Ask about this productRelated genes to: C1ql1 antibody
- Gene:
- C1QL1 NIH gene
- Name:
- complement C1q like 1
- Previous symbol:
- -
- Synonyms:
- CRF, C1QRF, C1QTNF14, CTRP14
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-06
- Date modifiied:
- 2018-07-16
Related products to: C1ql1 antibody
Related articles to: C1ql1 antibody
- Glioblastoma (GBM) cells form neuron-to-glioma malignant synapses on neurite-like tumor microtubes (TMs), driving infiltrative growth and recurrence. The mechanisms underlying coordinated crosstalk among GBM cells and with neurons to favor malignant over normal synapses remain largely unknown. Here, we demonstrate that glioma-secreted C1QL1 is a key messenger for glioma-neuron and glioma-glioma crosstalk to drive TM expansion and malignant synapse formation. C1QL1 binds to its receptor BAI3 on neighboring neurons and GBM cells, activating Rac1-mediated cytoskeleton rearrangement to prune normal synapses and outgrow TMs, promoting malignant synapse and glioma network formation. Targeted treatment with a non-GEF-targeting, first-in-class Rac1 inhibitor rescues C1QL1-mediated synaptic pruning, inhibiting TMs and malignant synapses to impede glioma recurrence. Our findings elucidate how crosstalk among GBM cells and neurons allows infiltrating GBM cells to sculpt and integrate into the existing neural network, highlighting a therapeutic strategy against GBM recurrence through simultaneous inhibition of TMs and glioma-induced synaptic pruning. - Source: PubMed
Publication date: 2026/02/27
Ding ChaoqiongDong JiayiPan ZhenzhongLiu ShijieSong QiuyueYang GaoxiaPeng YulingXie ChuanxingHuang ZongyaoYao WeiWu MengnanZhong YiZhang WeiZhang YanWang SonghuaMa WeiweiWang Yuan - Cell adhesion molecules (CAMs) are pivotal in establishing and maintaining synaptic connectivity. Emerging evidence indicates that some secreted factors within the synaptic cleft, including C1q-like proteins (C1qls), play a crucial role in bridging pre- and post-synapses by connecting the bilateral CAMs. However, the mechanisms of those secreted factors in synapse assembly remain incomplete. Here, we explore C1ql-mediated synaptic connectivity, focusing on the assembly of C1ql1 and its postsynaptic receptor brain-specific angiogenesis inhibitor 3 (BAI3, also called ADGRB3). Our biochemical, structural, and computational analyses reveal that the trimeric globular C1q (gC1q) domain of C1ql1 undergoes a calcium-modulated domain-swapping event to form a hexamer. Cryo-EM study manifests the stabilizing role of calcium ions on the C1ql1_gC1q hexamer in complex with the extended CUB domain of BAI3. Using the gC1q hexamer, full-length C1ql1 further assembles into linear clusters, possibly providing a scaffold to accumulate BAI3 receptors on the plasma membrane. Our cellular and in vivo studies support a role for the gC1q-mediated dynamic assembly of C1ql1 in receptor accumulation and synapse maintenance. Collectively, our findings provide a plausible mechanism of secreted factor-mediated synaptic connectivity, driven by the calcium-modulated assembly of C1qls and their interactions with CAMs. - Source: PubMed
Publication date: 2025/12/10
Liao LiangyuHan YingNiu FengfengWang YingjieLu YangXu ShunZhu HoumingLin LeishuXiao JinmanTou Hoi InGao JialiZhang BoWei Zhiyi - [This corrects the article DOI: 10.1371/journal.pone.0251412.]. - Source: PubMed
Publication date: 2025/09/29
Biswas JoyshreePijewski Robert SMakol RohitMiramontes Tania GThompson Brianna LKresic Lyndsay CBurghard Alice LOliver Douglas LMartinelli David C - Our earlier research discovered that C1QL1 was expressed less in breast cancer (BrCa) tissues than in normal breast tissues by analyzing the gene profile of RNA sequences. However, up to now, the biological function of C1QL1 and its molecular mechanism in BrCa remains unknown. Here public database analyses, quantitative PCR with reverse transcription, western blot, immunohistochemistry and quantitative methylation-specific PCR were used to analyze C1QL1 