ACADM Antibody (B01P)
- Known as:
- ACADM Antibody (B01P)
- Catalog number:
- ang-000034-b01p
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- ACADM Antibody (B01P)
Related genes to: ACADM Antibody (B01P)
- Gene:
- ACADM NIH gene
- Name:
- acyl-CoA dehydrogenase medium chain
- Previous symbol:
- -
- Synonyms:
- MCAD, MCADH, ACAD1
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: ACADM Antibody (B01P)
Related articles to: ACADM Antibody (B01P)
- The global rise in prediabetes and diabetes, with type 2 diabetes (T2DM) being predominant, highlights the association between T2DM and hypertriglyceridemia (HTG). Patients with both abnormal glucose levels and HTG require increased attention due to higher risks of complications and mortality. Therefore, this study aimed to find the key long non-coding RNA (lncRNA) of HTG in the abnormal glucose metabolism patients. We collected blood samples for RNA sequencing experiments and blood samples for validation in population. We have conducted RNA sequencing, weighted gene co-expression network analysis (WGCNA), quantitative real-time polymerase chain reaction (qRT-PCR) in a 82-vs-82-sample-size population and insulin induced HepG2, RNA- Fluorescence in situ hybridization (FISH) and Cell Counting Kit-8 (CCK-8). We also explored lipid metabolism related transcription factor and the related protein expression and processed key lncRNA by both interference expression and overexpression, and the related consequences were rescued by its target mRNA. ENST00000540317.5 (LINC317.5) was lower in HTG with abnormal glucose metabolism and was found in both cytoplasm and nucleus in HepG2, inversely regulating the accumulation of TG and its target mRNA TKFC. Relative expression of peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma (PPARγ) were decreasing, and SREBP-1c (sterol regulatory element-binding protein-1c) was increasing of the interference expression of LINC317.5. Interference expression of LINC317.5 significantly decreased the protein expression of ACADM and CPT1A, whereas increased the protein expression of FAS and ACC1. TKFC partly reduced the triglyceride (TG) accumulation of LINC317.5. In conclusion, we suggested LINC317.5-TKFC as a key for TG accumulation in the HepG2-insulin resistant (IR). These might provide information of non-invasive biomarkers for the HTG with abnormal glucose. - Source: PubMed
Publication date: 2024/04/26
Yang YixueSun MengziYan ShoumengYao NanLi XiaotongWu CaihongWu ZiboWang FengdanCui WeiweiLi Bo - Clear cell renal cell carcinoma (ccRCC) represents a highly frequent renal cancer subtype. However, medium-chain acyl-CoA dehydrogenase (ACADM) encodes an important enzyme responsible for fatty acid β-oxidation (FAO) and its association with prognosis and immunity in cancers has rarely been reported. Therefore, the present work focused on exploring ACADM's expression and role among ccRCC cases. We used multiple public databases and showed the hypo levels of ACADM protein and mRNA within ccRCC. Additionally, we found that ACADM down-regulation showed a remarkable relation to the advanced stage, high histological grade, as well as dismal prognostic outcome. As suggested by Kaplan-Meier curve analysis, cases showing low ACADM levels displayed shorter overall survival (OS) as well as disease-free survival (DFS). Moreover, according to univariate/multivariate Cox regression, ACADM-mRNA independently predicted the prognosis of ccRCC. In addition, this work conducted immunohistochemistry for validating ACADM protein expression and its prognostic role in ccRCC samples. KEGG and GO analyses revealed significantly enriched genes related to ACADM expression during fatty acid metabolism. The low-ACADM group with more regulatory T-cell infiltration showed higher expression of immune negative regulation genes and higher TIDE scores, which might contribute to poor response to immunotherapies. In conclusion, our results confirmed that downregulated ACADM predicted a poor prognosis for ccRCC and a poor response to immunotherapy. Our results provide important data for developing immunotherapy for ccRCC. - Source: PubMed
Publication date: 2024/04/25
Zhou LibinYin MinGuo FeiYu ZefengWeng GuobinLong Huimin - This study aims to explore the important factors affecting the characteristics of different parts of pork. - Source: PubMed
Publication date: 2024/04/10
Wu ZhuosuiWang ZhonggangWang PanCheng LeiyanLi JianhaoLuo YanfengYang LinfangLi LinfengZeng JianhuaHu Bin - Neutrophils rapidly accumulate in large numbers at sites of tissue damage, exhibiting not only their well-known bactericidal capabilities but also playing crucial roles in angiogenesis and tissue repair. While exosomes derived from human umbilical cord mesenchymal stem cells (HucMSC-Exo) have emerged as a promising therapeutic tool, their exact mechanisms of action remain partly elusive. We hypothesize that HucMSC-Exo treatment may modulate neutrophil phenotypes, thereby significantly influencing wound healing outcomes. - Source: PubMed
Publication date: 2024/04/13
Yang JiamanXie YulinXia ZhikuanJi ShuaifeiYang XinYue DanxiaLiu YuanyuanYang RongyaFan Yunlong - Most studies on fat appetite have focused on long-chain triglycerides (LCTs) due to their obesogenic properties. Medium-chain triglycerides (MCTs), conversely, exhibit anti-obesogenic effects; however, the regulation of MCTs intake remains elusive. Here, we demonstrate that mice can distinguish between MCTs and LCTs, and the specific appetite for MCTs is governed by hepatic β-oxidation. We generated liver-specific medium-chain acyl-CoA dehydrogenase (MCAD)-deficient (MCAD) mice and analyzed their preference for MCTs and LCTs solutions using glyceryl trioctanoate (C8-TG), glyceryl tridecanoate (C10-TG), corn oil, and lard oil in two-bottle choice tests conducted over 8 days. Additionally, we employed lick microstructure analyses to evaluate the palatability and appetite for MCTs and LCTs solutions. Finally, we measured the expression levels of genes associated with fat ingestion (, , and ) in the hypothalamus 2 h after oral gavage of fat. Compared to control mice, MCAD mice exhibited a significantly reduced preference for MCTs solutions, with no alteration in the preference for LCTs. Lick analysis revealed that MCAD mice displayed a significantly decreased appetite for MCTs solutions only, while the palatability of both MCTs and LCTs solutions remained unaffected. Hypothalamic expression in control mice was elevated by oral gavage of C8-TG but not by LCTs, and this response was abrogated in MCAD mice. In summary, our data suggest that hepatic β-oxidation is required for MCTs-specific appetite but not for LCTs-specific appetite. The induction of hypothalamic galanin upon MCTs ingestion, dependent on hepatic beta-oxidation, could be involved in the regulation of MCTs-specific appetite. - Source: PubMed
Publication date: 2024/04/10
Maruyama TsugunoriMatsui ShoKobayashi RyosukeHorii TakuroOguri YasuoTsuzuki SatoshiHorie TakahiroOno KohHatada IzuhoSasaki Tsutomu