ACP2
- Known as:
- ACP2
- Catalog number:
- 001031A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACP2
Related genes to: ACP2
- Gene:
- ACP2 NIH gene
- Name:
- acid phosphatase 2, lysosomal
- Previous symbol:
- -
- Synonyms:
- LAP
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-08-21
Related products to: ACP2
Related articles to: ACP2
- Nannochloropsis microalgae are widely recognized as sustainable cell factories for producing nutritional oils and biofuels due to their high-lipid content. However, a comprehensive understanding of the genetic basis of their oleaginous traits across diverse species has been limited. Here, we constructed a pan-genome of 17 Nannochloropsis species comprising 14,851 gene families. Our analysis defined a distinct genetic architecture for lipid metabolism: Gene families associated with vesicular transport formed a conserved core functional module, whereas the genetic collection for lipid metabolism showed greater plasticity and was primarily classified as part of the soft-core genome. This finding establishes a genetic blueprint for the coevolution between a stable cellular "logistics network" and an adaptable "biosynthetic factory." Evolutionary analysis further indicated that the DGAT and fatty acid desaturase families have species-specific expansions in Nannochloropsis, suggesting a potential role in enhancing lipid accumulation. By integrating 231 transcriptome datasets, we identified key genes (ACP2 and DGAT2) that were highly upregulated under nitrogen deprivation and pinpointed a set of core genes with high expression levels involved in vesicular transport. This "Infrastructure-Toolkit" model provides both genetic targets for strain improvement and a broader framework for understanding lipid accumulation in oleaginous microorganisms. - Source: PubMed
Publication date: 2026/08/19
Zhang PengjuanMiao LijunWang HuaWang JingZhang Ge - Glioma progression is shaped by molecular heterogeneity, therapy resistance, and an immunosuppressive tumor microenvironment. Lysosomal remodeling has emerged as a hallmark of glioma adaptation; however, the regulation of individual lysosomal enzymes to malignant progression remains poorly understood. Lysosomal acid phosphatase 2 (ACP2) has been implicated in developmental and metabolic disorders, but its role in glioma has not been systematically investigated. In this study, we conducted an integrative multi-omics analysis to define the transcriptional, clinical, functional, and cellular correlates of ACP2 in glioma. Bulk RNA-seq datasets from TCGA and CGGA were used to analyze gene expressions, survival modeling, and machine-learning-based prognostic classification to evaluate the predictive contribution of ACP2 across glioma grades. Immune infiltration was quantified using TIMER2.0. Functional pathways were assessed using MetaCore, KEGG, GO, and Hallmark GSEA. Single-cell RNA-seq and single-nucleus RNA-seq analyses provided cell-type and subtype-specific validation. Protein-protein interactions were examined using STRING and GeneMANIA. Further pharmacogenomic associations were examined using GDSC/CTRP, and molecular docking was performed to simulate the drug ability of ACP2. Findings of this study indicated that ACP2 was significantly overexpressed in glioma relative to normal tissues and demonstrated the strongest prognostic impact among ACP family members. Elevated ACP2 expression correlated with reduced overall survival across multiple independent cohorts and was associated with increased infiltration of macrophages, neutrophils, and dendritic cells. Enrichment analyses revealed consistent activation of PI3K/AKT, KRAS, E2F and extracellular matrix remodeling pathways. MetaCore identified APP processing and cytoskeletal remodeling as top ACP2-associated modules. Single-cell and single-nucleus analyses localized ACP2 expression mainly to malignant glioma and myeloid populations, with higher expression in recurrent and advanced malignant states. This multi-omics framework identified ACP2 as a lysosomal regulator of glioma aggressiveness and immune remodeling. ACP2 functions as a robust biomarker of malignancy and may represent a candidate target for therapeutic exploration in glioma. - Source: PubMed
Publication date: 2026/06/07
Palekkode NeethuLiu Chia-HuiChen Jian-BinSolomon Dahlak DanielKumar SachinKo Ching-ChungYen Meng-ChiYeh I-JengXuan Do Thi MinhLin Hung-YunFathima AymanLee Yung-KuoChang Kai-FuLin Hui-RuWang Chih-YangShih Chia-LungNguyen Ngoc Uyen Nhi - Plastid ACPs are not limiting factors for seed oil accumulation and show functional redundancy, while their differentiation affects fatty acid composition. Plastid acyl carrier proteins (ACPs) act as acyl carriers in the fatty acid biosynthesis, yet the specific functions of different isoforms and their roles in seed oil accumulation remain unclear. To investigate the functions of the five ACPs in Arabidopsis seeds, this study analyzed their structure, expression pattern, and phenotypes of mutants and seed-specific overexpression lines. The results showed that ACP1, ACP2, ACP3, and ACP5 are expressed in developing seeds. Total fatty acid content of seeds is not affected by mutations of single, double, or triple ACPs, or their overexpression. Comprehensive analysis of changes in fatty acid composition in loss-of-function and overexpression seeds revealed that ACP1 and ACP5 may promote the accumulation of longer-chain and more unsaturated fatty acids. ACP2 has similar, but weaker effects on fatty acid composition compared with ACP1 and ACP5. ACP3 may uniquely enhance the accumulation of 20:1. ACP4 differs from the other four ACPs in both protein structure and a function of increasing 16:0 and 18:2. Our results indicate that ACPs exhibit functional redundancy and may not be limiting factors in oil accumulation, yet these ACPs differentially affect fatty acid composition. - Source: PubMed
