Sulf1 (mouse)
- Known as:
- Sulf1 (mouse)
- Catalog number:
- Y213682
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Sulf1 (mouse)
Related genes to: Sulf1 (mouse)
- Gene:
- SULF1 NIH gene
- Name:
- sulfatase 1
- Previous symbol:
- -
- Synonyms:
- KIAA1077, SULF-1, hSulf-1
- Chromosome:
- 8q13.2-q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-26
- Date modifiied:
- 2018-02-13
Related products to: Sulf1 (mouse)
Related articles to: Sulf1 (mouse)
- Microvessels within atherosclerotic plaques are crucially involved in disease progression. Here, we generated a transcriptomic atlas of human atherosclerosis at single-cell resolution, encompassing 17,367 vascular endothelial cells (VECs) from five scRNA-seq studies, and verified key morphological characteristics using histology. SULF1 arterial endothelial cells (ArtECs) represented the primary subcluster undergoing endothelial-to-mesenchymal transition (EndMT). Capillary-like endothelial cells (CapECs) were identified as primary mediators of angiogenesis, and a trajectory model illustrated the transition between tip and stalk cells, with subclusters of ArtECs and CapECs predominantly expressing CXCL12, thereby driving the CXCL12/CXCR4 signaling axis. The largest plaque EC cluster, exhibiting the most heterogeneity, was found among post-capillary venule endothelial cells (VenECs), particularly ACKR1NR2F2 VenECs, which displayed distinct inflammatory transcriptional signatures characterized by adhesion molecules and chemokines. Overall, this atlas of atherosclerosis underscores endothelial heterogeneity and identifies SULF1 ArtECs and VenECs as potential therapeutic targets for EndMT and leukocyte recruitment, respectively. - Source: PubMed
Publication date: 2026/04/17
Wu YanzhaoXue ZhiweiSun TaoYu YindaLiang XiangjunXing WenchenMu FeiyuZhang ZhihanLv MeilinLing LuHan MengtaoCheng LianGisterå AntonWang Donghai - Gastric cancer (GC) progression is linked to immune escape in the tumor microenvironment, yet the molecules regulating tumor-associated macrophage polarization and CD8 T-cell exhaustion are unclear. This study analyzed TCGA data to examine SULF1 expression and its prognostic role. It used CRISPR/Cas9 and lentiviral methods in GC cells to test proliferation, invasion, and apoptosis, plus co-culture and flow cytometry to assess SULF1's impact on macrophages and CD8 T-cells. STAT3 signaling was studied via immunoblotting and nuclear translocation assays, and a mouse model tested SULF1's therapeutic relevance. Results showed SULF1 was up-regulated in GC, tied to advanced stages and poor survival. SULF1 knockdown inhibited the malignant phenotypes of gastric cancer cells, including proliferation, migration, and invasion abilities, while promoting cell apoptosis; conversely, SULF1 overexpression enhanced these pro-tumor phenotypes. SULF1 activated macrophage STAT3, promoting M2 polarization and CD8 T-cell dysfunction. In mice, SULF1 silencing reduced tumors and T-cell exhaustion, while supplementation reversed this. Conclusions: GC-secreted SULF1 creates an immunosuppressive microenvironment via STAT3-dependent pathways, and targeting SULF1-STAT3 may improve GC immunity. - Source: PubMed
Publication date: 2026/04/15
Lu XiaodanLu Di - Coronary endothelial dysfunction is considered one of the key pathological components in acute myocardial infarction (AMI). This study aimed to explore the expression patterns and potential significance of the differentially expressed genes SULF1 and EPB41L3 in AMI by integrating bioinformatics analysis and clinical validation. - Source: PubMed
Publication date: 2026/03/25
Zhu HouyongXu XiaoqunZhu XinyuHuang JinyuCai LongGao BeibeiYang ChaoWang ShiwangChen QilanFang XiaojiangZheng JianwuBao ChengChen Tielong - Convergence and extension (C&E) cell movements that elongate the primary embryonic axis are precisely timed during vertebrate gastrulation, but mechanisms controlling their onset remain unknown. Using zebrafish embryonic explants that recapitulate C&E and its timing, we identified sulfatase modifying factor 2 (sumf2) as a candidate trigger gene for C&E onset. sumf2 and its paralog sumf1 encode negative and positive sulfatase regulators, respectively, whose expression levels invert and increase heparan sulfate sulfation during gastrulation. Overexpressing sumf1 or sumf2 causes delayed or precocious C&E, respectively, whereas their loss shifts C&E timing in the opposite direction. We identified Sulf1, a modifier of heparan sulfate proteoglycans (HSPGs), as their key downstream effector and found that altering heparan sulfate sulfation levels shifts C&E onset and suppresses sumf1 and sumf2 mutant phenotypes. This work supports a model in which sumf2 expression reduces sulfatase activity, rewriting HSPG sulfation patterns to promote the onset of C&E morphogenesis. - Source: PubMed
Publication date: 2026/03/31
Cervino Ailen SoledadBasu AmritaWeiss Ryan JKaur Bajwa GursimranMarín-Juez RubénGrimm Sandra LCoarfa CristianWilliams Margot Kossmann - This research aimed to explore key glycosylation-related genes (signature genes) and associated molecular mechanism on chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), which further providing new perspectives for disease prognosis and diagnose. - Source: PubMed
Publication date: 2026/01/22
Yin Xiao LingZhai YingWang Lei