Ask about this productRelated genes to: CBLN1 antibody
- Gene:
- CBLN1 NIH gene
- Name:
- cerebellin 1 precursor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-06
- Date modifiied:
- 2015-09-11
Related products to: CBLN1 antibody
Related articles to: CBLN1 antibody
- The cerebellin (CBLN) family includes CBLN1, CBLN2, CBLN3, and CBLN4, which are important secreted glycoproteins that play roles in synaptogenesis and the maintenance and plasticity of synapses across various regions of the central nervous system (CNS). Generally known for their implications in cerebellar parallel fiber-Purkinje cell synapses, CBLNs also play a comprehensive role in synaptic regulation in the CNS. By forming trans-synaptic complexes with postsynaptic glutamate delta receptors (GluDs) and presynaptic neurexins (NRXNs), CBLNs significantly impact the synaptic specificity and potency. Each CBLN protein has its own expression signature and function. Current research points to a key role for CBLN1 in forming excitatory synapses, especially in the cerebellum, while CBLN2 is reported to regulate inhibitory synaptic transmission and serotonergic circuits. In addition, CBLN3 regulates synaptic stability and is associated with many neurodevelopmental problems. Apart from its role in the regulation of inhibitory synapse formation, CBLN4 is also linked to many neurodegenerative disorders. Dysfunction of pathways associated with CBLN signaling has been linked to several neuropsychiatric and neurological disorders, such as ataxia and schizophrenia. This review article compares existing data on the structure, expression, and functional properties of CBLN proteins, their roles in synapse organization, and their potential as therapeutic targets for neurological disease. - Source: PubMed
Zhao PanfengYang JianYang JieDu Jinfeng - The neurotoxicity of emerging contaminants, polyhalogenated carbazoles (PHCZs), is elusive. In this study, we investigated the potential toxicity of 13 prevalent PHCZs utilizing a network toxicology approach, which revealed shared molecular targets associated with Parkinson's disease (PD). Molecular docking simulations assessed the binding affinities of these PHCZs for eight key PD-related targets, identifying monoamine oxidase B (MAOB) as a critical target. Among the dihalogenated PHCZs, 2,7-dibromocarbazole (2,7-BCZ) exhibited the highest binding affinity to MAOB. Comparative molecular docking and dynamics simulations suggest that the inhibition of MAOB activity by 2,7-BCZ is a potential initiating event in PHCZ-induced neurological disorders. experiments confirmed that 2,7-BCZ exposure highly correlates with α-synuclein aggregation, a hallmark of PD pathology. Transcriptomic sequencing of 2,7-BCZ-exposed SH-SY5Y cells, combined with analysis of public PD microarray data, identified shared transcriptional alterations in genes including , , , , and . By integrating pathways from PD-related targets of PHCZs, differentially expressed genes in 2,7-BCZ-exposed cells, and public PD data sets, we further elucidated key biological pathways through which 2,7-BCZ may contribute to PD pathogenesis, particularly dopaminergic synapse function and neurodevelopmental regulation. Collectively, this study not only highlights the potential role of PHCZs in PD, elucidating the potential biological mechanisms by which PHCZs may exacerbate PD, but also exemplifies an innovative, animal-sparing approach using New Approach Methodologies (NAMs) to assess environmental pollutants' risks in neurodegenerative adverse outcomes. - Source: PubMed
Publication date: 2026/02/23
Lu XinheLuo YuhangPeng PeiXing XingyueXia WeiYin HongyanLi HanzengXu Shunqing - Central amygdala (CeA) is a component of the spino-parabrachio-amygdala nociceptive pathway. Neuroplasticity in this pathway, such as increased cellular excitability and excitatory neurotransmission, play a key role in the development and persistence of chronic pain. However, the underlying mechanisms of neuroplastic changes in the CeA remain poorly understood. We recently demonstrated that GRID1/GluD1 (glutamate ionotropic receptor delta type subunit 1) and its binding partner CBLN1 (cerebellin 1 precursor) are downregulated in models of inflammatory and neuropathic pain. Furthermore, we have shown that GRID1-CBLN1 signaling regulates autophagy in multiple brain regions. Here, we tested the causal relationship between GRID1-CBLN1 downregulation, macroautophagy impairment, and subsequent hyperalgesia, using models of inflammatory and neuropathic pain. During pain, the downregulation of GRID1 and CBLN1 was accompanied by neuroplastic changes, as evidenced by an increase in excitatory neurotransmission and AMPA receptor (AMPAR) expression. In addition, significant downregulation of BECN1 and upregulation of SQSTM1 and MAP1LC3B, demonstrating impaired autophagic flux, were observed in the pain state. These changes appear to be cell type-specific, as