Publication date: 2026/06/10
Guo NingxinChen YangyangZhao JialiangWen JiayinZhao CuizhuZhang Meng - Foot-and-mouth disease virus (FMDV) remains a major constraint to livestock health due to its high mutation rate and serotype diversity. Currently, FMDV vaccines, primarily inactivated whole-virus formulations, have significant limitations, including limited cross-protection, high production costs, and potential biosafety risks. To address the need for broad-spectrum protection, this study aimed to design a universal vaccine candidate by rationally constructing artificial chimeric proteins (ACPs) integrating conserved structural (VP1-VP3) and non-structural (3 A, 3 C) proteins from the predominant Egyptian FMDV serotypes A, O, and SAT 2. Three-dimensional modeling via AlphaFold3 and Swiss-Model confirmed the high structural quality of the constructs, with the ACP2 candidate exhibiting superior stability and reliability metrics (TM-score > 0.95, RMSD < 0.5, and overall quality > 88). Functional annotation revealed three conserved domains critical for virion assembly, receptor interaction, and host immune activation. Immunoinformatics analysis identified a robust antigenic profile for ACP1 and ACP2 proteins, comprising (21 and 36) cytotoxic T-lymphocyte (CTL), (18 and 20) helper T-lymphocyte (THL), and (15 and 19) B-cell epitopes prioritized for conservancy and population coverage. Based on these epitopes, three multiepitope vaccine constructs were assembled and analyzed computationally. Molecular docking demonstrated strong and stable binding affinities between the vaccine constructs and bovine TLR9 and TLR4 receptors (lowest binding energies of - 19.4 and - 16.9 kcal/mol, respectively), supported by stable interactions in 100 ns molecular dynamics simulations. These findings highlight the ACP2 construct as a novel, structurally stable, and highly immunogenic candidate capable of eliciting cross-serotype protection. The study provides a translational blueprint for a universal recombinant FMDV vaccine, warranting immediate in vitro expression and in vivo validation. - Source: PubMed
Publication date: 2026/06/09
Elrashedy AlyaaNayel MohamedSalama AkramZaghawa AhmedHasan Mohamed E - Esophageal squamous cell carcinoma (ESCC) continues to pose significant therapeutic challenges due to its aggressive behavior and suboptimal outcomes. The mitochondrial unfolded protein response (MUPR) pathway has emerged as a potential contributor to tumor progression, yet its role in ESCC prognosis and therapy remains insufficiently characterized. This study therefore seeks to systematically identify MUPR-associated prognostic genes in ESCC and to evaluate their potential as targets for therapeutic intervention. This study analyzed public databases to correlate MUPR pathway genes with ESCC prognosis, identifying YME1L1 and ACP2. These genes were used to construct a prognostic risk model, and single-cell RNA sequencing (scRNA-seq) was employed to determine their cellular expression patterns. Furthermore, the expression levels of the identified genes were experimentally validated in human ESCC cell lines using Reverse Transcription-quantitative PCR (RT-qPCR). Subsequently, the potential of these genes as drug targets was assessed. Following computational screening, lycorine emerged as a promising candidate. Rather than relying solely on molecular docking, this study performed molecular dynamics (MD) simulations to assess the stability of the binding interactions over time. The prognostic model was able to stratify patients into high- and low-risk groups that showed significantly different survival outcomes. At the cellular level, YME1L1 and ACP2 exhibited pronounced activity in B cells and neutrophils. RT-qPCR analysis demonstrated a significant downregulation of YME1L1 and ACP2 in ESCC cell lines compared to normal esophageal epithelial cells (P < 0.05), demonstrating high concordance between our bioinformatics predictions and experimental evidence. The drug screening identified lycorine as a promising candidate, with a predicted binding energy of − 9.0 kcal/mol to ACP2. MD simulations demonstrated the stability of these interactions: both the ACP2-lycorine and YME1L1-lycorine complexes remained stable throughout the simulation period, maintaining their structural integrity and key hydrogen bonds. This study identified ACP2 and YME1L1 as a novel prognostic signature in ESCC, supported by preliminary transcriptional validation, and proposed the natural compound lycorine as a computational candidate for inhibiting this axis. Our work established a conceptual link between prognostic biomarkers and a candidate therapeutic, providing a computationally derived rationale for future experimental and translational studies in ESCC. Further investigations are warranted to validate lycorine’s efficacy in vivo and to explore its potential synergy with existing therapies, with the ultimate goal of improving clinical outcomes. - Source: PubMed
Publication date: 2026/04/06
Chen FangZhang JunpengXu YingWang YalinCheng Jian