Ask about this productRelated genes to: AASDH Blocking Peptide
- Gene:
- AASDH NIH gene
- Name:
- aminoadipate-semialdehyde dehydrogenase
- Previous symbol:
- -
- Synonyms:
- NRPS998, LYS2, ACSF4
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-17
- Date modifiied:
- 2015-08-26
Related products to: AASDH Blocking Peptide
Related articles to: AASDH Blocking Peptide
- In recent years, liquid-liquid phase separation (LLPS) has garnered increasing attention in the field of oncology. However, its role in osteosarcoma remains largely unexplored. We aimed to construct a prognostic risk model associated with LLPS and to investigate the impact of LLPS-related genes on osteosarcoma briefly. - Source: PubMed
Publication date: 2025/12/29
Huang XinyuXiong LiangZeng JiaxingLi ShanhangCai YangjieZou ZhuanYang MingxiuLi HeningLiu YunHe Maolin - The enzyme 2-aminoadipic-6-semialdehyde dehydrogenase () plays a crucial role in metabolic pathways and has emerged as a significant player in multiple pathological conditions, including cancer and cardiomyopathies. has been implicated in colorectal cancer (CRC), particularly in microsatellite instability (MSI)-high tumors, in which genetic alterations may contribute to chemotherapy resistance and tumor progression. In addition to CRC, dysregulation of has been observed in hepatocellular carcinoma (HCC) and lung adenocarcinoma (LUAD), where it influences lipid metabolism and oncogenic pathways. Additionally, emerging evidence suggests a strong link between and cardiomyopathies, highlighting its potential as a biomarker of ischemic cardiomyopathy-induced heart failure. At the molecular level, functions in ATP binding and acid-thiol ligase activity, and plays a pivotal role in stress responses, lysine metabolism, and oxidative stress protection. Its association with metabolic reprogramming and the tumor microenvironment suggests that targeting could enhance current therapeutic strategies for cancer and cardiovascular diseases. This review comprehensively explores the diverse roles of , emphasizing its potential as a prognostic biomarker and therapeutic target for multiple diseases. A deeper understanding of may pave the way for novel treatment strategies that integrate metabolic modulation with conventional therapies and improve clinical outcomes in both oncology and cardiology. - Source: PubMed
Jaradat Jaber HJalali PooyaAmro RaghadAlsalhi Hamza KSerag IbrahimAl-Nusairi Ahmed MSaeed Anwaar - The resistance risk and mechanisms of cyclobutrifluram in are unclear. The baseline sensitivity of 111 isolates to cyclobutrifluram was 0.10 ± 0.07 μg/mL. Eight cyclobutrifluram-resistant mutants of were generated in the laboratory, exhibiting high-level and relative stable resistance. Cross-resistance was found between cyclobutrifluram and boscalid or pydiflumetofen, yet no cross-resistance was observed between cyclobutrifluram and iprodione, azoxystrobin, mefentrifluconazole, or difenoconazole. Each resistant mutant exhibited a reduced compound fitness index (CFI) compared to their parental isolates. An S73L substitution in AaSdhC or a P113T, H134N, or D145N mutation in AaSdhD conferred cyclobutrifluram resistance. Allele-specific PCR (AS-PCR) methods for the detection of mutations AaSdhC, AaSdhD, AaSdhD, and AaSdhD were successfully developed. In summary, exhibits a moderate risk for developing resistance to cyclobutrifluram, attributed to the S73L substitution in AaSdhC or the P113T, H134N, or D145N mutations in AaSdhD, which are detectable using specific AS-PCR methods. - Source: PubMed
Publication date: 2025/02/10
Peng QinTang LijunTang ShiqiWang ShuaiMiao JianqiangLiu Xili - Ischemic cardiomyopathy (ICM) induced heart failure (HF) is one of the most common causes of death worldwide. This study aimed to find candidate genes for ICM-HF and to identify relevant biomarkers by machine learning (ML). - Source: PubMed
Publication date: 2023/03/17
Kong XiangJinSun HouRongWei KaiMingMeng LingWeiLv XinLiu ChuanZhenLin FuShunGu XingHua - Acyl-CoA synthetases (ACSs) are responsible for acyl-CoA synthesis from nonpolar hydrophilic fatty acids and play a vital role in many metabolic processes. As a category of ACS isozymes, members of ACS family (AACS, ACSF2-3, AASDH) participate in lipid metabolism; however, their expression patterns, regulatory mechanisms and effects in hepatocellular carcinoma (HCC) are poorly understood. Here, through evaluating the expression profiles of ACSF gene family, we found that upregulated AACS might be more significant and valuable in development and progression of HCC. Consequently, the mRNA expression levels of AACS and ACSF2 was accordantly increased in HCC. Kaplan-Meier plotter revealed that HCC patients with high level of AACS were highly related to a shorter overall survival time and relapse-free survival. Genetic alterations using cBioPortal revealed that the alteration rate of AACS were 5%. We also found that the functions of ACSF gene family were linked to several cancer-associated pathways, including long-term potentiation, phospholipase D signaling pathway and purine metabolism. TIMER database indicated that the AACS and ACSF2 had a strong relationship with the infiltration of six types of immune cells (macrophages, neutrophils, CD8+ T-cells, B-cells, CD4+ T-cells and dendritic cells). Next, Diseasemeth database revealed that the global methylation levels of ACSF2 was higher in HCC patients. In conclusion, this study firstly demonstrated that Acyl-CoA synthesis gene family, in particular, AACS, could be associated with immune microenvironment, thereby influencing the development and prognosis of patients with HCC. - Source: PubMed
Publication date: 2022/10/04
Zhao ZijinLiu MiaomiaoXu ZhijieCai YuanPeng BiLiang QiujuYan YuanliangLiu WeiKang FanhuaHe QingchunHong QianhuiZhang WenqinLi JianboPeng JinwuZeng Shuangshuang