ACACA_BOVIN ACACA ELISA tesk kit
- Known as:
- ACACA_BOVIN ACACA Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16513
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- ACACA_BOVIN ACACA ELISA tesk kit
Related genes to: ACACA_BOVIN ACACA ELISA tesk kit
- 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
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- 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 - : Promoting white adipose tissue (WAT) browning into thermogenic beige adipocytes is a promising anti-obesity strategy. (YST) has been used traditionally to alleviate obesity-related conditions. Catalpol and rhoifolin are major bioactive components of (Gaertn.) and (Thunb.) with known metabolic or anti-inflammatory effects. However, their direct roles in adipocyte browning and the mechanisms via β3-adrenergic receptor (β3-AR) signaling are not well defined, and this study addresses this gap. : To evaluate browning potential, 3T3-L1 adipocytes were treated with catalpol and rhoifolin during differentiation. The expression of browning markers and lipid metabolism or catabolism transcription factors was analyzed using Western blotting and quantitative real-time polymerase chain reaction. The involvement of the β3-AR and adenosine monophosphate-activated protein kinase (AMPK) signaling pathways was further validated using specific agonists and antagonists. : Both compound treatments significantly upregulated beige-specific (, , , , , ) and mitochondrial biogenesis markers (, , ), accompanied by a marked increase in thermogenic markers (UCP1, PGC-1α, ). Concurrently, lipolysis-related genes such as , , and were elevated, while lipogenesis targets (, , , ) were downregulated through activation of the β3-AR signaling pathway. : These findings suggest that catalpol and rhoifolin, key phytochemicals of YST, promote WAT browning and lipolysis. Our findings indicate that these compounds induce browning and modulate metabolism via the β3-AR pathway. These results serve as a cornerstone for natural anti-obesity therapy, pending further validation in vivo and clinical studies. - Source: PubMed
Publication date: 2026/05/18
Choi Seung MinLim Sung HoLee Ho SeonChoi GayoungKim Myeong JiKim HyunwooChoi Chang-Ik - Cervical cancer, primarily driven by persistent high-risk HPV infection, remains a major global health issue. Xiao-ai-fei honey ointment, a traditional Uyghur multi-ingredient preparation, has shown clinical promise in cancer treatment, but its mechanisms against cervical cancer are not fully understood. This study aimed to investigate the potential molecular mechanisms of ethanolic extract of Xiao-ai-fei honey ointment (XAFHO) in cervical cancer using network pharmacology, single-cell RNA sequencing, and experimental validation. Differentially expressed genes (DEGs) in cervical cancer were identified from TCGA database. Active components and corresponding targets of XAFHO were retrieved from the TCMSP database, and disease targets were obtained from GeneCard, OMIM, and the TTD. Intersection targets were subjected to multivariate Cox and LASSO regression to construct a prognostic model. Immune infiltration, TMB, and MSI were compared between risk groups. Single-cell RNA-seq data were analyzed to determine cellular origins and inter-cellular communication. In vitro assays were performed on HeLa and SiHa cells to assess the anti-cancer activity of XAFHO. Molecular docking evaluated binding affinities between active compounds and core targets. The expression and functional roles of and were further validated by RT-qPCR, Western blotting, and siRNA transfection. Sixty-three potential XAFHO targets were identified, and an 11-gene prognostic model was established, effectively stratifying patients into high- and low-risk groups with significantly different overall survival (AUC > 0.7). The high-risk group exhibited an immunosuppressive microenvironment and higher TMB. Single-cell analysis revealed that and were predominantly expressed in tumor cells, while was enriched in macrophages/monocytes. Tumor cells communicated with immune cells via the TGFB1-TGFβR1/R2 axis, promoting immune evasion. In vitro, XAFHO significantly inhibited proliferation, colony formation, migration, and invasion of cervical cancer cells. Molecular docking confirmed the strong binding of quercetin, kaempferol, and isorhamnetin to and (binding energy < -6.0 kcal/mol). Functional validation indicated that upregulated and contribute to malignant behaviors in cervical cancer cells. This study integrates network pharmacology with single-cell and experimental approaches to demonstrate that XAFHO exerts multi-target and multi-cell anti-cervical cancer effects, potentially by modulating lipid metabolism and immune-related pathways via and . These findings provide a scientific basis for the therapeutic application of XAFHO in cervical cancer. - Source: PubMed
Publication date: 2026/04/27
Abasi XiariwanaLiang DiRezhake RemilaTuerxun GulixianZhuo QianJu XianSu HongyuYang JingAbulizi Guzhalinuer - Heat stress (HS) has emerged as a major environmental stressor, inducing oxidative stress and hepatic steatosis and impairing production performance and health in laying hens, with limited evidence-based nutritional interventions available. This study investigated the hepatoprotective effects of dietary silibinin (SIL) against chronic HS. In a 10-week trial, 252 43-week-old Hy-Line Brown hens were exposed to daily HS (32 ± 1 °C, temperature-humidity index [THI] > 73) and fed either a basal diet or one supplemented with 100 mg/kg SIL. SIL significantly increased laying rate ( < 0.05) and improved albumen height, Haugh units, and shell strength by week 8 ( < 0.05). Histological analysis showed a 48% reduction in non-alcoholic fatty liver disease (NAFLD) activity score, with significantly decreased hepatic triglyceride content ( < 0.05); Oil Red O staining confirmed reduced lipid droplet accumulation. SIL restored redox balance by increasing plasma, hepatic total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px) ( < 0.05), increasing hepatic catalase (CAT) and glutathione (GSH) levels while decreasing malondialdehyde (MDA) ( < 0.05). Untargeted plasma metabolomics identified 11 key metabolites related to 2-oxoglutarate and purine metabolism, while hepatic transcriptomics revealed 835 differentially expressed genes primarily in the PPAR signaling and fatty acid biosynthesis pathways. SIL suppressed de novo lipogenesis via downregulation of ACACA and FASN, and enhanced β-oxidation through upregulation of CPT1A and ACSL1 ( < 0.05). Molecular docking indicated favorable binding affinities between SIL and these targets, which was further supported by corresponding changes in protein expression via Western blotting. Correlation analysis revealed a consistent alignment between the upregulation of ACSL1/CPT1A and improvement in performance and antioxidant status, suggesting a coordinated metabolic shift. These findings emphasize the potential of SIL as a sustainable animal nutrition antioxidant additive, which can alleviate HS-induced lipid disorders in the liver of laying hens. Importantly, these hepatoprotective effects were demonstrated exclusively under chronic heat stress conditions; further studies incorporating a normothermic baseline are required to distinguish stress-specific mitigation from general metabolic stimulation. - Source: PubMed
Publication date: 2026/05/11
Gao JiangRen HongruiWu XuanfuZou CunzhiHe BinMa Wenqiang