Ask about this productRelated genes to: CLECL1 antibody
- Gene:
- CLECL1 NIH gene
- Name:
- C-type lectin like 1
- Previous symbol:
- -
- Synonyms:
- DCAL1
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2007-06-21
- Date modifiied:
- 2017-03-23
Related products to: CLECL1 antibody
Related articles to: CLECL1 antibody
- Tumor associated macrophages (TAMs) in Head and neck squamous cell carcinoma (HNSCC), particularly M2-polarized subtypes, are pivotal drivers of tumorigenesis, angiogenesis, and metastasis, contributing to adverse clinical outcomes. Current prognostic markers lack precision, underscoring the need for novel biomarkers and risk stratification models. Single-cell RNA sequencing (scRNA-seq) was applied to profile the transcriptional landscape of TAMs in HNSCC at single-cell resolution. 1,208 M2 TAMs were integrated from scRNA-seq data with bulk RNA sequencing to identify molecular signatures. Weighted correlation network analysis (WGCNA) and Uniform Manifold Approximation and Projection (UMAP) analysis were applied to dissect TAMs heterogeneity and interactions within the tumor microenvironment. experiments validated the efficacy of the prognostic signature model. In this study, high infiltration of M2 TAMs was strongly associated with advanced clinical stages, lymph node metastasis, and reduced overall survival (P<0.001). TCGA datasets were utilized for cross-platform verification. Multivariate Cox regression and survival analyses were performed to establish prognostic relevance. 11 prognostic signature genes (FCGBP, GIMAP5, WIPF1, RASGEF1B, GIMAP7, IGFLR1, GPR35, NCF1, CLECL1, HEXB, IL10) were identified through integrative analysis, which formed the basis of a robust risk stratification model. The distribution of biomarkers in the high-risk group, as determined by the signature we constructed, can serve as a better indicator for assessing poor prognosis. In clinical samples, prognosis signature has the potential to predict the prognosis effectively in patients with HNSCC.M2 TAMs-driven prognostic signature for HNSCC offers a clinically actionable tool for risk stratification and outcome prediction. - Source: PubMed
Publication date: 2025/08/12
Wang JialeLi HuanShi MingruiRen ChenghaoWei WuZhao QiHe XinxinYang ZihuiWei JianhuaYang Xinjie - Nicotinamide adenine dinucleotide (NAD) is well known as a coenzyme involved in many redox reactions in cellular energy metabolism, or as a substrate for many NAD-consuming enzymes, including those that generate the second messenger cyclic ADP-ribose or deacetylate proteins (e.g., histones). The role of NAD in non-catalytic proteins is poorly understood. IRBIT and L-IRBIT (the IRBITs) are two cytosolic proteins that are structurally related to dehydrogenases but lack catalytic activity. Instead, by interacting directly with their targets, the IRBITs modulate the function of numerous proteins with important roles, ranging from Ca signaling and intracellular pH (pH) regulation to DNA metabolism to autophagy. Among the targets of the IRBITs is the Na-HCO cotransporter NBCe1-B, which plays a central role in intracellular pH (pH) regulation and epithelial electrolyte transport. Here, we demonstrate that NAD modulates NBCe1-B activation by serving as a cofactor of IRBIT or L-IRBIT. Blocking NAD salvage pathway greatly decreases NBCe1-B activation by the IRBITs. Administration of the oxidized form NAD enhances, whereas the reduced form NADH decreases NBCe1-B activity. Our study represents the first example in which the redox state of NAD, via IRBIT or L-IRBIT, modulates the function of a membrane transport protein. Our findings reveal a new role of NAD and greatly expand our understanding of NAD biology. Because the NAD redox state fluctuates greatly with metabolic status, our work provides insight into how, via the IRBITs, energy metabolism could affect pH regulation and many other IRBIT-dependent processes. - Source: PubMed
Publication date: 2025/02/20
