mTOR Polyclonal Antibody
- Known as:
- Mammalian target on rapamycin Polyclonal Antibody
- Catalog number:
- A-0422-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- mTOR Polyclonal Antibody
Related genes to: mTOR Polyclonal 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 Polyclonal Antibody
Related articles to: mTOR Polyclonal Antibody
- A prospective observational study has shown that intrapancreatic fat deposition (IPFD) increases pancreatic ductal adenocarcinoma (PDAC) risk; however, the underlying mechanisms remain unclear. In this study, we established a C57BL/6J mouse model of IPFD by feeding them Gubra Amylin NASH (GAN), a high-fat diet, to evaluate the effect of IPFD on PDAC. Mice in the GAN 30-week group exhibited significantly higher IPFD than controls. RNA sequencing of pancreatic tissue from this group revealed increased fatty acid-binding protein (FABP) 5 and MKI67 expression, along with an upregulation of the JAK/STAT, PI3K/AKT/mTOR, and Ras/Raf/MEK/ERK signaling pathways. In a syngeneic orthotopic PDAC mouse model using KPC cells, mice fed a GAN diet showed rapid tumor growth, a high incidence of liver metastasis, and intraperitoneal dissemination. In vitro, FABP5 promoted PDAC cell proliferation and migration by upregulating RAC1, a Rho family small GTPase associated with cellular movement. Inhibition of FABP5 using BMS-309,403 suppressed syngeneic KPC subcutaneous tumor growth without serious side effects. Conclusively, this study demonstrates that high IPFD enhances PDAC carcinogenesis, growth, and metastasis with enrollment of FABP5 upregulation, indicating that FABP5 inhibition may represent a potential therapeutic strategy for PDAC. - Source: PubMed
Publication date: 2026/06/06
Hamamoto KaoriShinoda ShuheiSuenaga ShigeyukiMatsumoto ToshihikoYamamoto NaokiNakamura NaohikoHamada ShinMasamune AtsushiYamamoto MasatoTakami Taro - Individual growth heterogeneity in Litopenaeus vannamei severely constrains aquaculture uniformity and yield, yet the systemic cellular regulatory mechanisms underlying this phenomenon remain elusive. Here, we combined scRNA-seq and weighted gene co-expression network analysis (WGCNA) to systematically compare hemocyte profiles between fast-growing (FG) and slow-growing (SG) groups, to elucidate the cellular and molecular basis of the "growth-immunity trade-off." We identified six major hemocyte clusters and reconstructed a continuous differentiation trajectory spanning from progenitor-like cells (Cluster 5/0) through a high-metabolic biosynthetic transition state (Cluster 1/3) to mature immune effectors (Cluster 2/4). Pseudotime analysis indicated divergent hemocyte distribution patterns between the two groups: FG hemocytes were predominantly enriched near the trajectory origin (Cluster 5), a population characterized by high expression of tissue development-related genes. In contrast, cells from the SG group were shifted toward the intermediate and terminal stages, showing specific enrichment in the energy-demanding "biosynthetic" subpopulation (Cluster 3). Differential expression analysis showed that Cluster 3 cells in the SG group significantly upregulated mitochondrial complex I subunit (Ndufs3), oxidative phosphorylation, the TCA cycle, and ribosome pathways, exhibiting typical characteristics of high immuno-metabolism. WGCNA further uncovered the upstream regulatory networks driving this trade-off: the FG group systematically activated the dark-orange module (centered on IRS1 and CCND1), which synergistically maintains progenitor reserves via mTOR and insulin signaling. Conversely, the SG group showed higher activity of the turquoise module, characterized by aminoacyl-tRNA biosynthesis and the expression of the antimicrobial peptide Crustin in progenitor-like cells, suggesting a stress-associated immune activation state. These findings suggest that slow growth may be associated with a transcriptomic shift from progenitor-like states toward energetically demanding immune-related states, providing a cellular hypothesis for the growth-immunity trade-off in L. vannamei. These findings provide a novel cellular perspective on crustacean growth traits and identify key molecular targets for breeding superior strains that balance disease resistance and growth. - Source: PubMed
Publication date: 2026/06/05
