Ask about this productRelated genes to: ACY3 antibody
- Gene:
- ACY3 NIH gene
- Name:
- aminoacylase 3
- Previous symbol:
- -
- Synonyms:
- HCBP1, MGC9740, ACY-3
- Chromosome:
- 11q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-10
- Date modifiied:
- 2015-03-09
Related products to: ACY3 antibody
Related articles to: ACY3 antibody
- Floods and tropical cyclones (TCs), two of the most frequent and costliest climate-related disasters worldwide, have been linked to sustained health risks extending beyond acute hazards. However, evidence on the underlying epigenetic mechanisms remains scarce. We aimed to characterize DNA methylation patterns associated with exposure to floods and TCs of varying intensities. - Source: PubMed
Publication date: 2026/04/20
Huang WenzhongXu RongbinWu YaoYang ZhengyuYe ZhoufengWong Ee MingSouthey Melissa CHopper John LAbramson Michael JLi ShanshanLi ShuaiGuo Yuming - Cells counteract proteotoxic conditions by launching transcriptional stress responses. While synthesis of heat shock proteins (HSPs) upon acute stress is well characterized, how distinct proteotoxic conditions reshape the transcriptome remains poorly understood. Here, we analyse polyA+ RNA expression under heat shock, HSP90 inhibition, and polyglutamine (polyQ) aggregation. We find fundamentally distinct transcriptional responses to proteotoxic stressors and a systemic deficiency of mice under chronic stress to launch acute responses. While heat shock and HSP90 inhibition induce chaperones, polyQ aggregation increases expression of RNAs linked to transcription repression, chromatin remodeling, and autophagy. Analysing wild-type and Huntington's Disease (HD) mice reveals tissue-specific transcriptional adaptations to polyQ, including repressed cell-type specific functions and altered energy metabolism. Despite profound reprogramming, remarkably few genes exhibit consistently increased (Acy3, Abhd1, Tmc3) or decreased (Fos) RNA levels across HD brain regions. These results emphasize cellular background in disease manifestation and support energy metabolism and detoxifying enzymes as therapeutic targets in late-stage HD. Moreover, the systemic deficiency of chronically stressed mice to launch responses challenges strategies that rely on induced transcription. Altogether, we characterize transcription signatures to proteotoxic stresses, identify key trans-activators driving proteotoxic stress responses, provide an interactive gene-by-gene viewer of global changes, and delineate tissue-specific transcription programs in HD mice. - Source: PubMed
Publication date: 2026/01/29
Rabenius AdelinaSalim IntisarLindström HilmarPak AnastasiyaAktay SerhatVihervaara Anniina - Acute coronary syndrome (ACS) is a critical cardiovascular condition with diverse clinical presentations, necessitating personalized therapeutic approaches. This study explores the genetic variation associated with ACS subtypes in the Han and Uyghur Chinese populations to support the development of precision medicine approaches tailored to ethnic-specific genetic backgrounds. - Source: PubMed
Publication date: 2025/08/15
Lai HongmeiZhu JinhangTao JingGuo ZitongYu XiaolinShen XinWang TingWang YingCai HuanCai XiaoWei ZhenbangYang Yining - The molecular heterogeneity of endometrial stromal tumors (ESTs) is demonstrated by the presence of the same fusion gene in distinct pathologic entities, such as endometrial nodules and low-grade endometrial stromal sarcoma, both exhibiting the chimeric transcript. Given the limited knowledge on these tumors, which is based on a small number of cases studied with a restricted range of techniques, we analyzed 47 ESTs to explore their methylation and transcriptomic landscapes. - Source: PubMed
Publication date: 2025/05/22
Brunetti MartaVitelli ValeriaNaas Anca MihaelaZahl Eriksson Ane GerdaHaugland Hans KristianKrakstad CamillaMicci Francesca - Breast cancer (BRCA) is a prevalent female malignancy. PANoptosis, integrating diverse cell death traits, is pivotal in BRCA, thus necessitating deeper study. - Source: PubMed
Publication date: 2025/04/15
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