ACMSD
- Known as:
- ACMSD
- Catalog number:
- 001012A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACMSD
Related genes to: ACMSD
- Gene:
- ACMSD NIH gene
- Name:
- aminocarboxymuconate semialdehyde decarboxylase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-08
- Date modifiied:
- 2015-08-24
Related products to: ACMSD
Related articles to: ACMSD
- Colorectal liver metastasis (CRLM) remains the primary cause of mortality in patients with colorectal cancer (CRC), yet effective predictive tools and reliable biomarkers are still lacking. DeepMetabio-mCRC Screener, an integrated multi-omics framework combining large-scale transcriptomic profiles with serum metabolomics, was developed to address this gap. In a cohort of 1,077 CRC samples, 620 metabolism-related genes were used to train a convolutional neural network, yielding an area under the receiver operating characteristic curve of 0.92 in the validation cohort and 0.97 in the independent testing cohort, outperforming the performance of the 10 established machine learning models. Model-derived transcriptomic risk scores revealed 22 core metabolic features associated with metastatic progression and CRLM occurrence, particularly retinol and tryptophan metabolism. Cross-omics integration revealed aminocarboxymuconate-semialdehyde decarboxylase (ACMSD) as a promising biomarker associated with impaired nicotinamide adenine dinucleotide biosynthesis. Clinical validation in 100 CRC patients confirmed elevated ACMSD levels in patients with CRLM, which correlated with advanced stage, recurrence risk, an immune-inflamed tumor microenvironment, and heightened sensitivity to epidermal growth factor receptor/vascular endothelial growth factor receptor-targeted therapies. In vitro, ACMSD knockdown was associated not only with suppressed CRC cell migration caused by inhibition of the transforming growth factor-β/epithelial-to-mesenchymal transition pathway but also with decreased proinflammatory and immune-responsive pathways and reduced immune cell infiltration. These findings collectively validate the DeepMetabio-mCRC Screener as a substantial early risk prediction tool and underscore ACMSD, identified through this framework, as a multifunctional biomarker for diagnosis, prognosis, molecular characterization, and therapeutic decision-making in patients with CRLM. - Source: PubMed
Publication date: 2026/05/25
Zhang HongyuWang KeGuo RunqiuWu XiaochuanChen QingquanHe QiaojunYang BoZhuang YanyanYang WanlingZhu Hong - L-tryptophan (Trp) metabolism through the L-kynurenine (Kyn) pathway contributes to immune escape in neoplasms, including bladder cancer (BC). Indoleamine 2,3-dioxygenase-1 (IDO1) is a key enzyme, and its catabolites-Kyn, 3-hydroxykynurenine (3HK), and 3-hydroxyanthranilate (3HAA)-depend on other enzymes and play a crucial role in immunomodulation. - Source: PubMed
Lemes Douglas EdgardSantos Aline Áurea de Souzade Oliveira Jéssica LopesRoman-Ramos HenriqueMoreno Ana Carolina RamosCamacho Cleber PintoPontes-Junior JoséDellê Humberto - The residual feed intake (RFI) is a crucial economic trait in chickens. However, the genetic network and regulatory mechanisms that underpin RFI traits and the effects of RFI on meat quality and slaughter performance in chickens remain unclear. In this study, a total of 315 male Huainan chickens were reared from 7 to 13 weeks of age, and feed intake and weight gain were recorded for each individual bird. Based on the calculated RFI values, the 30 chickens with the highest RFI values are classified into the high residual feed intake (HRFI) group, while the 30 chickens with the lowest RFI values are classified into low residual feed intake (LRFI) group. The results revealed a significantly lower abdominal fat percentage in the LRFI group; however, no significant differences were detected in other meat quality traits or slaughter performance parameters. This phenotypic difference may be associated with the high expression of PCK1 in the HRFI group, which is likely to enhance glucose metabolism and thereby promote abdominal fat deposition. Two groups randomly selected 9 samples each for RNA seq analysis. The obtained transcriptome data were subjected to differential gene expression analysis, which revealed that 170 genes exhibited down-regulation while 109 genes displayed