Niu PanpanJiang ShanshanTian CaijuanZhong HaoLiu MianyuKong JieLuan ShengMeng XianhongXing QunLuo KunGao Huan - Immobilization induces skeletal muscle atrophy by disrupting muscle protein homeostasis, leading to progressive loss of muscle mass and function. Shikimic acid (SA), a plant-derived organic acid with anti-inflammatory and antioxidant properties, has not been previously evaluated in immobilization-associated muscle atrophy. This study aimed to determine whether SA attenuates skeletal muscle atrophy by regulating inflammation and muscle protein turnover using cellular and animal models. In tumor necrosis factor-alpha (TNFα)-induced L6 myotubes, SA significantly suppressed inflammatory cytokine expression through inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling and attenuated forkhead box O3a (FoxO3a)-dependent protein degradation, while restoring protein kinase B (Akt)/mechanistic target of rapamycin (mTOR)-dependent anabolic signaling to promote myogenic differentiation and protein synthesis. In an immobilization-induced muscle atrophy model in mice, SA administration prevented declines in grip strength and exercise capacity and preserved skeletal muscle mass and myofiber cross-sectional area. At the molecular level, SA alleviated inflammatory responses and restored the imbalance between protein synthesis and degradation in the tibialis anterior muscle. Furthermore, molecular docking analysis revealed that SA interacts with the activation pocket of phosphoinositide 3-kinase (PI3K), providing structural insight into the mechanism of anabolic signaling reactivation. Collectively, these findings demonstrate that SA mitigates immobilization-induced skeletal muscle atrophy by suppressing NF-κB-mediated inflammatory signaling and restoring muscle protein turnover through reactivation of the PI3K/Akt/mTOR signaling pathway, highlighting its potential as a functional compound for preserving skeletal muscle health under immobilization conditions. - Source: PubMed
Publication date: 2026/06/05
Kim Mi-BoYoo JiheeMoon Chae YoungHwang Jae-KwanKang Hyunju - Accumulating evidence indicates that diabetes is associated with increased risk of several cancers. The strongest evidence has been reported for cancers of the breast, colorectum, endometrium, liver, pancreas, and gallbladder. However, distinguishing causal relationships from associations driven by shared risk factors such as obesity, aging, and lifestyle behaviors remains challenging. Several biological mechanisms have been proposed to explain these associations. Key pathways include the effects of insulin resistance and compensatory hyperinsulinemia on mitogenic signaling pathways, including PI3K/AKT/mTOR and MAPK, as well as the influence of adiposity, chronic inflammation, and altered metabolic substrates on tumor initiation and progression. Hyperglycemia may also contribute by promoting tumor metabolism and cellular proliferation, although its independent contribution remains debated. These mechanisms likely interact to create a protumorigenic metabolic environment in individuals with diabetes. Obesity, which frequently co-occurs with diabetes, further amplifies these risks through altered adipokine secretion and increased estrogen production, highlighting the interrelated contributions of metabolic and hormonal factors. The relationship between diabetes and cancer has important clinical implications. Diabetes has been associated with worse cancer prognosis and higher cancer-related mortality, highlighting the importance of integrated management strategies. The impact of antihyperglycemic therapy on cancer risk and progression has been extensively studied, and ongoing research continues to evaluate potential protective or tumor-modifying effects. In this article, we summarize the epidemiologic and pathophysiologic evidence describing the relationship between diabetes and cancer and discuss strategies for risk mitigation, screening, and management. - Source: PubMed
Publication date: 2026/06/06
Lipscombe Lorraine LAli SameenLega Iliana C - This study aims to investigate the mechanism by which extract of Dendrobium officinale leaves (EDL) extends the lifespan of Caenorhabditis elegans. Untargeted metabolomics and network pharmacology analyses revealed that EDL primarily contains active components such as fatty acids, flavonoids, and polyphenols, which are predicted to potentially modulate pathways including MAPK, AMPK, mTOR, and longevity-related signaling pathways. Experimental results showed that 2 mg/mL EDL significantly extended the mean lifespan of nematodes by 11.4%, enhanced pharyngeal pumping rate and muscular endurance, but reduced brood size. EDL treatment also significantly decreased lipid droplet accumulation, cell apoptosis, and lipofuscin levels. Transcriptomic analysis indicated that EDL regulated the expression of multiple genes related to energy metabolism, particularly activating longevity-regulating pathways and the AMPK signaling pathway. RT-qPCR results demonstrated that EDL significantly increased the mRNA level of sod-3 in C.elegans. In conclusion, EDL may upregulate the expression of the sod-3 gene via the DAF-16/SOD-3 axis, thereby extending lifespan in C. elegans, providing a scientific basis for the high-value utilization of Dendrobium officinale leaves. - Source: PubMed
Publication date: 2026/06/06
Gong ChengFeng ShuChen YuanfengLuo HuiqingZhou SiyuZhao ShikuanZhou RuiFeng LiGe YunfeiYang RuijuanFang ChongyeDu Xiaocui