mTOR polyclonal
- Known as:
- Mammalian target on rapamycin pab
- Catalog number:
- ASA905687100
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- mTOR polyclonal
Related genes to: mTOR polyclonal
- 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 polyclonal
Related articles to: mTOR polyclonal
- Obesity is prevalent and linked to cognitive impairment via hippocampal atrophy and insulin resistance. Here, we investigated whether the primary catechin of green tea, epigallocatechin‑3‑gallate (EGCG), could attenuate this neuropathology. Epidemiological analysis of UK Biobank adults with obesity provided an initial clue, showing a positive linear trend between green tea intake and hippocampal volume (p = 0.07). To elucidate the underlying mechanisms, we administered a human‑achievable dose of EGCG (50 mg/kg) to high‑fat diet-fed mice. EGCG treatment significantly reduced body weight and inflammatory signaling while improving insulin sensitivity, attenuating hippocampal atrophy, and mitigating cognitive deficits. Mechanistically, EGCG rescued synaptic structural integrity by suppressing the pro-inflammatory JNK pathway, restoring hippocampal insulin signaling (IRS1/Akt), and stimulating neuronal autophagy through the AMPK/mTOR/ULK1 axis. Together, these data provide translational evidence that EGCG counteracts obesity-linked neurodegeneration by linking metabolic health to hippocampal integrity through the inflammation-insulin-autophagy axis, motivating dietary trials to mitigate cognitive impairment. - Source: PubMed
Publication date: 2026/06/04
Huang KunyiLi XinChen YujieQi YiyunZhang WeiyingTan Jia EeChan Jia YingLu JiashuoHao FangyiShi JiayiYan ShutingHuang ZhenzhenWu XiaojunXu QiMa Zhiwei - Pancreatic cancer (PC) remains a major therapeutic challenge because of its profound plasticity and adaptability. Although our previous studies established that calreticulin (CRT) promotes epithelial-mesenchymal transition (EMT), its role in linking endoplasmic reticulum stress (ERS), autophagy-associated responses, and tumor cell plasticity has remained incompletely defined. The functional role of CRT was examined using in vitro and in vivo PC models, together with CRISPR/Cas9-mediated gene silencing, overexpression approaches, and pharmacological modulation of ERS and autophagy. Clinical relevance was evaluated in human PC specimens and correlated with patient survival. Thapsigargin-induced ERS activated autophagy-associated signaling through the PERK/eIF2α-ATG5/ATG12/LC3B axis and promoted EMT in a CRT-dependent manner. Under serum-free conditions, CRT was required for AMPK/mTOR/ULK1-associated autophagy activation and stemness-associated traits. Mechanistically, CRT interacted with LC3 through a conserved LC3-interacting region (LIR; WDFL), and this interaction contributed to stress-associated autophagy and malignant phenotypes. Furthermore, GATA6 was identified as a direct transcriptional activator of CRT, defining a GATA6-CRT regulatory axis. In vivo, targeting this axis through CRT silencing or autophagy inhibition by chloroquine or ATG5 knockdown suppressed tumor growth and metastasis. Clinically, high CRT expression was associated with GATA6, LC3B, and markers linked to stemness and EMT, as well as poor prognosis. Together, these findings support a model in which the GATA6-CRT axis functions as an important stress-responsive regulator associated with autophagy, phenotypic plasticity, and aggressiveness in PC, and nominate this axis as a potential therapeutic vulnerability while highlighting the need for further work to define its full mechanistic scope. - Source: PubMed
Publication date: 2026/06/04
Wang Ming-QingLiu YangChan Bo-YuanWu Hong-JiaZhang Wan-XiangWang Zhong-YangGeng Qi-LongChang Run-XinWang WeijieZhang Shu-YuanZu Fu-QiangCao GuodongRenz Bernhard WTang Jing-TongWang Hua-QinSheng Weiwei - - Source: PubMed
Publication date: 2026/06/04
Bian PengHu WeiLiu ChuanLi Liang - This study aimed to conduct an in vitro assessment of the concentration- and time-dependent cytotoxic effects of cetalkonium chloride (CKC), a preservative used in ophthalmic preparations, on human corneal keratocytes and to investigate its underlying cellular mechanisms of toxicity. Primary human corneal keratocytes were treated with a range of CKC concentrations (0 to 4.0 × 10% w/v) for up to 72 h, after which cell viability, intracellular reactive oxygen species (ROS) production, mitochondrial integrity, and the expression of key proteins in cell survival and apoptosis pathways were analyzed. The results showed that CKC induced a significant, concentration- and time-dependent reduction in keratocyte viability and a dose-dependent increase in ROS production. CKC exposure also led to the collapse of the mitochondrial network, cell shrinkage. Mechanistically, CKC suppressed the phosphorylation of pro-survival proteins Akt, mTOR, and ERK, while increasing the pro-apoptotic BAX/Bcl-xL ratio. In conclusion, CKC exhibits toxicity to keratocytes through mechanisms involving increased ROS, mitochondrial damage, cell membrane damage, and alterations of key survival/apoptosis signaling pathways. These findings provide a critical basis for defining safe concentration limits for CKC, guiding the development of ophthalmic preservative systems that minimize stromal keratocyte damage. - Source: PubMed
Publication date: 2026/06/03
Son YengwooPark Joo-HeePark Choul Yong - This study investigated the impact of a high-carbohydrate diet (HC: 25% carbohydrate) on skin wound healing in turbot versus a control diet (CC: 16% carbohydrate). Following 10 weeks of triple replicates of fish (n = 40), standardized 8 mm skin wounds were created and healing assessed macroscopically and molecularly at baseline, 1, 3, and 7 days post-wounding (dpw). While growth performance remained unaffected, HC-fed fish exhibited persistent hyperglycemia and hyperinsulinemia, indicative of systemic insulin resistance. Macroscopic analysis showed significantly impaired wound contraction in the HC group at 3 and 7 dpw compared to CC controls. Histological assessment revealed defective re-epithelialization characterized by aberrant keratinocyte migration, suppressed provisional matrix formation, ill-defined epidermal stratification, and persistent goblet cell aggregation in HC fish. Molecular analyses demonstrated HC-mediated suppression of re-epithelialization markers (suppressed MMP9, EGF, FGF2, and KRT2 gene expression; reduced MMP9 protein distribution), dysregulated inflammation (reduced MPO and NAG activity; lower IL1B, IL6, IL8, TGFB1, and TNF expression; elevated IL10 expression), and impaired tissue form ation and remodelling (downregulated FN1, VEGF, CCN1, LAMB2, and COL1A mRNA; reduced collagen deposition; attenuated CD31-based angiogenesis). Importantly, HC feeding promoted skin AGEs accumulation, which was accompanied by reduced MTOR phosphorylation, decreased HIF1A protein levels, and blunted post-wounding induction of glycolytic genes, including PFK, HK2, and PK. Collectively, these findings indicate that HC feeding compromises multiple phases of skin wound healing in turbot and suggest that AGE-associated suppression of MTOR-HIF1A-mediated glycolytic adaptation is an important metabolic mechanism associated with delayed healing. - Source: PubMed
Publication date: 2026/06/03
Chen ZhichuLi YuantingFang YuanyuanHuang DongÁngeles Esteban MariaChen XinhuaZhang Yanjiao