APBB2
- Known as:
- APBB2
- Catalog number:
- 001742A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- APBB2
Related genes to: APBB2
- Gene:
- APBB2 NIH gene
- Name:
- amyloid beta precursor protein binding family B member 2
- Previous symbol:
- -
- Synonyms:
- FE65L, FE65L1, MGC35575
- Chromosome:
- 4p14-p13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-25
- Date modifiied:
- 2018-02-13
Related products to: APBB2
Related articles to: APBB2
- Skeletal muscle fiber composition plays a critical role in determining muscle growth and meat quality in livestock species. However, the molecular mechanisms underlying muscle fiber-type transformation in meat rabbits remain poorly understood. - Source: PubMed
Publication date: 2026/05/07
Jia ChengQianwen WuZhengwei JiZhongqiang YaoLing WangHongzhao LuWenxian Zeng - Fibrosis is a severe pathological outcome of many chronic diseases, yet the therapeutic potential of targeting the altered major histocompatibility complex (MHC) class I immunopeptidome remains largely unexplored. Here we characterized the MHC class I immunopeptidomes from both fibrotic foci of human idiopathic pulmonary fibrosis lung explants and bleomycin-treated mice, identifying a diverse repertoire of fibrosis-associated peptides. Parallel profiling of bleomycin-induced pulmonary fibrosis in mice enabled the computational prioritization of therapeutic targets. In vivo, therapeutic vaccination with three candidate peptides (MAF, APBB2 and TNS3) effectively mitigated fibrosis progression in bleomycin-treated mice. Furthermore, leveraging its evolutionary conservation, we found that MAF elicited specific human cytotoxic T lymphocytes that lysed human idiopathic pulmonary fibrosis-derived myofibroblasts and M2-like macrophages. This study indicates that immunopeptidome profiling provides a robust platform for discovering translatable antifibrotic immunotherapies. - Source: PubMed
Publication date: 2026/04/20
Bai ZiyiLan TianxiaHong WeiqiQue HaiyingZhu MinXiao XinWan DandanAi JiayuanHuang ShaoxiongWang JiayuHong QiaonanLiu YanyanXiao ChengxinZhao ChengjianWang XinZhang XiaolongYang TingXu HengDai LunzhiPowell Charles ARicheldi LucaLuo FengmingDong HaohaoYuan YongPu QiangWei Xiawei - Temporal lobe epilepsy (TLE) remains a major clinical challenge, with over one-third of patients resistant to existing medications. Microglia, the brain's resident immune cells, are highly plastic, yet their potential to adopt a protective state in epilepsy is unclear. Using time-resolved single-nucleus RNA sequencing (snRNA-seq) in a kainic acid (KA)-induced seizure model, we identified an early-emerging microglial subpopulation transcriptionally distinct from homeostatic microglia. This subpopulation was characterized by high expression of insulin-like growth factor 1 (Igf1), along with Myo1e and Apbb2. Through in vitro co-culture assays, we demonstrated that TGFB1 stimulation, but not LPS, drives the generation of this IGF1 phenotype. These induced IGF1 microglia significantly suppressed the secretion of pro-inflammatory cytokines under inflammatory conditions. Importantly, conditioned medium from IGF1 microglia enhanced the proliferation and survival of KA-exposed HT22 neuronal-like cells. Mechanistically, we found that TGFB1 activates the Wnt/β-catenin pathway, promoting the nuclear translocation of β-catenin, which in turn upregulates IGF1 expression. In vitro, we abolished the TGFB1-induced neuroprotective phenotype by knocking down β-catenin using siRNA; however, exogenous supplementation with IGF1 partially rescued this effect. Our findings define a TGFB1-β-catenin-IGF1 axis that drives microglia into a neuroprotective state, revealing a novel endogenous mechanism and therapeutic direction for epilepsy. - Source: PubMed
Publication date: 2026/03/29
Yuan ZiweiLiu YanDuan RanZhang XiaogangHu LiqinSong FeiLiu JingMeng YuanKe PingyangXiao Fei - Schizophrenia (SCZ) is a complex psychiatric disorder, and its pathogenic mechanisms are not yet fully understood. The identification of reliable blood biomarkers and molecular subtypes for early diagnosis and effective therapy remains a significant challenge. To address this issue, we utilized a combination of bioinformatics and machine learning (ML) to identify potential biomarkers for SCZ. Our approach involved the integration of 12 different ML algorithms to develop a diagnostic signature based on data from several datasets, including GSE18312, GSE27383, GSE38485, GSE54913, and GSE165604. A nomogram was constructed using these datasets for potential clinical applications. In addition, clustering analysis was performed on SCZ patients using consensus clustering and non-negative matrix factorization (NMF) algorithms. We further evaluated subtype differences in biological functions and immune cells through various methods, such as gene set enrichment analysis (GSEA), gene set variation analysis (GSVA), Proteomaps, and IOBR analyses. Our results identified a diagnostic signature composed of 16 genes (APBB2, CLCN1, SYDE1, PAX5, SNAI1, DAZL, UNC93B1, PLAGL2, HS3ST1, ITPKB, PILRA, BTLA, SWAP70, AZI2, ADM, and AVPR2), which demonstrated robust performance in diagnosing SCZ across eight different datasets. A nomogram based on these genes was created, providing clinical benefits for SCZ patients. Among the identified genes, AZI2 was found to be the most critical, influencing inflammation and immunity. We also identified potential chemical compounds that could target these 16 genes. Unsupervised clustering and NMF algorithms revealed two distinct subtypes of SCZ, each associated with unique immune cell profiles, biological functions, and protein expression levels. In conclusion, this study not only developed a diagnostic signature and a novel nomogram for SCZ but also provided new insights into the subtypes of SCZ. These findings may pave the way for personalized diagnosis and treatment strategies for SCZ patients. - Source: PubMed
Publication date: 2026/03/24
Li ZhijunSun QingLi HaoyuGuan NaiyuNi JingWang JingXu XiaoleiShen YeSun SiyuLi Yan - Prior studies identified subsets of patients with Takayasu arteritis (TAK) based on angiographic patterns of disease in cohorts from India and North America. This study aimed to validate these patterns in a TAK cohort from Turkey and determine the role of genetics in arterial patterns. - Source: PubMed
Publication date: 2025/11/08
Casares-Marfil DesiréGribbons K BatesSaruhan-Direskeneli GuherKaymaz-Tahra SemaQuinn Kaitlin AAlibaz-Oner FatmaGrayson Peter CDireskeneli HanerSawalha Amr HMerkel Peter A