Human Polyclonal ACACA Ab
- Known as:
- Human Polyclonal ACACA Antibody
- Catalog number:
- a0110
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal ACACA
Related genes to: Human Polyclonal ACACA Ab
- Gene:
- ACACA NIH gene
- Name:
- acetyl-CoA carboxylase alpha
- Previous symbol:
- ACAC, ACC
- Synonyms:
- ACC1
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-09-11
- Date modifiied:
- 2018-05-03
Related products to: Human Polyclonal ACACA Ab
Related articles to: Human Polyclonal ACACA Ab
- The impact of metabolic reprogramming on immune cell functions is increasingly recognized. However, it remains largely unexplored in terms of immune cells adaptation during reproduction. Dendritic cells (DC) are crucial for establishing and maintaining pregnancy by orchestrating maternal immune adaptation essential for embryo implantation and decidualization. Here, we characterized the phenotypic and metabolic characteristics of DCs during early pregnancy in an allogeneic mouse model and in response to the specific deletion of hormonal receptors on DCs. Frequency of uterine CD11c DCs on gestational day (gd) 7.5 remained equal to that of non-pregnant mice. However, we observed a functional shift from cDC1 to cDC2 in pregnant mice. In parallel, a metabolic switch in uterine DCs was identified by upregulation of genes representing fatty acid synthesis (, ), fatty acid oxidation (), and glutamine-related metabolic pathways (). The cell-specific deletion of the glucocorticoid receptor in DCs reduced their MHCII expression, accompanied by a reduction in expression. Glutamine deprivation i dramatically reduced the absolute number of cultured bone marrow cells and the frequency of cDC1s while simultaneously increasing the frequency of cDC2s. Collectively, these findings establish glutamine metabolism as a key driver of DC adaptation during early pregnancy, revealing novel metabolic-immunological crosstalk at the maternal-fetal interface. - Source: PubMed
Publication date: 2026/06/15
Cai SongchenWieczorek AgnesUrbschat ChristopherSolano Maria EmiliaZeng YongArck Petra ClaraDiao LianghuiThiele Kristin - The interaction between fatty acids and nanoparticles (NPs) is increasingly recognized. This study investigated how stearic acid (SA)/linolenic acid (LNA) and SiO NPs co-exposure affects mRNA abundance of efflux, autophagy, fatty acid metabolism, and synthesis genes in adult zebrafish, and Si concentrations and lipid accumulation in Caco-2 and HepG2 cells. In vivo, SA or LNA inhibited SiO NPs from inducing abcg1 expression, and SiO NPs and SA/LNA co-exposure decreased agap1 expression in intestines. In livers, SiO NPs and SA co-exposure increased abcg1 expression. SiO NPs increased autophagic gene expression (map 1lc3b, atg7, and becn1) in intestines but not in livers. In contrast, SiO NPs + LNA increased map 1lc3b and atg7 expression, and SiO NPs + SA increased atg5 and becn1 expression in livers. For fatty acid β-oxidation genes, SiO NPs increased acox1 expression but decreased pparaa expression in intestines, an effect altered by SA or LNA. In livers, SiO NPs decreased acox1, cpt1aa, and pparaa but increased pnpla2 expression, which was also changed by SA. For fatty acid synthesis genes, LNA increased acaca and fasn expression in SiO NP-exposed intestines. In livers, SiO NPs decreased acaca, fasn, and scd expression, which was increased by LNA. In vitro, LNA increased Si accumulation in SiO NP-exposed Caco-2 cells, whereas both fatty acids reduced Si levels in HepG2 cells. Lipid accumulation was enhanced in HepG2 cells exposed to LNA and SiO NPs + LNA. Overall, our findings highlighted the complex interplay between SiO NPs and fatty acids, with outcomes dependent on fatty acid structure and cell/tissue type. - Source: PubMed
Publication date: 2026/06/12
Lin WeiqiLi ShanmanNing JiaxinyuGan LuCao Yi - Prenatal valproic acid (VPA) exposure is strongly linked to developmental cardiotoxicity, yet no targeted pharmacological countermeasure exists. Converging mechanistic evidence indicates that VPA cardiotoxicity centers on AMPK/PGC-1α suppression, positioning the AMPK activator metformin (MET) as a rational candidate for protection. We examined MET's protective effects against VPA-induced developmental cardiotoxicity in zebrafish embryos. Embryos were randomly allocated to four groups (Control, VPA 0.1 mM, MET 10 mM, VPA + MET) immediately after fertilization and chronically exposed until 96 hpf. Oxidative stress biomarkers (MDA, NO, SOD, GSH) and the expression of cardiac (), AMPK (), and mitochondrial/energy-related genes () were quantified. Compared