up-regulation in HRFI group relative to LRFI group. A total of 23097 genes were used to construct the weighted gene co-expression network analysis (WGCNA), and 27 co-expression gene modules were identified. Among these modules, the magenta module (R = 0.66, P = 0.003) has a significant positive correlation with RFI, while the pink module(R=﹣0.6,P = 0.009) has a significant negative correlation. The hub genes within the above modules were identified based on MM > 0.8 and GS > 0.4. Combining differential and hub genes, 56 key genes were identified as being significantly correlated with RFI traits. Several genes were identified as central regulator genes due to their involvement in the regulation of mitochondrial function (e.g., ACE2, ACMSD), glucose metabolism (e.g., FABP2, FETUB, PCK1) and lipid metabolism (e.g., APOA1). The findings will contribute to a more profound comprehension of the genetic expression and regulation of RFI traits, thereby providing a foundation for genetic breeding. - Source: PubMed
Publication date: 2026/02/21
Wang HaoChen ZihanZhang ChuchuWei WeiLiu YanghaoXing ChaohuiZou AofanCheng JianshengJiang Runshen - Imbalance of Nicotinamide adenine dinucleotide (NAD) homeostasis is a key contributor to various cardiac pathologies, including doxorubicin (DOX)-induced cardiomyopathy (DIC). The kynurenine pathway (KP), initiated by indoleamine 2,3-dioxygenase 1 (IDO1), serves as the primary route for de novo NAD biosynthesis. While this pathway regulates critical biological processes such as cellular metabolism, inflammatory responses, oxidative stress, and aging, its specific role in DIC remains poorly understood. Here, we reveal a protective function of the KP in DIC by facilitating NAD synthesis. Genetic ablation of IDO1 exacerbates DOX-induced cardiac injury and structural damage in mice. In cardiomyocytes, DOX treatment upregulates α-amino-β-carboxy-muconate-semialdehyde decarboxylase (ACMSD) while downregulating quinolinate phosphoribosyl-transferase (QPRT), thereby reducing levels of the intermediate metabolite quinolinic acid (QA) and NAD levels. These effects can be pharmacologically reversed by TES-1025, an ACMSD inhibitor that enhances QPRT activity and potentiates the cardioprotective effects of the KP pathway against DIC. Mechanistically, we show that DOX modulates the STING/interferon γ/5'-AMP-activated protein kinase (p-AMPK) signaling axis to elevate ACMSD and suppress QPRT. Our findings establish a novel therapeutic potential that targets the metabolic switch ACMSD to QPRT, restoring NAD redox homeostasis and conferring protection against DIC in murine models. - Source: PubMed
Publication date: 2025/12/06
Li DanleiZhang YangKuang YuanyuanLin ZhongWang PingJiang JianjunPi WenhuMa Qilin - Acute kidney injury (AKI) is a severe and prevalent nephrotic syndrome which lack of definitive therapies. Alpha-amino-β-carboxymuconic acid-ε-semialdehyde decarboxylase (ACMSD) is a metabolic enzyme mainly expressed in the kidney which exacerbated AKI injury by promoting TCA cycle and inhibiting nicotinamide adenine dinucleotide (NAD) production, whereas lack of effective intervention strategies for ACMSD-targeted therapy. Herein, we knocked out ACMSD through CRISPR-Cas9 method, and developed a reactive oxygen species (ROS)-responsive neutrophil-derived cellular vesicles (CVs) drugs (RNAi@ROS-CVs), which efficiently mediated ACMSD knockdown , exploring the mechanism of ACMSD-induced ferroptosis process in AKI. ACMSD knockout effectively alleviated cisplatin (CP)-induced mitochondrial damage, suppressed TCA cycle progression, promoted NAD synthesis, and inhibited ferroptosis in HK2 cells. In mice AKI model, RNAi@ROS-CVs effectively targeted the injured kidneys, downregulated ACMSD expression in renal tubular epithelial cells, reduced ROS production and lipid peroxidation, and alleviated CP or ischemia/reperfusion (I/R)-induced ferroptosis. These findings highlight the therapeutic potential of ACMSD-targeted knockout in AKI intervention and introduce a versatile and efficient controlled-release drug delivery platform for AKI-targeted therapy, with potential applicability to other acute renal diseases. - Source: PubMed
Publication date: 2026/01/01
Zhang YunjingDeng QingXu YangtaoWu WeiWu TianHuang JiaHu YugangLin WeiqiangXu XimingWu Jicheng