Dataset Information

MS assay of proteins after CO-IP with GPNMB antibody in hippocampus area

ABSTRACT: Three mice were excised at day 7 after pilocarpine treatment to induce abundant GPNMB expression (Figures 1 and 2). Hippocampal proteins were extracted and pulled down by anti-GPNMB immunoprecipitation for mass-spectrometer assay.

ORGANISM(S): Mus Musculus

SUBMITTER: Rongqing Chen

PROVIDER: PXD066376 | iProX | Mon Jul 21 00:00:00 BST 2025

REPOSITORIES: iProX

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Publications

GPNMB and ATP6V1A interact to mediate microglia phagocytosis of multiple types of pathological particles.

Liu Mei M Zhu Jianping J Zheng Jiawei J Han Xuan X Jiang Lijuan L Tong Xiangzhen X Ke Yue Y Guo Zhipeng Z Huang Weiyuan W Cong Jin J Liu Meiqiu M Lin Su-Yan SY Zhu Shuang S Mei Li L Zhang Xingmei X Zhang Wangming W Xin Wen-Jun WJ Zhang Zhenhai Z Guo Yanwu Y Chen Rongqing R

Cell reports 20250223 3

Pronounced elevation of glycoprotein non-metastatic melanoma B (GPNMB) is a common phenomenon in a variety of brain diseases, but the expression patterns, functions, and molecular signaling of GPNMB have not been well studied. Here, we showed that pathological factors, including neuronal degeneration caused by seizures, caspase-3-induced neuronal apoptosis, neuronal debris, and β-amyloid, induced "on-demand" GPNMB expression in hippocampal microglia. Genetic ablation of GPNMB did not affect acut ...[more]

PMID: 39992792

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Project description:Short-term folate deficiency has been linked to cognitive defects. Given folate’s role in regulating nucleotide synthesis and DNA and histone methylation, these changes are often linked to altered gene expression. We hypothesize that chronic folate deficiency will induce memory deficits that can be linked to tissue-specific changes in gene expression. This study placed mice on folic acid deficient or replete diets, containing either no source of folate or AIN-93G normal folic acid intake, beginning post-weaning and persisting through the end of adult life at 18 months. Cognitive outcomes were assessed using the novel object test for memory. Changes in hippocampal gene expression were examined by RNA microarray analysis and confirmed by qPCR. qPCR was also use to compare a subset of significant hippocampal genes to potential changes in liver and heart expression. Ontological categories were determined using GeneCodis for genes whose expression significantly changed in the deficient condition. Significantly enriched motifs in the deficient genes were examined using the HOMER bioinformatics analysis tool to identify transcription factors associated with changing genes. Folic acid deficient mice showed significant memory impairment (P<0.05) compared to replete counterparts beginning at 5 mo and persisting through 17 mo. These deficits were associated with 363 significantly downregulated and 101 significantly upregulated genes (P<0.05, fold change > 2) in the deficient condition. Of the 16 genes whose differential hippocampal expression was confirmed by qPCR, none were also differentially regulated in the heart, and only one was differentially regulated in the liver (P<0.05). Significant ontological categories for differential genes included nucleotide regulation, ion channel activity, and MAPK signaling. Two enriched motifs were identified and determined to be associated with MafB and Zfp410 binding sites. These genes and enriched motifs may represent targets for treatment or investigation of memory-related diseases.

Dataset Information

MS assay of proteins after CO-IP with GPNMB antibody in hippocampus area

Publications

GPNMB and ATP6V1A interact to mediate microglia phagocytosis of multiple types of pathological particles.

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