with controls, VPA reduced (p < 0.01) and elevated (p < 0.05), triggered pericardial edema (p < 0.0001), suppressed , and (p < 0.05, p < 0.001, and p < 0.0001, respectively), upregulated (p < 0.0001), increased MDA and NO (p < 0.0001), and lowered SOD and GSH (p < 0.0001 and p < 0.001, respectively). Relative to the VPA group, MET co-treatment restored expression (p < 0.001), attenuated pericardial edema (p < 0.0001), increased (p < 0.05), (p < 0.01), and (p < 0.0001), suppressed (p < 0.0001), and normalized MDA (p < 0.05), NO (p < 0.0001), SOD, and GSH (both p < 0.0001). The restoration of , mitochondrial, and antioxidant capacity by MET suggests that the AMPK/PGC-1α axis may serve as a central target in VPA cardiotoxicity. - Source: PubMed
Publication date: 2026/06/08
Üstündağ Ünsal VeliÜstündağ Fümet DuyguAyşit Neşe - Background Acute kidney injury (AKI) frequently causes remote organ injury including hepatic steatosis, yet whether lipid accumulation reflects increased synthesis or impaired clearance has not been resolved. Methods We used a murine ischemia-reperfusion AKI model. Unbiased liver proteomics was performed at 24 hours after reperfusion, and dysregulated pathways were identified by Gene Set Enrichment Analysis. Results were validated by Western blotting, qPCR, and immunohistochemistry. These findings were complemented by retrospective analysis of two ICU databases (MIMIC-IV and eICU-CRD). Results AKI significantly increased serum ALT and AST and induced hepatic lipid accumulation. Proteomic analysis revealed that key lipogenic enzymes (Scd1, Fasn, Acly, Acaca) were uniformly suppressed rather than upregulated. Proteins essential for VLDL assembly (ApoB, MTTP, ApoE) were significantly downregulated. Plasma triglycerides were decreased while liver triglycerides were increased, consistent with impaired hepatic lipid export. As in renal tubular cells, AKI also disrupted ER protein folding homeostasis in the liver, triggering ER stress. This was evidenced by upregulated levels of the ER chaperone GRP78, increased XBP1 splicing indicative of UPR activation, and elevated expression of the ER stress-induced pro-apoptotic transcription factor CHOP, suggesting that prolonged ER stress may also promote hepatocyte cell death. TLR4/MyD88 signaling was activated, yet inflammatory cytokines were paradoxically reduced, accompanied by Kupffer cell depletion (decreased F4/80) and monocyte infiltration (increased CD68). In 6,996 propensity-matched ICU patients (MIMIC-IV), AKI independently increased the risk of clinically significant liver injury 4-fold (adjusted OR = 4.41). Analysis of 22,727 patients across 208 hospitals (eICU-CRD) identified a lipid dissociation pattern: elevated triglycerides alongside decreased total cholesterol, HDL, and LDL, with dose-dependent scaling across KDIGO stages. Conclusions These data support ER stress-mediated impairment of VLDL export as a primary driver of AKI-induced hepatic steatosis. Clinical validation across two independent ICU databases identifies a dual metabolic insult: enhanced peripheral lipid delivery compounds impaired hepatic export, amplifying hepatic lipid retention. ER stress and lipid export machinery represent potential therapeutic targets for AKI-associated liver injury. - Source: PubMed
Publication date: 2026/05/19
Li MinghuaNi RunzeWilliams KristofMelaika MiriameSun Lucas EliFu LiyingSubramanian VijayDhanireddy KiranLiu Ruisheng - Breast cancer remains a major threat to women's health and survival worldwide. Iroquois homeobox 1 (IRX1), a developmentally regulated transcription factor, acts as a tumor suppressor in several cancers. However, its mechanistic role in breast cancer remains elusive. In this study, we demonstrate that IRX1 is downregulated in breast cancer tissues and cell lines due to promoter hypermethylation. IRX1 functioned as a tumor suppressor both in vitro and in vivo. Mechanistically, IRX1 interacts with NME1 and promotes its nuclear localization. Subsequently, NME1 facilitates the transcriptional regulation of ACACA by IRX1. The IRX1-NME1 axis modulates de novo fatty acid synthesis and breast cancer progression by targeting ACACA. In conclusion, our findings reveal that the IRX1- NME1/ACACA axis plays a critical role in de novo fatty acid synthesis and breast cancer progression, providing new insights into gene regulatory interactions and highlighting its potential as a novel therapeutic target for breast cancer. - Source: PubMed
Publication date: 2026/06/01
Liu Wen-BoHai Lin-YueZhang Yuan-YuanYue Hao-RanLiu Xiao-FengLiu Bo-WenWang XinCao Xu-ChenYu Yue