SAAL1 (Center) antibody Host rabbit
- Known as:
- SAAL1 (Center) (anti-) Host host: rabbit
- Catalog number:
- 'ARP52597_P050
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- ACR
- Gene target:
- SAAL1 (Center) antibody Host rabbit
Related genes to: SAAL1 (Center) antibody Host rabbit
- Gene:
- SAAL1 NIH gene
- Name:
- serum amyloid A like 1
- Previous symbol:
- -
- Synonyms:
- FLJ41463
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-28
- Date modifiied:
- 2015-11-20
Related products to: SAAL1 (Center) antibody Host rabbit
Related articles to: SAAL1 (Center) antibody Host rabbit
- Small extracellular vesicles (sEVs)-derived circular RNA (circRNA) serves as a crucial biomarker for diagnosing gastric cancer and as a key regulator of tumor progression, orchestrating intercellular crosstalk within the tumor microenvironment (TME). In gastric cancer (GC), tissue-derived mesenchymal stem cells (GC-MSCs) critically drive tumor progression; however, the interplay between sEVs and circRNA in GC-MSCs remains incompletely understood. We identified sEVs-hsa_circ_0006718 (circ6718) as significantly upregulated in gastric cancer patients. Elevated levels of sEVs-circ6718 correlated with clinical stage, distant metastasis and poor prognosis, confirming its utility as both an early diagnostic and prognostic biomarker in GC. Mechanistically, circ6718 functions as a competing endogenous RNA (ceRNA) by sequestering hsa-miR-561-3p, thereby derepressing the expression of SAAL1 (Serum amyloid A-like 1). SAAL1 enhances the transcriptional activity of PRRX1 (Paired related homeobox 1), which directly activates the TGFβ1 promoter. Consequently, the TGFβ1/Smad2/3 signaling pathway drives the transdifferentiation of GC-MSCs into cancer-associated fibroblasts (CAFs)-promoting stromal remodeling and tumor aggressiveness. Our findings unveil a novel sEVs-circRNA-mediated axis in GC progression, revealing dual utility in diagnostics and targeted therapy. - Source: PubMed
Publication date: 2026/05/11
Zhang FanZang XueyanWang DongliLi RongQian HuiXu WenrongJiang JiajiaYan Yongmin - Metabolic reprogramming, particularly toward oxidative phosphorylation (OXPHOS), is a hallmark of lung squamous cell carcinoma (LUSC) and contributes to its aggressive phenotype and immunosuppressive microenvironment. While OXPHOS activation is increasingly recognized as a key metabolic feature in LUSC, its prognostic implications and associated gene signatures remain underexplored. This study aimed to identify OXPHOS-related differentially expressed genes (DEGs) and construct a robust prognostic signature for LUSC. - Source: PubMed
Publication date: 2025/12/04
Dai NinghuangFang ChenGu YuWang BinFeng WeiPan KaifangJiang WeiLi GuangbinMa Haitao - Palbociclib, a dual CDK4/6 kinase inhibitor used for breast cancer, has been explored as a treatment option for rheumatoid arthritis (RA). Preclinical studies have reported palbociclib-induced myelosuppression, but no such effects have been observed in or single-deficient mice. Synoviocyte proliferation-associated in collagen-induced arthritis 1/serum amyloid A-like 1 (SPACIA1/SAAL1) is involved in G1 phase progression. Given that SPACIA1/SAAL1 upregulates (but not ) expression, we aimed to determine whether suppressing CDK6 expression alone could prevent synovial hyperplasia without myelosuppression. The effects of CDK6 expression on TNF-α-induced rheumatoid arthritis synovial fibroblast (RASF) proliferation and synovial hyperplasia in collagen-induced arthritis (CIA) mice were investigated by modulating the transcriptional level with a expression inhibitor (indole-3-carbinol), small interfering RNA (siRNA), and -deficient mice. Indole-3-carbinol or siRNA inhibited TNF-α-induced RASF proliferation without suppressing CDK4 expression and reduced retinoblastoma protein phosphorylation. In CIA mice, indole-3-carbinol did not cause myelosuppression, considerably delayed CIA onset and progression, and reduced arthritis severity. -deficient mice showed similar improvements in CIA pathogenesis but had lower serum anti-type II collagen IgG levels. Notably, synovial hyperplasia was not observed in -deficient mice. CIA-synovial hyperplasia depends on CDK6, but not CDK4, expression. - Source: PubMed
Publication date: 2025/01/28
Komatsu RieFujii RyojiOgasawara ToruSuzuki-Takahashi YukiChen SandySugishita YodoNiki HisateruYudoh Kazuo - Lung adenocarcinoma (LUAD) carries a poor prognosis at advanced stages underscoring the need to elucidate the underlying molecular mechanisms driving its pathogenesis. This study aimed to investigate the roles of eukaryotic translation initiation factor 3 subunit M () and its associated effector, serum amyloid A-like 1 (), in LUAD development and progression. Bioinformatic analyses such as TNMplot, The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and other public databases were used to evaluate and expression levels, methylation status, clinical associations, and potential transcriptional regulators across LUAD datasets. Patient samples were analyzed for / expression by qRT-PCR, immunohistochemistry, and ELISA. and were overexpressed in LUAD tumor tissues compared with normal lung tissues, correlated with advanced stage, nodal metastasis, and poor survival outcomes. High / levels associated with increased cell proliferation, epithelial-mesenchymal transition, metastasis, and regulatory T cell dysfunction based on gene set enrichment analysis (GSEA). Mechanistically, / upregulation was linked to promoter hypomethylation, and transcriptionally regulated by JMJD1C, via hTFtarget prediction. The / promote oncogenic cellular programs and immunosuppressive microenvironments that conferred unfavorable prognosis. These findings nominate EIF3M/SAAL1 as potential therapeutic targets and biomarkers in LUAD. - Source: PubMed
Publication date: 2024/10/15
Chiang Hung-HsingWu Kuan-LiTsai Hung-PeiOng Chai-TungChang Chao-YuanWu Yu-YuanShen Tzu-YenHung Jen-YuLee Hsiao-ChenHsu Ya-LingTsai Ying-Ming - Inhibition of Serum Amyloid A-like 1 (SAAL1) expression could inhibit cancer progression and improve the prognosis of cancer patients. At present, the correlation between SAAL1 and lung adenocarcinoma (LAC) remains unclear. Therefore, this study surveyed the worth and pathway of SAAL1 in LAC progression and immunity. - Source: PubMed
Publication date: 2023/03/27
Tong SongJiang NiWan Jun-HaoChen Chong-RuiWang Si-HuaWu Chuang-YanGuo QiangXiao Xiao-YueHuang HuanZhou Ting