 in CAFs is mediated by Mpp6, a member of the palmitoylated membrane protein subfamily of the peripheral membrane-associated guanylate kinases (MAGUK). Finally, we interrogated whether these observations could be translated to a human scenario. Indeed, , the ortholog of murine Saa3, is overexpressed in human CAFs. Moreover, high levels of in the stromal component correlate with worse survival. These findings support the concept that selective inhibition of SAA1 in CAFs may provide potential therapeutic benefit to PDAC patients. - Source: PubMed
Publication date: 2018/01/19
Djurec MagdolnaGraña OsvaldoLee AlbertTroulé KevinEspinet ElisaCabras LaviniaNavas CarolinaBlasco María TeresaMartín-Díaz LauraBurdiel MirandaLi JingLiu ZhaoqiVallespinós MireiaSanchez-Bueno FranciscoSprick Martin RTrumpp AndreasSainz BrunoAl-Shahrour FátimaRabadan RaulGuerra CarmenBarbacid Mariano - - Source: PubMed
Publication date: 2015/11/10
Wang Ya-tingXu Dan-yan - To examine whether the long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is altered in the endothelial cells in response to glucose and the significance of such alteration. We incubated human umbilical vein endothelial cells with media containing various glucose levels. We found an increase in MALAT1 expression peaking after 12 hrs of incubation in high glucose. This increase was associated with parallel increase in serum amyloid antigen 3 (SAA3), an inflammatory ligand and target of MALAT1 and was further accompanied by increase in mRNAs and proteins of inflammatory mediators, tumour necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). Renal tissue from the diabetic animals showed similar changes. Such cellular alterations were prevented following MALAT1 specific siRNA transfection. Results of this study indicate that LncRNA MALAT1 regulates glucose-induced up-regulation of inflammatory mediators IL-6 and TNF-α through activation of SAA3. Identification of such novel mechanism may lead to the development of RNA-based therapeutics targeting MALAT1 for diabetes-induced micro and macro vascular complications. - Source: PubMed
Publication date: 2015/03/19
Puthanveetil PrasanthChen ShaliFeng BiaoGautam AnirudhChakrabarti Subrata - - Source: PubMed
Publication date: 2015/03/06
Knee OlatejumoyeGupta AashishCurley AnnaCharnock-Jones D StephenSmith Gordon C SBelteki Gusztav - S100A4 is implicated in metastasis and chronic inflammation, but its function remains uncertain. Here we establish an S100A4-dependent link between inflammation and metastatic tumor progression. We found that the acute-phase response proteins serum amyloid A (SAA) 1 and SAA3 are transcriptional targets of S100A4 via Toll-like receptor 4 (TLR4)/nuclear factor-κB signaling. SAA proteins stimulated the transcription of RANTES (regulated upon activation normal T-cell expressed and presumably secreted), G-CSF (granulocyte-colony-stimulating factor) and MMP2 (matrix metalloproteinase 2), MMP3, MMP9 and MMP13. We have also shown for the first time that SAA stimulate their own transcription as well as that of proinflammatory S100A8 and S100A9 proteins. Moreover, they strongly enhanced tumor cell adhesion to fibronectin, and stimulated migration and invasion of human and mouse tumor cells. Intravenously injected S100A4 protein induced expression of SAA proteins and cytokines in an organ-specific manner. In a breast cancer animal model, ectopic expression of SAA1 or SAA3 in tumor cells potently promoted widespread metastasis formation accompanied by a massive infiltration of immune cells. Furthermore, coordinate expression of S100A4 and SAA in tumor samples from colorectal carcinoma patients significantly correlated with reduced overall survival. These data show that SAA proteins are effectors for the metastasis-promoting functions of S100A4, and serve as a link between inflammation and tumor progression. - Source: PubMed
Publication date: 2014/01/27
Hansen M TForst BCremers NQuagliata LAmbartsumian NGrum-Schwensen BKlingelhöfer JAbdul-Al AHerrmann POsterland MStein UNielsen G HScherer P ELukanidin ESleeman J PGrigorian M