Ask about this productRelated genes to: C2orf40 antibody
- Gene:
- ECRG4 NIH gene
- Name:
- ECRG4 augurin precursor
- Previous symbol:
- C2orf40
- Synonyms:
- augurin
- Chromosome:
- 2q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-31
- Date modifiied:
- 2019-04-18
Related products to: C2orf40 antibody
Related articles to: C2orf40 antibody
- Papillary thyroid carcinoma (PTC) is less aggressive when associated with lymphocytic thyroiditis (LT), even in the presence of oncogenic BRAF, including smaller tumours, less lymph node involvement, and reduced extrathyroidal extension (1). To investigate possible immune mechanisms underlying this association, we compared the tumour microenvironment of PTC-BRAF with and without LT using single-cell RNA sequencing (scRNA-seq). Single-cell libraries were generated from fresh and fixed tumour samples with post-dissociation viability >70% using the 10x Genomics Chromium platform and sequenced on an Illumina NovaSeq 6000. We analysed scRNA-seq data from 11 PTC-BRAF tumours, including four with LT (one publicly available sample) and seven without LT. Downstream analyses included quality control, batch correction, dimensionality reduction, and differential gene expression analysis. We found neutrophils were the predominant myeloid cell type in PTCs without LT. Thyrocytes without LT showed significant expression of the neutrophil recruitment chemokine ECRG4. In the absence of LT, neutrophils expressed oncogenic genes with poor clinical outcomes. In contrast, thyrocytes from tumours with LT showed increased expression of MHC-II antigen presentation, consistent with effective immune surveillance. Thyrocytes and macrophages in the presence of LT showed enrichment of interferon gamma response pathways. Our data suggests LT in thyroid cancer is associated with enhanced antigen presentation and fewer features of pro-tumorigenic innate immune activity. These results identify previously under recognized innate immune cell population and associated transcriptomic features which suggests new mechanisms to target immune treatments in PTC refractory to other therapies. - Source: PubMed
Publication date: 2026/08/12
Perampalam SumathyGild MattiAmoakowa Sey AdwoaTacon Lyndal JFadia MitaliKing CathalPapachristos AlexanderSywak MarkGill Anthony JBullock MartynClifton-Bligh Roderick J - Dendritic spine dysfunction may contribute to the etiology and symptom expression of neuropsychiatric disorders. The intimate relationship between spine morphology and function suggests that decoding disease-related abnormalities from spine morphology can aid in developing synapse-targeted interventions. Here, we describe a population analysis of dendritic spine nanostructure applied to the objective grouping of multiple mouse models of neuropsychiatric disorders. This method has identified two major groups of spine phenotypes linked to schizophrenia and autism spectrum disorder (ASD). An increase in spine subpopulation with small volumes characterized the spines of schizophrenia-associated mouse models, whereas a spine subset with large volumes increased in ASD models. Schizophrenia-associated mouse models showed higher similarity in spine morphology, driven by reduced size and growth of nascent spines. The expression of , a gene encoding small secretory peptides, was increased in schizophrenia-associated mouse models, and functional studies confirmed its critical involvement in impaired spine dynamics and shape. These results suggest that population-level spine analysis provides rich insights into heterogeneous spine pathology, facilitating the identification of new molecular targets related to core synaptic dysfunction. - Source: PubMed
Publication date: 2026/08/11
