Ask about this productRelated genes to: mTOR 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 antibody
Related articles to: mTOR antibody
- Reduced response to targeted therapy in human epidermal growth factor receptor 2 (HER2)-positive breast cancer underscores the need for novel therapeutic strategies and molecular targets. Cluster of differentiation 24 (CD24), an oncogenic molecule closely associated with aggressive tumor phenotypes, was investigated for its expression in HER2-positive breast cancer and its potential as a candidate target for combination therapy. - Source: PubMed
Publication date: 2026/05/16
Lu YiZhou XingluGao YueZhu ZiDeng BaoLv WubinFu ZhenkunDing HeZhong Lei - Thioredoxin-interacting protein (TXNIP) critically regulates cellular redox homeostasis. It drives multi-organ fibrosis by integrating oxidative stress, inflammation, metabolic dysregulation, and autophagic dysfunction. TXNIP contributes to organ-specific fibrotic responses in the liver, kidney, heart, and lung through multiple core signaling pathways, including the NLRP3 inflammasome, TGF-β1/Smad, NF-κB, and mTOR cascades. Notably, TXNIP exhibits cell- and organ-specific dual regulatory characteristics during fibrogenesis, adding further complexity to its mechanistic involvement. In recent years, targeting TXNIP has emerged as a promising strategy in anti-fibrotic research. Clinically relevant small-molecule drugs, natural products and bioactive components of traditional Chinese medicine, as well as emerging precision technologies such as epigenetic modulation and exosome-based delivery systems, have demonstrated significant anti-fibrotic potential by modulating TXNIP expression and its downstream signaling networks. This review systematically summarizes recent advances in understanding the role of TXNIP in multi-organ fibrosis, with a focus on its core molecular mechanisms and organ-specific functions. It also explores current therapeutic strategies targeting TXNIP and discusses future research directions, summarize current insights that may inform future research into TXNIP-centered anti-fibrotic strategies. - Source: PubMed
Publication date: 2026/05/14
Li DandanShi LingchangLiu ChuweiLiao QianhuiWu WeiyuChen ShuangshuangTang QunWen LixiangMeng Bin - Excessive dietary fructose intake is gradually recognised to exacerbate intestinal inflammation in Ulcerative Colitis (UC) through disruption of epithelial barrier integrity and microbial dysbiosis, resulting in hyper immune activation. Inflammation in UC is generally linked with PI3K/Akt/mTOR pathway activation; however, the underlying molecular mechanisms behind fructose-mediated immune hyper-activation remains incompletely understood. Hence, this study is aimed to investigate the role of phosphatidylinositol-4-phosphate 5-kinases (PIP5Ks), a probable upstream regulator of PI3K, in high-fructose diet-induced colonic inflammation. In vitro and in vivo models of high fructose exposure were employed to evaluate the expression and functional role of PIP5Ks through pharmacological inhibition using ISA 2011B (PIP5K1A inhibitor) and IITZ01 (PIP5K1B inhibitor). Inflammatory responses, epithelial integrity, and disease severity were assessed using molecular, histological, and clinical indices in the high fructose + DSS induced UC in rodent model. High fructose exposure enhanced PIP5K expression, leading to increased levels of phosphatidylinositol 4,5-bisphosphate (PIP2), a key substrate for PI3K. This activation triggered downstream signalling that amplified inflammatory responses and compromised epithelial barrier function. Inhibition of PIP5Ks markedly attenuated fructose-induced inflammation in both cellular and animal models. Notably, IITZ01 demonstrated superior efficacy compared to ISA 2011B, as evidenced by improved disease activity index, restored epithelial structure, and reduced inflammatory burden. Collectively, our findings identify PIP5Ks as a critical mediator of fructose-induced intestinal inflammation and establish the PIP5K-PI3K signalling axis as a key regulator of macrophage activation and epithelial dysfunction. Targeting PIP5Ks may represent a promising therapeutic strategy for the management of UC. - Source: PubMed
Publication date: 2026/05/15
Rajdev BishalKundu SnehashisPanja PallabiMandal ArijitN P SyamprasadJain SiddhiGangasani Jagadeesh KumarNaidu V G M - Diabetes is known to cause severe disruptions in metabolic and reproductive health, often leading to testicular dysfunction and impaired fertility. - Source: PubMed
Publication date: 2026/05/12
Elmorsy Ekramy MAl-Ghafari Ayat BAl Doghaither Huda AJan MuhammadShah Syed Sajid HussainSyed AsmaraMarghani Basma HElshopakey Gehad E - Cellular metabolism is precisely regulated in response to nutrient availability. As an extremely energy-consuming anabolic process, ribosome biogenesis should be tightly controlled in response to nutrient supply. However, how the nucleolus responds to different nutrient statuses remains poorly understood. Here, we show that C7orf50 is a nucleolus-localized protein and functions as a coordinator between ribosome biogenesis and autophagy, acting as what we term a "nutrient-responding nucleolar factor." C7orf50 undergoes reversible nucleolus-nucleoplasm translocation in response to nutrient deprivation and supply, with its nucleolus and nucleoplasm location dictating ribosome biogenesis and autophagic augmentation, respectively. The location-dependent function of C7orf50 is determined by acetylation at the lysine-71/lysine-72/lysine-76 residues by N-alpha-acetyltransferase 10, a substrate of mammalian target of rapamycin and a nutritional status-responsive acetyltransferase. In vivo and in vitro assays show that C7orf50 acts as an oncoprotein that promotes tumor growth. Our findings reveal a nucleolus-localized coordinating mechanism for the regulation of anabolism and catabolism transition by nutrient status. - Source: PubMed
Publication date: 2026/05/15
Sun JingyuYang MeiLi QianLiang JiaweiFeng HaipingGao LijieWang YunLiu HongmeiGuo CaixiaTang Tie-Shan