C1qL1 ELISA kit
- Known as:
- C1qL1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-C1qL1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- C1qL1 ELISA kit
Related genes to: C1qL1 ELISA kit
- 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
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- Glioblastoma (GBM) exhibits pronounced intratumoral heterogeneity, yet the interactions between macrophages and astrocyte-like (AC-like) cells remain incompletely understood. - Source: PubMed
Publication date: 2026/06/06
Gao MenggeLiu QiongYang BoLiu Xiaofang - Glioblastoma (GBM) cells secrete C1QL1, which binds BAI3 on nearby neurons and tumor cells to activate RAC1, promoting tumor microtube growth, malignant synapse formation, and remodeling of normal synapses. Blocking RAC1 with a targeted inhibitor disrupts this process and may help prevent GBM recurrence. See related article by Ding et al., p. 1176. - Source: PubMed
Li YujiaBorniger Jeremy C - Glioblastoma (GBM) cells form neuron-to-glioma malignant synapses on neurite-like tumor microtubes (TM), driving infiltrative growth and recurrence. The mechanisms underlying coordinated cross-talk 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 cross-talk 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 cross-talk 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
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