observed by the higher localization of BECN1 and LAMP1, a marker for autolysosomes, to PRKCD neurons, in which GRID1 is preferentially expressed. Using a GRID1 C-terminal-derived peptide (Tat-HRSPN), we demonstrate that GRID1 directly facilitates autophagy and subsequently reduces AMPAR expression in normal animals. This effect may be attributable to the direct interaction of GRID1 with mediators of autophagy, such as neuronal (n)GOPC/nPIST, BECN1 and LAMP1. Together, these results identified a novel GRID1/GluD1-dependent trans-synaptic autophagy mechanism, the deficit of which drives chronic pain.: aCSF: artificial cerebro spinal fluid; AMPARs: α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors; ATG: autophagy related; BAPTA: 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; BECN1: beclin 1; CBLN1: cerebellin 1 precursor; CeA: central amygdala; CFA: complete Freund's adjuvant; CRH/CRF: corticotropin releasing hormone; CTD: carboxy-terminal domain; DHPG: dihydroxy phenyl glycine; GOPC/PIST: golgi associated PDZ and coiled-coil motif containing; GRID1/GluD1: glutamate ionotropic receptor delta type subunit 1; GRIN/NMDAR: glutamate ionotropic receptor NMDA type; iGluRs: ionotropic glutamate receptors; KO: knockout; LA/BLA; lateral amygdala/baso-lateral amygdala; LAMP1: lysosomal associated membrane protein 1; LTD: long-term depression; MAP1LC3: microtubule associated protein 1 light chain 3; mEPSCs: miniature excitatory post-synaptic currents; GRM: glutamate metabotropic receptor; MTOR: mechanistic target of rapamycin kinase; nGOPC/nPIST: neuronal GOPC/PIST; NRXN1a: neurexin 1 alpha; PB: parabrachial nucleus; PBS: phosphate-buffered saline; PB-CeLC: parabrachio-central laterocapsular amygdala; PI3K: phosphoinositide 3-kinase; PRKCD+: protein kinase C delta positive; rCBLN1: recombinant CBLN1; SDS-PAGE: sodium dodecyl sulfate-polyacrylamide gel electrophoresis; SQSTM1: sequestosome 1; SNL: spinal nerve ligation; SST+: somatostatin positive; TBD11: Tat-beclin 1 D11; TBST: Tris-buffered saline with Tween 20; WT: wild type. - Source: PubMed
Publication date: 2025/10/28
S Narasimhan Kishore KumarChettiar Poojashree BKiritoshi TakakiJi GuangchenNeugebauer VolkerDravid Shashank M - Postherpetic neuralgia (PHN) is a chronic, treatment-resistant pain condition following herpes zoster. Neuroinflammation plays a key role in its pathogenesis but the mechanisms are unclear. Cerebellin-1 (CBLN1), a synaptic protein of the C1q/TNF family, may modulate pain via interaction with GluD1. However, its role in PHN progression is also unclear. Herein, we investigated the role of CBLN1 in resiniferatoxin (RTX)-induced PHN in mice and uncover the mechanism. We found that CBLN1 was downregulated in the spinal dorsal horn of PHN model mice. Recombinant CBLN1 administration alleviated RTX-induced mechanical and thermal hypersensitivity, reduced proinflammatory cytokine levels, and decreased neuronal apoptosis. It also increased GluD1 expression. These effects were abolished by GluD1 inhibition, suggesting that CBLN1 exerts its protective role via the GluD1 pathway. Therefore, CBLN1 inhibits the inflammatory response by targeting GluD1 thereby alleviating RTX-induced postherpetic neuralgia in mice. - Source: PubMed
Cui LongjiJia Xu - Somatic symptom and related disorders (SSRD) are characterized by a mixture of neurological and psychiatric features and include functional neurological (FND) and somatic symptom disorders (SomD). While these complex neuropsychiatric disorders show evidence of genetic susceptibility, there are no genome-wide association studies (GWAS) of SSRD, and the heritability is unknown. We did a GWAS of a total of 22,203 patients with SSRD, and 1,831,107 controls of European ancestry. We identified one genome-wide significant locus (chromosome 8:65565084) in SSRD, and one additional locus (chromosome 16:49074278) in the SomD subgroup (n cases = 18,536). The observed-scale SNP heritability was estimated to be 7.3 % for SSRD, 15.7 % for FND and 7.7 % for SomD. FND and SomD were strongly genetically correlated (rg=0.94, SE=0.11, p=3.9E-18). SSRD showed significant genetic correlation with psychiatric disorders (highest with anxiety, post-traumatic stress disorders, depression, rg=0.3-0.8), neurological disorders (migraine, chronic pain, rg=0.4-0.6) and immune-related diseases (rg=0.2-0.3). Functional follow-up analysis of SSRD loci implicated the genes , and , which are involved in metabolic and brain-related processes, suggesting common underlying pathways. We identified genomic loci associations with SSRD and showed strong genetic correlation between FND and SomD and with neurological and psychiatric disorders, as well as immune-related diseases. The current findings highlight shared underlying pathophysiological processes between SSRD diagnostic categories. - Source: PubMed
Publication date: 2025/07/17
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