ACYP2
- Known as:
- ACYP2
- Catalog number:
- 001121A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACYP2
Related genes to: ACYP2
- Gene:
- ACYP2 NIH gene
- Name:
- acylphosphatase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p16.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-21
- Date modifiied:
- 2016-02-26
Related products to: ACYP2
Related articles to: ACYP2
- Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with a poor prognosis. Temozolomide (TMZ) is the most widely used chemotherapeutic agent and can significantly improve patient survival rates. However, numerous patients develop TMZ resistance, leading to limited therapeutic benefits. Therefore, it is crucial to investigate the mechanisms of TMZ resistance in patients with GBM and identify the sensitizing targets of TMZ to improve its clinical efficacy. In this study, we demonstrated that acylphosphatase 2 (ACYP2) was involved in regulating the sensitivity of GBM to TMZ. ACYP2 knockdown significantly reduced the IC50 values of TMZ in GBM cells, whereas overexpression of ACYP2 increased their IC50 values. The combination of ACYP2 knockdown and TMZ treatment not only inhibited the malignant behavior of GBM cells in vitro but also slowed the progression of intracranial GBM in mice. Additionally, comet tail and γ-H2AX staining assays showed that ACYP2 knockdown enhanced the TMZ-induced DNA damage. Mechanistically, ACYP2 upregulates the transcription factor c-Myc to promote the transcription of its downstream target PARP1, an important regulatory molecule for DNA damage repair, ultimately inducing TMZ resistance in GBM cells. Thus, this study demonstrated that ACYP2 is a potential therapeutic target for TMZ-resistant patients with GBM. - Source: PubMed
Sui MengjunCai QingSun ZhiweiLi JinjinZhang YiyangLi MengdanDai PenggaoLi Gang - Substance use disorder (SUD) significantly increases the risk of neurotoxicity, inflammation, oxidative stress, and impaired neuroplasticity. The activation of inflammatory pathways by substances may lead to reactive astrogliosis and chronic neuroinflammation, potentially mediated by the release of extracellular particles (EPs), such as extracellular condensates (ECs) and extracellular vesicles (EVs). These particles, which reflect the physiological, pathophysiological, and metabolic states of their cells of origin, might carry molecular signatures indicative of SUD. In particular, our study investigated neuroinflammatory signatures in SUD patients by isolating EVs from the dorsolateral prefrontal cortex (dlPFC) Brodmann's area 9 (BA9) from postmortem subjects. We isolated BA9-derived EVs from postmortem brain tissues of eight individuals (controls: n = 4, SUD: n = 4). The physical properties (concentration, size, zeta potential, morphology) of the EVs were analyzed, and the EVs were subjected to integrative multiomics analysis to profile the lipidomic and proteomic characteristics. We assessed the interactions and bioactivity of EVs by evaluating their uptake by glial cells. We further assessed the effects of EVs on complement mRNA expression in glial cells and on microglial migration. No significant differences in EV concentration, size, zeta potential, or surface markers were observed between the SUD group and the control group. However, lipidomic analysis revealed significant enrichment of glycerophosphoinositol bisphosphate (PIP2) in SUD-derived EVs. Proteomic analysis revealed the downregulation of SERPINB12, ACYP2, CAMK1D, DSC1, and FLNB and the upregulation of C4A, C3, and ALB in SUD-derived EVs. Gene Ontology (GO) and protein‒protein interactome analyses revealed functions associated with the identified proteins, such as cell motility, focal adhesion, and acute phase response signaling. Both control and SUD-derived EVs increased C3 and C4 mRNA expression in microglia, but only SUD-derived EVs upregulated these genes in astrocytes. SUD-EVs also significantly enhanced microglial migration in a wound healing assay. This study successfully isolated EVs from postmortem brains and used a multiomics approach to identify EV-associated lipids and proteins in SUD. Elevated C3 and C4 in SUD-derived EVs and the distinct effects of EVs on glial cells suggest a crucial role for these cells in acute phase response signaling and neuroinflammation. - Source: PubMed