expression and promoter methylation. The effects of C1QL1 on BrCa proliferation, cell cycle, apoptosis and metastasis were assessed using the Cell Counting Kit-8, flow cytometry analysis, terminal deoxynucleotidyl transferase dUTP nick end labeling assays, transwell in vitro and nude mice experiments in vivo. Liquid chromatography-tandem mass spectrometry, co-immunoprecipitation and western blot were performed to identify factors that mediate the effects of C1QL1. In BrCa, C1QL1 is often silenced due to promoter methylation, and its expression is favorably connected with prognosis. Overexpression of C1QL1 inhibits BrCa cell proliferation, metastasis and promotes cancer cell apoptosis both in vitro and in vivo. Conversely, C1QL1 knockdown increases the proliferation and spread of BrCa cells. Mechanistically, C1QL1 is located at endoplasmic reticulum and interacts with HSP90α and VCP to facilitate their ubiquitin-mediated degradation. This leads to the caspase-dependent apoptosis that occurs in BrCa cells as a result of ER stress (ERS)/unfolded protein response (UPR). Our results support that C1QL1 can act as a tumor suppressor of BrCa by modulating the C1QL1/HSP90α/VCP-ERS/UPR pathway, implying that the promoter methylation status of C1QL1 or the expression of C1QL1 may represent a potential marker for the diagnosis or prognosis of BrCa. - Source: PubMed
Publication date: 2025/06/30
Zhang NingningShao QingXiang XinniYan ChunTao DanLi QianRong HuanZhao YiXiang TingxiuZeng Xiaohua - Cardiomyopathy often results in heart failure and mortality, significantly impairing patients' quality of life. Advancements in genomics and proteomics now enable the identification of proteins associated with cardiomyopathy, offering valuable insights for its diagnosis and treatment. However, numerous potential pathogenic proteins remain unidentified, underscoring the need for further exploration of novel drug targets for cardiomyopathy. This study aims to employ Mendelian randomization (MR) to explore genetic associations between plasma proteins and cardiomyopathies, with the objective of identifying potential drug targets. Two-sample MR was employed to investigate causal relationships between cardiomyopathies and plasma proteins, using summary data from genome-wide association studies of different cardiomyopathy subtypes, such as dilated cardiomyopathy, hypertrophic cardiomyopathy (HCM), and restrictive cardiomyopathy (RCM). Cis-protein quantitative trait loci retrieved from the deCODE database served as genetic instruments. Steiger filtering was applied to assess and validate reverse causality. Enrichment analysis was conducted to elucidate potential biological effects, while protein-protein interaction networks were examined to explore interactions among proteins. Molecular docking was employed to evaluate the binding affinity between drugs and their targets. The MR analysis identified 70 significant proteins linked to cardiomyopathy, 12 to dilated cardiomyopathy, 60 to HCM, and 103 to RCM. Intersection analysis revealed 24 significant proteins. Following multiple hypothesis testing, 2 significant proteins (CCL17, SERPINA4) were identified for HCM, and 16 significant proteins (APOL3, C1QL1, CNDP1, CRLF1, CSF2RB, CTSH, GABARAPL2, GP1BA, ICAM5, NPPB, NTM, PDCD5, PTPRS, RNASET2, RTN4R, TCN2) were identified for RCM. Reverse causality testing provided no evidence of reverse causality for any positive genes. Enrichment analysis of protein-protein interaction networks indicated a potential biological role for the positive proteins. Moreover, potential drug targets for treating cardiomyopathy were identified. The genetic associations between plasma proteins and cardiomyopathy were analyzed, leading to the identification of specific proteins as potential biomarkers. Additionally, novel drug targets were identified, providing valuable insights for the diagnosis and treatment of cardiomyopathy. - Source: PubMed
Ji YandiDai GuohuaFan MaoxiaChen ChenLiu RuixiaDong XueyanGao Wulin