Ask about this productRelated genes to: SAA1 protein
- 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 protein
Related articles to: SAA1 protein
- Serum amyloid A1 (SAA1) is closely associated with malignant progression and unfavorable prognosis in multiple cancers. However, the specific cellular sources and mechanisms of SAA1 within the breast cancer tumor microenvironment (TME) remain incompletely understood. This study aims to investigate the SAA1 expression in the breast cancer and to elucidate its functional roles in tumor progression. - Source: PubMed
Publication date: 2026/04/28
Lin JialiHuang XiaozhiPan LiuxianLi MingliLei LanghuanYang XingShi WeiDing YanpingJiang ZiqiongLi WeiLiang Qiuyu - Patients with advanced high-grade serous ovarian carcinoma (HGSOC) often experience extremely poor prognoses due to extensive peritoneal metastases, yet the underlying driving mechanisms remain unclear. This study reveals that serum amyloid A1 (SAA1) is markedly upregulated in late-stage HGSOC and is closely associated with poor prognosis and distant metastasis. These findings were validated through both single-cell RNA sequencing and clinical specimen analyses. Surprisingly, SAA1 does not directly promote tumour cell proliferation or migration. Instead, it reshapes the immunosuppressive tumour microenvironment by activating FPR2 tumour-associated macrophages (TAMs). Mechanistically, the SAA1-FPR2 signalling axis triggers the JAK2/STAT3 pathway in macrophages, enhancing the transcription and secretion of CXCL1. This, in turn, induces epithelial-mesenchymal transition (EMT) in tumour cells and endows them with greater metastatic potential. Animal models further confirmed that SAA1 knockdown, macrophage depletion, or CXCL1 blockade all significantly suppressed peritoneal dissemination. Collectively, this study identifies a novel SAA1-TAM-CXCL1 immune-inflammatory signalling axis, elucidates its critical role in ovarian cancer metastasis, and provides a robust theoretical foundation for the development of innovative anti-metastatic therapeutic strategies. KEY POINTS: A distinct SAA1-enriched tumour cell subset with metastasis-associated features is identified in ovarian cancer. Tumour-derived SAA1 reprograms TAM through FPR2-mediated JAK2-STAT3 signalling to induce an immunosuppressive phenotype. The SAA1-TAM-CXCL1 axis facilitates metastatic progression in ovarian cancer. - Source: PubMed
Zhou XuanMeng HuangyangChang QianjingRen JingjingWen MeichenZhang LinCheng Wenjun - Renal injury is a key determinant of prognosis of patients afflicted with occupational medicamentosa-like dermatitis due to trichloroethylene (OMDT). Prior investigations have identified damage to renal vascular endothelial cells and elevated serum amyloid A1 (SAA1) levels in individuals with OMDT. Nevertheless, the precise relationship between SAA1 and endothelial cell damage necessitates further elucidation. In the present study, utilizing a trichloroethylene (TCE)-sensitized mouse model alongside cellular experiments, SAA1 inhibitor SGA360 and TLR2 siRNA were employed to explore the specific correlation between SAA1 and endothelial cell damage. The findings demonstrated that TCE-sensitized mice exhibited pronounced renal injury and damage to renal vascular endothelial cells, which were associated with the activation of the NLRP3 inflammasome. Pretreatment with SGA360 effectively inhibited NLRP3 inflammasome activation and mitigated renal injury. Further investigations revealed that SAA1 interacts with TLR2, rather than TLR4, to activate the NLRP3 inflammasome. In vitro experiments, wherein human umbilical vein endothelial cells (HUVECs) were exposed to 1.25 μg/mL of SAA1 and TLR2 small interfering RNA (siRNA), demonstrated that SAA1 activates the NLRP3 inflammasome through its interaction with TLR2. This activation promotes GSDMD-mediated pyroptosis, thereby compromising the endothelial barrier. The study concluded that SAA1 interacts with TLR2 receptors located on the surface of renal vascular endothelial cells, leading to the activation of the NLRP3 inflammasome. This activation initiates pyroptosis and the substantial release of inflammatory cytokines, which undermine the integrity of the renal vascular endothelial barrier. Consequently, this disruption impairs glomerular filtration and tubular reabsorption functions. - Source: PubMed
Publication date: 2026/05/16
You ChenQin ZhuohuiLi RuiChen JianZhu QixingXie Haibo - Pediatric severe traumatic brain injury (sTBI) remains a leading cause of death and long-term disability, yet its molecular characterization is incomplete. Single-biomarker approaches fail to capture the biological heterogeneity underlying variable clinical outcomes. Comprehensive proteomic profiling across neuropathologic domains to identify clinical endotypes has not been performed in pediatric sTBI. This study addresses this gap using high-throughput plasma neuro-proteomic profiling during the acute injury phase. - Source: PubMed
Publication date: 2026/05/14
Cela EnisVan Nynatten Logan RTweddell DavidDaley MarkMorello MariaCepinskas GediminasFraser Douglas D - Non-glycosylated liver-derived acute-phase amyloid A1 and A2 proteins (SAA1 and SAA2, 104 amino acids), generated by two different genes in humans (/) and other mammalian species, are considered the prime acute-phase reactants following inflammatory conditions during host defense in cells, tissues, and the circulation. While human has been identified as a pseudogene, genes in other mammalian species are coding for primarily extrahepatically expressed Saa3 proteins that also may act as suitable inflammatory markers. The discovery of SAA4 (112 amino acids, carrying an octapeptide insert) in humans and mice has paved a new avenue for the exploration of different functions of this so far unknown member of the SAA superfamily. SAA4 has originally been termed a "constitutively" expressed SAA protein, apparently due to its nature not to act as an inflammatory marker. The present overview aimed to cover possible functions-so far identified-for human SAA4 (following its expression in various diseases on mRNA and protein level) and to work out whether SAA4 might be considered-at least in part-an acute-phase protein. Alternatively, we are raising the question whether SAA4 may solely act as a bystander or even underdog within the whole SAA family, where SAA1 and SAA2 proteins (commonly termed acute-phase SAA) hold undoubtedly an eminent status during inflammatory conditions, not only as host defense reactants but also as long-lasting markers for chronic diseases and malignancies in humans. - Source: PubMed
Publication date: 2026/04/28
Malle ErnstMadreiter-Sokolowski CorinaWindpassinger Christian