ACACA (Human) Recombinant Protein (Q01)
- Known as:
- ACACA (Human) Recombinant Protein (Q01)
- Catalog number:
- H00000031-Q01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ACACA (Human) Recombinant Protein (Q01)
Related genes to: ACACA (Human) Recombinant Protein (Q01)
- 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: ACACA (Human) Recombinant Protein (Q01)
Related articles to: ACACA (Human) Recombinant Protein (Q01)
- Endometriosis (EMs) is one of the most common gynecologic diseases, and the roles of ferroptosis in EMs have not been fully clarified. The induction of ferroptosis has been demonstrated to inhibit the growth of ectopic lesions in EMs. Although acetyl-CoA carboxylase 1 (ACC1), the rate-limiting enzyme for fatty acid biosynthesis, has been shown to regulate ferroptosis, the detailed mechanism involved has not been fully elucidated. In addition, the role of ACC1, encoded by ACACA, in EMs remains unclear. Thus, the present study aimed to explore the role of ACC1 in ferroptosis and the potential therapeutic effect of the ferroptosis inducer the ferroptosis inducer 56 (FIN56) in EMs. - Source: PubMed
Publication date: 2026/06/29
Zeng ChengZhu JingwenLu RuihuiWu PeiliLi XinLi FangyuanPeng ChaoZhou YingfangXue Qing - This study investigated the molecular characteristics and functions of buffalo prolactin (PRL) in the lactation. The buffalo gene's complete coding sequence (CDS) is 690 bp, encoding 229 amino acids, with structure and function highly consistent with other Bovidae species. expression was significantly higher in the buffalo mammary gland during lactation compared to the non-lactating period, highlighting its crucial role in lactation. overexpression in buffalo mammary epithelial cells (BuMECs) promotes cell proliferation and increases the casein secretion and triglyceride (TAG) accumulation. This occurs through the activation of the JAK2-STAT5 (cell differentiation, casein () gene transcription, and lipid factor transcription), PI3K-AKT-mTOR (cell growth, milk protein gene translation, and lipid factor activation), and mitogen-activated protein kinase (MAPK; cell proliferation and stress mitigation) signaling pathways. Specifically, overexpression upregulated the mRNA expression of genes in these pathways, such as , , , , , , and , while decreasing and . Overexpression also increased the expression of cell cycle genes (, , /), and enhanced cell viability. Furthermore, overexpression led to increased expression of casein genes (, ) and milk-fat-synthesis-related genes (, , , , ). Population genetic analysis identified five single-nucleotide polymorphisms (SNPs) in the buffalo CDS, with c.34C T and c.430T C being non-synonymous substitutions that were predicted to affect protein function. This research provides a theoretical foundation for genetic interventions aimed at improving buffalo lactation traits. - Source: PubMed
Publication date: 2025/12/03
Huang LigeFan XinyangTeng XiaohongQian LindongBao ZhipengMiao Yongwang - This study evaluated whether chlorogenic acid (CGA) attenuates hepatic injury in broilers under high stocking density (HSD). A total of 216 experimental male Arbor Acres broilers were assigned to normal density without CGA (ND; 14 birds/m), high density without CGA (HD; 22 birds/m), normal density with 0.1% CGA (NDCGA), or high density with 0.1% CGA (HDCGA) groups, with six cages per treatment. CGA was supplied from day 7 to 42. At 42 d, live-weight densities were 35.00, 50.25, 34.48, and 49.38 kg/m, respectively. Compared with their corresponding normal-density groups, the high-density groups had lower body weights at 21, 28, 35, and 42 d, and lower average daily gain (ADG) during days 21-42 ( < 0.05), whereas CGA did not significantly alter body weight or ADG within either stocking density ( > 0.05). At 35 and 42 d, the HD group had lower hepatic T-AOC, SOD, and CAT activities and higher MDA content than the ND group ( < 0.05). Compared with the HD group, the HDCGA group had higher T-AOC and CAT activities and lower MDA content at both ages, and higher SOD activity at 42 d ( < 0.05). Qualitative histological and transcript-level alterations were evident at 28 d. Compared with HD, the HDCGA group showed treatment-associated shifts in AMPK, SREBP1, ACACA, PLA2G4A, COX-2, ALOX5, and NOX5 mRNA abundance ( < 0.05). Under the experimental conditions, 0.1% CGA was associated with partial attenuation of HSD-related hepatic oxidative, lipid-metabolic, and inflammatory disturbances without a significant growth response. - Source: PubMed
Publication date: 2026/08/15
Bai DongyingZhang YiZheng BoGuo FangshenZhen WenruiZhao ZiyueLei KeyuanZhang ChenjieZhang CaiZhang YushuZhang BingkunMa Yanbo - Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive form of metabolic dysfunction-associated steatotic liver disease with limited pharmacological treatment options. Wogonoside (WOG), a flavonoid isolated from Scutellaria baicalensis, exhibits anti-inflammatory, antioxidant, and lipid-lowering activities; however, its effects and underlying mechanisms in MASH remain unclear. - Source: PubMed
Publication date: 2026/08/07
Wang DaopingMou YuWu XuemeiWang HongjiWang QianjunRao QingHu EnmingLi QingZheng XiuyanHuang Lei - Dysregulation of brain cholesterol homeostasis is increasingly recognized as a critical driver of Alzheimer's disease (AD) pathogenesis. G protein-coupled receptor 146 (GPR146) has emerged as a pivotal regulator of systemic cholesterol metabolism; however, its role in the central nervous system and AD remains elusive. Here, we report that GPR146 deficiency in mice modulates ERK/PKA signaling without affecting baseline physiology or general behavior. Following intracerebroventricular (i.c.v.) injection of amyloid-β (Aβ)42 oligomers, GPR146 was associated with altered Aβ42-evoked ERK/PKA/Akt signaling both in vivo and in vitro. Mechanistically, Gpr146 ablation potentiated microglial Aβ phagocytosis, which correlated with the transcriptional upregulation of phagocytic receptors, including TREM2, GPR34, P2Y6, and CR3, alongside increased expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). Moreover, GPR146 deficiency was linked to elevated levels of blood-brain barrier (BBB)-associated markers Cldn-5 and Glut-1 protein levels, while attenuating Aβ‑induced inflammatory responses in brain endothelial cells. At the metabolic level, GPR146 knockout modulated the expression of key enzymes governing glucose (GLUT1, GLUT3, G6PD, PFK, HK) and lipid (HMGCS1, ACACA, FASN, SCD1) metabolism and markedly reduced Aβ‑elicited lipid droplet accumulation in the cortex and hippocampus. Collectively, our findings establish GPR146 as a novel neurometabolic regulator whose deficiency correlates with enhanced Aβ phagocytosis, maintenance of BBB-associated proteins, and altered cerebral metabolism, thereby presenting a potential therapeutic axis for early AD intervention. - Source: PubMed
Publication date: 2026/08/05
Yang ShaobinLi YanhongGuo YanlingLi YumengLi MeiqiLi HongxiaZhang Yimeng