Kashiwagi YutaroLiu QingruiGo YasuhiroSaito RyoAiba AtsuNakazawa TakanobuOkabe Shigeo - BackgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) and the formation of neurofibrillary tangles. Although the amyloid cascade hypothesis underscores the centrality of Aβ accumulation, the precise initiators of this process remain unknown.ObjectiveIn this study, we investigate the potential role of Esophageal Cancer-Related Gene 4 (ECRG4) in AD. We hypothesized that ECRG4, which is associated with cognitive impairment and upregulated in AD, directly contributes to amyloid pathology.MethodsWe performed cell-based assays, co-immunoprecipitation, in vivo experiments using APP knock-in mouse, and immunohistochemistry of human hippocampal sections.ResultsECRG4(133-148) associated with the amyloid precursor protein (APP) intracellular domain (AICD), leading to increased APP/Aβ accumulation. Furthermore, intracerebral injection of synthetic ECRG4(133-148) into AD model mice significantly augmented APP/Aβ deposition. Notably, the co-localization of ECRG4(133-148)-containing peptides with AICD-containing peptides increased with AD severity in human hippocampal tissue.ConclusionsOur findings establish that the carboxy-terminal fragment of ECRG4 acts as a potential initiator of amyloid pathology in AD through its interaction with AICD. - Source: PubMed
Publication date: 2026/06/30
Chung Michael Lai KitTakeda ShujiRyu JunnanMurayama ShigeoKoshimizu UichiKondo Toru - Current treatments for Alzheimer's disease (AD) primarily focus on slowing disease progression, emphasizing the urgent need for a reliable diagnostic method for early-stage Alzheimer's (EAD). Our investigation, which is based on the finding that the secretory protein Esophageal Cancer Related Gene 4 (ECRG4) is elevated in the hippocampus of AD patients, led to the creation of a novel ELISA system for ECRG4 detection. We observed that ECRG4 peptides, particularly the fragment spanning amino acids 108-132, were elevated in the plasma of approximately 25% of patients with mild cognitive impairment (MCI) and 50% of those with AD, compared to individuals without dementia. RNA sequencing of plasma samples revealed decreased levels of carbohydrate sulfotransferase 3 () mRNA, which is mainly expressed in oligodendrocyte (OLG)-lineage cells, in ECRG4-positive patients. Functional analyses demonstrated that the ECRG4 (71-107) peptide induced cytotoxicity in oligodendrocytes in vitro and reduced the expression of the OLG marker galactocerebroside in the corpus callosum following intracerebral injection. Additionally, peptide injection resulted in extravascular IgG leakage and the accumulation of OLG precursor cells (OPCs), which are crucial for myelin regeneration, around the blood vessels. These phenomena were similarly observed in the hippocampi of patients with EAD. Collectively, these findings establish ECRG4 as a novel serum marker for AD and suggest its association with ECRG4-dependent OLG dysfunction. - Source: PubMed
Publication date: 2026/05/15
Zhang LifuIkeda NaokiTakeda ShujiOikawa NaotoMurayama ShigeoKoshimizu UichiYabe IchiroKondo Toru - Esophageal cancer-related gene-4 (ECRG4) is a hormone-like protein that acts as a tumor suppressor by inducing cell death through apoptosis and cell-cycle arrest. ECRG4 is expressed in various organs, including the brain, and it influences the viability and function of neural cells such as oligodendrocytes and microglia. However, the effects of ECRG4 on astrocytes, which are essential neural cells that play significant roles in maintaining brain homeostasis, remain unclear. In this study, we demonstrate that ECRG4, specifically the region encompassing amino acids 71-107 (ECRG4(71-107)), induces cell death in mouse primary astrocytes. The ECRG4(71-107)-induced astrocyte death is associated with lysosomal damage and is mediated by cathepsins, indicating a lysosome-dependent cell death mechanism. Notably, ECRG4(71-107) promotes the secretion of cathepsins into the extracellular space. The introduction of exogenous cathepsins into the medium induced astrocyte death, while the removal of cathepsins from the conditioned medium reduced the toxicity associated with ECRG4(71-107). These findings suggest that extracellular cathepsins mediate the toxicity of ECRG4(71-107) in astrocytes. Overall, this study reveals a novel mechanism of cell death induced by ECRG4 in astrocytes and suggests a potential involvement of ECRG4 in pathophysiological functions of the brain. - Source: PubMed
Publication date: 2026/04/23
Oikawa NaotoZhang LifuKondo Toru