Publication date: 2025/08/15
Okeoma Chioma MNaushad WasifaOkeoma Bryson CGartner CarlosSantos-Ortega YulicaVary CalvinLima-Bastos SavioCarregari Victor CorasollaLarsen Martin RNoghero AlessioWalss-Bass ConsueloGrassi-Oliveira Rodrigo - : Chronic inflammation is associated with leukocyte telomere length (LTL) shortening and type 2 diabetes (T2D). The latter is also associated with LTL shortening, while the three variables are associated with aging. It is tempting to test whether inflammation, age, or both are behind the telomere system aberrations in diabetic patients. : In this cross-sectional observational study, blood samples collected from 118 T2D patients were analyzed via ELISA to estimate the plasma levels of four inflammatory markers, IL6, IL8, TREM1, and uPAR, and the telomerase enzyme (TE). Moreover, the extracted DNA was used for the LTL estimation via qPCR and for single nucleotide polymorphisms (SNP) genotyping of TE genes (TERT, TERC, and ACYP2) via rtPCR. The results showed no correlation between the levels of all tested inflammatory markers and the LTL, TE level, and age. There were no significant differences between the marker levels in diabetic patients in the four quartiles of the LTL and TE levels. Moreover, there were no significant differences in the levels of the markers between carriers of the different TE genotypes. There were no associations between the tested inflammatory markers' levels and the LTL, TE plasma levels, or age in T2D. Explanations for the dissociation between the above-known associations in T2D were proposed; however, the subject is worth further investigation. - Source: PubMed
Publication date: 2025/02/20
Sater Mai SAlDehaini Dhuha M BMalalla Zainab H AAli Muhalab EGiha Hayder A - Patients with schizophrenia (SCZ) experience constipation at significantly higher rates compared with the general population. This relationship suggests a potential genetic overlap between these two conditions. - Source: PubMed
Publication date: 2025/03/03
Luo QinghuaAn MingweiWu YunxiangWang JiawenMao YuantingZhang LeichangWang Chen - Bisphenol A (BPA) is a widely found endocrine-disrupting chemical (EDC). Nanoplastics (NPs) represent a novel environmental pollutant, and the combined toxicity of these pollutants on the hepatopancreas of marine arthropods is understudied. To investigate the potential risks associated with co-exposure to BPA and NPs on the hepatopancreas, Portunus trituberculatus was treated with 100 μg/L BPA, 10 particles/L NPs, and a combination of 100 μg/L BPA + 10 particles/L NPs for 21 days, respectively. Histological observation demonstrated that co-exposure severely damaged both hepatopancreas tissue and mitochondrial structure. Transcriptome analysis revealed that 1498 transcripts were differentially expressed under different exposure conditions, and these transcripts are involved in biological processes such as cellular processes and carbohydrate metabolism. BPA and NPs co-exposure modulate pyruvic acid (PA) levels by increasing the activity of pyruvate kinase (PK), leading to changes in glycogen and glucose (GLU) content within tissues, thus affecting glycolysis. The dysregulation of the CHI3L1, ACSS2 and ACYP2 genes induced by BPA and NPs co-exposure may collectively regulate the process of carbohydrate metabolism. Notably, the downregulation of the VPS4 gene and the upregulation of the GBA1, Pin1 and CCND2 gene may affect the cell cycle, potentially impacting cell proliferation after BPA and NPs co-exposure. These data indicate that co-exposure to BPA and NPs is more significantly cytotoxic and leads to changes in carbohydrate metabolism, cell proliferation, and histological damage in the hepatopancreas of P. trituberculatus. This knowledge emphasizes the need for proactive measures to mitigate the adverse effects of these environmental pollutants on human and ecological health while also providing valuable insights into the relevant molecular mechanisms. - Source: PubMed
Publication date: 2024/11/08
Wang XiaotianZhou ShangjieHuang YutongChu PengfeiZhu LongChen Xiaocong