Gui TianxiangLiu YingFu MingfengWu HanSu PanFeng XuhuiZheng MengmengHuang ZixuanLuo XudongBoron Walter FChen Li-Ming - Targeted therapy and immunotherapy has brought new hope to patients with lung adenocarcinoma (LUAD) with their applications. However, the prognosis of LUAD patients is still unpromising. - Source: PubMed
Luo HaichaoChen RanWang ChangyingChen Qitian - Inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) are high-conductance channels that allow the regulated redistribution of Ca2+ from the endoplasmic reticulum (ER) to the cytosol and, at specialized membrane contact sites (MCSs), to other organelles. Only a subset of IP3Rs release Ca2+ to the cytosol in response to IP3. These 'licensed' IP3Rs are associated with Kras-induced actin-interacting protein (KRAP, also known as ITPRID2) beneath the plasma membrane. It is unclear whether KRAP regulates IP3Rs at MCSs. We show, using simultaneous measurements of Ca2+ concentration in the cytosol and mitochondrial matrix, that KRAP also licenses IP3Rs to release Ca2+ to mitochondria. Loss of KRAP abolishes cytosolic and mitochondrial Ca2+ signals evoked by stimulation of IP3Rs via endogenous receptors. KRAP is located at ER-mitochondrial membrane contact sites (ERMCSs) populated by IP3R clusters. Using a proximity ligation assay between IP3R and voltage-dependent anion channel 1 (VDAC1), we show that loss of KRAP reduces the number of ERMCSs. We conclude that KRAP regulates Ca2+ transfer from IP3Rs to mitochondria by both licensing IP3R activity and stabilizing ERMCSs. - Source: PubMed
Publication date: 2024/06/27
Atakpa-Adaji PeaceIvanova AdelinaKujawa KarolinaTaylor Colin W - Atherosclerosis (AS) is the pathologic basis of various cardiovascular and cerebrovascular events, with a high degree of heterogeneity among different arterial beds. However, mechanistic differences between arterial beds remain unexplored. The aim of this study was to explore key genes and potential mechanistic differences between AS in different arterial beds through bioinformatics analysis. Carotid atherosclerosis (CAS), femoral atherosclerosis (FAS), infrapopliteal atherosclerosis (IPAS), abdominal aortic atherosclerosis (AAS), and AS-specific differentially expressed genes (DEGs) were screened from the GSE100927 and GSE57691 datasets. Immune infiltration analysis was used to identify AS immune cell infiltration differences. Unsupervised cluster analysis of AS samples from different regions based on macrophage polarization gene expression profiles. Weighted gene co-expression network analysis (WGCNA) was performed to identify the most relevant module genes with AS. Hub genes were then screened by LASSO regression, SVM-REF, and single-gene differential analysis, and a nomogram was constructed to predict the risk of AS development. The results showed that differential expression analysis identified 5, 4, 121, and 62 CAS, FAS, IPAS, AAS-specific DEGs, and 42 AS-common DEGs, respectively. Immune infiltration analysis demonstrated that the degree of macrophage and mast cell enrichment differed significantly in different regions of AS. The CAS, FAS, IPAS, and AAS could be distinguished into two different biologically functional and stable molecular clusters based on macrophage polarization gene expression profiles, especially for cardiomyopathy and glycolipid metabolic processes. Hub genes for 6 AS (ADAP2, CSF3R, FABP5, ITGAX, MYOC, and SPP1), 4 IPAS (CLECL1, DIO2, F2RL2, and GUCY1A2), and 3 AAS (RPL21, RPL26, and RPL10A) were obtained based on module gene, gender stratification, machine learning algorithms, and single-gene difference analysis, respectively, and these genes were effective in differentiating between different regions of AS. This study demonstrates that there are similarities and heterogeneities in the pathogenesis of AS between different arterial beds. - Source: PubMed
Publication date: 2024/03/19
Wu XizePan XueZhou YiPan JiaxiangKang JianYu J J JiajiaCao YingyueQuan ChaoGong LihongLi Yue