Ask about this productRelated genes to: Clec1b antibody
- Gene:
- CLEC1B NIH gene
- Name:
- C-type lectin domain family 1 member B
- Previous symbol:
- -
- Synonyms:
- CLEC2
- Chromosome:
- 12p13.31-p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-09
- Date modifiied:
- 2018-02-13
Related products to: Clec1b antibody
Related articles to: Clec1b antibody
- The high global mortality of hepatocellular carcinoma (HCC) underscores the need for reliable non-invasive diagnostic biomarkers. In this study, transcriptomic analyses were performed on peripheral blood mononuclear cell (PBMC) and tumor datasets from HCC patients to identify differentially expressed genes (DEGs) using an adjusted p-value 〈 0.01 and |log2FC| 〉 1. Functional enrichment analyses revealed predominant immune-related pathways in PBMCs and metabolic pathway dysregulation in tumor tissues. Integration of PBMC and tumor profiles identified STEAP4, EPC1, CLEC1B, and LCN2 as shared DEGs. Survival analyses indicated that elevated expression of STEAP4, EPC1, and CLEC1B was associated with poorer overall survival in HCC patients. Collectively, these findings highlight consistent transcriptional alterations in PBMCs and tumor tissues and suggest that STEAP4, EPC1, and CLEC1B may serve as potential non-invasive biomarkers with diagnostic and prognostic relevance in HCC. - Source: PubMed
Publication date: 2026/02/26
Khojand SoheylaZahmatkesh NedaHassani ArezooDamerchiloo ZahraNikoo ZahraHeidarzadehpilehrood Roozbeh - To explore associations between circulating proteomic pathways and structural, functional, and symptomatic measures of small- and large-fiber neuropathy and corneal immune activation in people with Type 2 diabetes (T2D). - Source: PubMed
Publication date: 2026/03/18
Ponirakis GeorgiosAl-Janahi IbrahimElgassim EinasDalloul Rajaa S DPetropoulos Ioannis NGad HodaKhan AdnanZaghloul Hadeel BAli HamdaSiddique Mashhood AMohamed Fatima F SAhmed Lina H MDakroury YoussraEl Shewehy Abeer M MSaeid RubaMahjoub FadwaAl-Noubi Muna NSarwath HinaPaul PradiptaKaul RidhimaSalivon IuliiaZirie Mahmoud AAl-Ansari YousufAtkin Stephen LSchmidt FrankMalik Rayaz A - C-type lectin-like receptor 2 (CLEC2) is a transmembrane receptor highly expressed on platelets which regulates platelet aggregation and immune response. Yet, the function of CLEC2 in lung epithelium and its contribution to acute lung injury (ALI) is unclear. In this study, lung epithelial-specific CLEC2 knockout mouse (Clec1b AT2-KO) was generated and performed for ALI models. In both lipopolysaccharide (LPS)- and acid-induced lung injury models, the ALI signs of Clec1b AT2-KO mice were further exacerbated. The therapeutic application of epithelial-restricted CLEC2 overexpression using adeno-associated virus (AAV) or CLEC2 activation using its endogenous ligand podoplanin (PDPN) serves as a lung epithelial protective agent in the setting of ALI. Transcriptomic analyses reveal that CLEC2-regulated genes are highly enriched in chemotaxis, cytokine, and extracellular matrix (ECM) components. Lung injury was partially attenuated in Ccl5-/-, Csf3-/- and Cxcl1-/- mice pretreated with AAV-si-CLEC2, followed by LPS challenge. Loss of CLEC2 leads to ECM degradation, which could be reversed by exogenous transforming growth factor (TGF)-β. Furthermore, interferon regulatory factor 1 (IRF1) was identified as the key molecule that regulates CLEC2-related cytokine/chemokine production and ECM degradation. These findings suggest that epithelial CLEC2 protects against ALI by modulating spleen tyrosine kinase (Syk)/IRF1-mediated cytokine/chemokine production and TGF-β-mediated ECM remodeling. - Source: PubMed
Publication date: 2026/01/23
Jiang TianWu LinfengWang YingYang XuHuang RenhuiRen ChanghaoZhang QiHu YunfanZhang ShaoyuanYang XinyuYin JunWang LanTan Lijie - Neuro-related proteins are promising biomarkers and therapeutic targets for Parkinson's disease (PD), yet their specific roles remain uncertain. - Source: PubMed
Publication date: 2026/02/21
Zhou HangWang ZihaoTan ZixinDeng BinYang WanlinHuang ZifengGuo XingfangLi JintaoWang XinhaoYu YinghuaDeng ChaoZheng WenhuaZhang XuChen XiYue JianhuiYang ChengwuCui XiaoyingPoplawska-Domaszewicz KarolinaChaudhuri K RayZhou ZhidongXiao BinChan Ling-LingFoo Jia NeeTan Eng-KingWang Qing - Hepatocellular carcinoma (HCC), a prevalent liver malignancy, is closely associated with dysregulated lipid metabolism. Endocrine disrupting chemicals (EDCs) can bind to nuclear receptors (NRs) and potentially induce carcinogenesis, but their specific influence on HCC progression remains unclear. To investigate this relationship, we combined bioinformatic analyses with experimental validation in the present study. Differential expression analysis of public HCC datasets (GSE14323, GSE17548, and GSE25097) identified candidate genes, which were further refined via weighted gene co-expression network analysis (WGCNA) and machine learning algorithms (RF and SVM-RFE), pinpointing NPY1R and CLEC1B as key genes. Their downregulation in HCC was validated in an independent dataset (GSE54236) and in clinical liver tissues (n = 118). Molecular docking and dynamics simulations prioritized perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS) as high-affinity binders to the proteins encoded by these genes. In vitro, exposure to PFOA/PFOS dose-dependently suppressed NPY1R and CLEC1B expression in HepG2 cells. Chromatin immunoprecipitation assays revealed that PFOA/PFOS inhibit the binding of estrogen receptors (ERα and ERβ) to the promoters of these genes, leading to reduced transcription and increased lipid accumulation. Knockdown of ERα/ERβ exacerbated, while their overexpression rescued, the lipid-metabolic disruption induced by PFOA/PFOS. These findings indicate that EDCs such as PFOA and PFOS may promote HCC progression by disrupting lipid metabolism via interference with NR-dependent gene regulation, highlighting a novel environmental-toxicological axis in hepatocarcinogenesis. - Source: PubMed
Publication date: 2026/01/21
Xu ShujingQiao ShikaiZhang ShuoLiu ChunChen LiDai BinghuaYang ChangqingXia LuXiong GuangsuZhao LuyingLi Jing