MTOR (phospho-Ser2448) Antibody
- Known as:
- MTOR (phosphorilated-Ser2448) Antibody
- Catalog number:
- abx000164
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- MTOR (phospho-Ser2448) Antibody
Related genes to: MTOR (phospho-Ser2448) Antibody
- Gene:
- MTOR NIH gene
- Name:
- mechanistic target of rapamycin kinase
- Previous symbol:
- FRAP, FRAP2, FRAP1
- Synonyms:
- RAFT1, RAPT1, FLJ44809
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 1995-07-18
- Date modifiied:
- 2019-04-23
Related products to: MTOR (phospho-Ser2448) Antibody
Related articles to: MTOR (phospho-Ser2448) Antibody
- To what extent and via what mechanism does the concomitant administration of rapamycin (a follicle activation pathway inhibitor and antitumour agent) and cyclophosphamide (a highly toxic ovarian anticancer agent) prevent cyclophosphamide-induced ovarian reserve loss and inhibit tumour proliferation in a breast cancer xenograft mouse model? - Source: PubMed
Publication date: 2024/05/11
Tanaka YujiAmano TsukuruNakamura AkikoYoshino FumiTakebayashi AkieTakahashi AkimasaYamanaka HiroyukiInatomi AyakoHanada TetsuroYoneoka YutakaTsuji ShunichiroMurakami Takashi - Vitiligo is a common autoimmune skin disease. Capsaicin has been found to exert a positive effect on vitiligo treatment, and mesenchymal stem cells (MSCs) are also confirmed to be an ideal cell type. This study aimed to explore the influence of capsaicin combined with stem cells on the treatment of vitiligo and to confirm the molecular mechanism of capsaicin combined with stem cells in treating vitiligo. - Source: PubMed
Publication date: 2024/05/11
Wu YifeiWang XiaochuanZhang JiayuDu ShaWang ZhiqiongLi JinrongZhang WenheXiang JieLi RenfuLiu JingBi Xin - - Source: PubMed
Publication date: 2024/05/10
Zhang GangHuang ChaoWang RenGuo JiangrongQin YongLv Songcen - Impairment of the insulin signaling pathway is a key contributor to insulin resistance under arsenic exposure. Specifically, O-GlcNAcylation, an important post-translational modification, plays a crucial role in insulin resistance. Nevertheless, the concrete effect and mechanism of O-GlcNAcylation in arsenic-induced impairment of the insulin signaling pathway remain elusive. Herein, C57BL/6 mice were continuously fed arsenic-containing food, with a total arsenic concentration of 30mg/kg. We observed that the IRS/Akt/GSK-3β insulin signaling pathway was impaired, and autophagy was activated in mouse livers and HepG2 cells exposed to arsenic. Additionally, O-GlcNAcylation expression in mouse livers and HepG2 cells was elevated, and the key O-GlcNAcylation homeostasis enzyme, O-GlcNAc transferase (OGT), was upregulated. In vitro, non-targeted metabolomic analysis showed that metabolic disorder was induced, and inhibition of O-GlcNAcylation restored the metabolic profile of HepG2 cells exposed to arsenic. In addition, we found that the compromised insulin signaling pathway was dependent on AMPK activation. Inhibition of AMPK mitigated autophagy activation and impairment of insulin signaling pathway under arsenic exposure. Furthermore, down-regulation of O-GlcNAcylation inhibited AMPK activation, thereby suppressing autophagy activation, and improving the impaired insulin signaling pathway. Collectively, our findings indicate that arsenic can impair the insulin signaling pathway by regulating O-GlcNAcylation homeostasis. Importantly, O-GlcNAcylation inhibition alleviated the impaired insulin signaling pathway by suppressing the AMPK/mTOR-autophagy pathway. This indicates that regulating O-GlcNAcylation may be a potential intervention for the impaired insulin signaling pathway induced by arsenic. - Source: PubMed
Publication date: 2024/05/09
Zhang WenxinZeng ShuxianHuang JieliangTian XianbingWu JiegenGuo LianxianLiang Yi - Monocytes (Mos) are crucial in the evolution of metabolic dysfunction-associated steatotic liver disease (MASLD) to metabolic dysfunction-associated steatohepatitis (MASH), and immunometabolism studies have recently suggested targeting leukocyte bioenergetics in inflammatory diseases. Here, we reveal a peculiar bioenergetic phenotype in circulating Mos of patients with MASH, characterized by high levels of glycolysis and mitochondrial (mt) respiration. The enhancement of mt respiratory chain activity, especially complex II (succinate dehydrogenase [SDH]), is unbalanced toward the production of reactive oxygen species (ROS) and is sustained at the transcriptional level with the involvement of the AMPK-mTOR-PGC-1α axis. The modulation of mt activity with dimethyl malonate (DMM), an SDH inhibitor, restores the metabolic profile and almost abrogates cytokine production. Analysis of a public single-cell RNA sequencing (scRNA-seq) dataset confirms that in murine models of MASH, liver Mo-derived macrophages exhibit an upregulation of mt and glycolytic energy pathways. Accordingly, the DMM injection in MASH mice contrasts Mo infiltration and macrophagic enrichment, suggesting immunometabolism as a potential target in MASH. - Source: PubMed
Publication date: 2024/05/07
Sangineto MorisCiarnelli MartinaColangelo TommasoMoola ArchanaBukke Vidyasagar NaikDuda LorenVillani RosannaRomano AntoninoGiandomenico StefaniaKanwal HinaServiddio Gaetano