SAA1
- Known as:
- SAA1
- Catalog number:
- 000386A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SAA1
Related genes to: SAA1
- Gene:
- SAA1 NIH gene
- Name:
- serum amyloid A1
- Previous symbol:
- SAA
- Synonyms:
- PIG4, TP53I4
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-01-18
- Date modifiied:
- 2015-09-09
Related products to: SAA1
Related articles to: SAA1
- Clear cell renal cell carcinoma (ccRCC) is the most common kidney malignancy. Yet, no rapid, non-invasive biomarkers are available for diagnosis or screening. Urine represents an ideal analyte matrix due to its accessibility, low invasiveness, longitudinal sampling, and the kidney's central role in filtration. Here, we integrated proteomic, lipidomic, and metabolomic analyses of urine from ccRCC patients and controls to identify diagnostic biomarkers. Multi-omics profiling revealed urogenital metabolic dysregulation in ccRCC, including increased lipid metabolism, altered mitochondrial respiration signatures, and elevated urinary lipid content. We identified three urinary protein biomarkers: serum amyloid A1 (SAA1), haptoglobin (HP), and lipocalin 15 (LCN15). Using a parallel reaction monitoring mass spectrometry workflow, we developed a rapid and sensitive assay and combined these markers into a diagnostic UrineScore. The UrineScore achieved 0.96 in an area under the receiver operating characteristic curve analysis in the discovery cohort, and 0.95 in an independent validation cohort. Together, these results support the feasibility of multi-omics-guided urinary biomarker discovery and represent a step toward accessible diagnostic platforms for ccRCC. - Source: PubMed
Publication date: 2026/08/11
Jonsson GustavOliveira TiagoHofmann MauraLemberger UrsulaStejskal KarelKrššáková GabrielaSakic IrmaNovatchkova MariaMereiter StefanGrabmann GerlindeKöcher ThomasKoglgruber RubinaKikic ZeljkoCamano Páez SoniaLuna Sanchez BárbaraDíez Nicolás VíctorRechberger Gerald NZüllig ThomasHagelkruys AstridEnglinger BernhardSchmidinger ManuelaPenninger Josef M - Histopathological growth patterns (HGPs) have emerged as prognostic and predictive biomarkers in colorectal liver metastases (CLM). The desmoplastic/encapsulating HGP (EHGP) is associated with improved survival after surgery, whereas the replacement HGP (RHGP) is associated with poorer outcomes. However, HGPs can only be reliably assessed postoperatively, limiting their use as preoperative biomarkers. A deeper molecular understanding of HGPs could inform biomarker development and therapeutic strategies, including approaches to promote EHGP. - Source: PubMed
Publication date: 2026/07/28
Escriva Conde MariaAndersson AxelVermeulen PeterNilsson MatsNyström Hanna - Periodontitis is a chronic inflammatory disease characterized by irreversible destruction of alveolar bone, periodontal ligament attachment, and supporting tooth structures. Emerging evidence suggests that periodontal tissue breakdown and regenerative failure are primarily driven by dysregulation of the local immune microenvironment rather than by direct bacterial insult. Therefore, conventional therapies focused primarily on microbial control are insufficient to restore immune homeostasis and functional regeneration of the cementum-periodontal ligament-alveolar bone complex. Effective periodontal regeneration requires coordinated infection management, immune modulation, oxidative stress clearance, and inflammatory microenvironment reprogramming to relieve the suppression of regenerative cells, particularly periodontal ligament stem cells. This review summarizes key regulatory networks of the periodontal immune microenvironment, with emphasis on macrophage polarization, neutrophil heterogeneity, and the imbalance between Th17 cells and regulatory T cells. We further discuss recent immune-engineering strategies for restoring periodontal homeostasis, including surface-modified biomaterials, ion-delivery systems, stem cell-derived extracellular vesicles, gene-editing technologies, and smart responsive therapeutic scaffolds. Advances in single-cell and spatial transcriptomics have revealed previously unrecognized functional subpopulations, such as NLRP3 macrophages and SAA1 fibroblasts, offering new opportunities for precision immunomodulation. Collectively, this review provides an integrated and translational framework for leveraging immune microenvironment-based interventions to achieve functional and predictable periodontal regeneration. - Source: PubMed
Zhang RuyiZhang HuachangZeng WenhuaZhao JiqingXia HaoZhang NanLi Keyi - Silent corticotroph adenomas (SCAs) represent a high-risk subtype of pituitary neuroendocrine tumors, characterized by significant clinical heterogeneity and unclear pathogenesis. The multimicrocystic sign is a typical radiological feature of SCAs; however, its biological significance remains unclear. Here, we show that the characteristics of cystic changes reflect tumor evolutionary stages and are correlated with invasiveness and proliferative activity. We performed multi-omics analysis to identify key molecular drivers and revealed that serum amyloid A1 (SAA1) is highly expressed in microcystic tumors corresponding to the bone invasion stage. Our results demonstrate that SAA1 activates the TLR4/NF-κB pathway in macrophages, promoting pro-inflammatory macrophage polarization, TNF-α and CSF-1 secretion, and osteoclast differentiation. Spatial transcriptomics confirmed a significant correlation between the proportion of SAA1+ tumor cells and that of TNF-α+ macrophages. Serum amyloid A (SAA) levels in serum exhibited strong diagnostic value for SCAs. These findings highlight the potential clinical and biological significance of cyst size in SCAs and uncover a novel mechanism by which SAA1 drives tumor bone invasiveness through macrophage-mediated osteoclast differentiation. Our findings highlight that serum SAA levels may serve as a promising biomarker for the preoperative identification of SCAs, advancing our understanding of SCA heterogeneity. - Source: PubMed
Publication date: 2026/07/15
Jia JingyuanJiang ChenggangXie JindouYi ZhaoyiDi HanLi XuejingZhou LeiBai LuLiu YuweiZhang RenlongGong LeiWang HongyunLiu ZhaoqiXie WeiyanLi ChuzhongXing XudongZhang Yazhuo - Depression is one of the most prevalent psychiatric disorders worldwide, yet its pathogenesis remains unclear. Here, we aimed to investigate the effects of formyl peptide receptor 2 (FPR2), a key regulator of innate immunity and inflammation, on lipopolysaccharide (LPS)-induced depression-related behaviors in mice after intraperitoneal administration, and to elucidate its regulatory mechanisms in microglia. FPR2 knockout (Fpr2) significantly attenuated LPS-induced depressive and anxiety-like behaviors in mice. LPS markedly increased FPR2 expression in microglia of the prefrontal cortex (PFC) and hippocampus, while only a minimal increase was observed in neurons. FPR2 deficiency alleviated LPS-induced microglial activation and reduced neuronal synaptic alterations. RNA sequencing and validation experiments confirmed that FPR2 deletion substantially decreased LPS-induced microglial NLRP3 inflammasome activation and IL-1β levels in the brain. Mechanistically, FPR2 regulated downstream NLRP3 activation by modulating CSF1, and FPR2/CSF1 activation was governed by its upstream ligand, serum amyloid A (SAA). Analysis of public clinical datasets revealed that SAA1 levels were significantly upregulated in the orbital ventral PFC of patients with major depressive disorder (MDD) and in the plasma of patients with late-life depression. These findings demonstrate that the SAA/FPR2/CSF1/NLRP3 pathway mediates LPS-induced depressive-like behaviors by regulating microglial activation and neuroinflammation. - Source: PubMed
Publication date: 2026/07/16
Wang HanqiChen YijunChang JunnaLiu ZhenYu Yang