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
- Inflammaging refers to chronic low‑grade inflammation that develops with age and promotes multiple age‑related diseases. It arises from the close crosstalk between metabolic disturbance and inflammation, yet how this coupling acts across tissues remains poorly understood. As a hallmark of aging, sarcopenia often coincides with metabolic‑inflammatory dysfunction in the gut, liver, and adipose tissue, all tied together by insulin resistance (IR). In this review, we systematically examine the pathophysiological basis of the "metabolic-inflammatory axis" during aging, clarifying its conceptual boundaries with related terms such as "inflammaging," "immunometabolism," and "metabolic inflammation." We delineate the roles of three core molecular modules-nutrient sensing pathways (AMP‑activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR)), mitochondrial stress (mitochondrial reactive oxygen species (mtROS)-p53), and epigenetic regulation (acetyl‑Coenzyme A (AcCoA)-histone acetyltransferase (HAT))-in mediating metabolic-inflammatory coupling. Using sarcopenia as a clinical anchor, we construct a tissue-specific atlas of the metabolic-inflammatory axis and elucidate the principles of organ crosstalk-and its mediators-within the gut-liver-adipose-muscle (GLAM) core axis. We then summarize current intervention strategies stratified by evidence level and identify knowledge gaps and future research directions. This review establishes a mechanistic link between molecular pathways and age-related multi-organ dysfunction, supporting a paradigm shift from single-disease management to multi-system healthspan interventions in aging. - Source: PubMed
Publication date: 2026/04/13
Liang Tian - Glucocorticoid-induced skeletal muscle atrophy is characterized by progressive loss of muscle mass and function, yet effective pharmacological interventions remain limited. Prostaglandin E (PGE) plays an important role in maintaining muscle regeneration, and its degradation is primarily controlled by 15-hydroxyprostaglandin dehydrogenase (15-PGDH). Here we investigated whether phillyrin, a natural lignan compound, protects against dexamethasone (DEX)-induced muscle atrophy in mice. Phillyrin treatment significantly attenuated DEX-induced reductions in muscle mass and improved grip strength and motor endurance. Histological analysis showed that phillyrin alleviated myofiber atrophy and preserved mitochondrial ultrastructure. Mechanistically, phillyrin suppressed the upregulation of 15-PGDH and restored intramuscular PGE levels, accompanied by recovery of EP4 signaling. These changes were associated with inhibition of FOXO3a-mediated proteolysis and partial restoration of mTOR and PGC-1α signaling in skeletal muscle. Collectively, these findings indicate that phillyrin protects against glucocorticoid-induced muscle atrophy, potentially through modulation of the 15-PGDH/PGE pathway. These findings suggest that phillyrin may represent a potential therapeutic candidate for the treatment of glucocorticoid-induced skeletal muscle atrophy. - Source: PubMed
Publication date: 2026/04/08
Liu Jin-ChanYang Ren-JuLiu Ya-WenHe Fei - Hepatic fibrosis, a hallmark of chronic liver diseases, arises from persistent activation of hepatic stellate cells (HSCs). Golgi protein 73 (GP73) is a recognized fibrosis biomarker, yet its active role in driving fibrogenesis and the underlying molecular mechanisms remain poorly defined. Using wild-type, GP73 knockout, and knock-in mouse models, we demonstrate that GP73 expression is not merely a marker but a key functional modulator of fibrotic progression, correlates strongly with fibrosis severity. While these genetic models do not develop spontaneous hepatic fibrosis under basal conditions-notwithstanding the potential metabolic roles of GP73-our results demonstrate that GP73 expression levels significantly dictate the severity of CCl-induced fibrotic progression. Mechanistically, endogenous co-immunoprecipitation (Co-IP) revealed that GP73 physically interacts with TGF-β receptor 1 (TGFBR1), mTOR, and the recycling endosome marker Rab11. GP73 enhances HSC activation by amplifying TGF-β and mTOR signaling through the inhibition of key fibrotic factors' degradation, such as TGFBR1 and mTOR. Protein half-life and rescue experiments confirmed that GP73 prevents the lysosomal degradation of TGFBR1 and mTOR; notably, re-introducing GP73 into knockdown cells successfully restored receptor stability and downstream signaling. Furthermore, pharmacological disruption of endocytic trafficking with Brefeldin A (BFA) abolished the protective effect of GP73, leading to accelerated receptor degradation. Suppressing GP73 reduced HSC activation and attenuated collagen deposition in vivo. Our findings identify GP73 as a molecular scaffold that reroutes fibrotic signaling complexes into the recycling pathway and away from degradation. Consequently, our results position GP73-mediated endocytic recycling as a potential therapeutic target and a viable adjunctive strategy for managing chronic liver diseases. - Source: PubMed
Publication date: 2026/04/17
Guo YueLiu Meng-YuanMo Yun-QiWan Lin-YanWang Ya-NanWang Sheng-YongNi Yi-RanLi Zhi-YingWang YingWang Xiao-LianMa LanZhang Rui-TaoZhang Yan-QiongLiu Chang-BaiZhang Hong-BingLi Bo-TaoWu Jiang-Feng - Resina Draconis is a prestigious traditional Chinese medicine agent used to invigorate blood and resolve stasis. In traditional theory, malignancies are often characterized by severe blood stasis and pathological accumulation ("Zhengjia"). Thus, its traditional stasis-resolving efficacy offers a rationale for cancer therapy. - Source: PubMed
Publication date: 2026/04/16
Du WeiPeng Xi-YuanLi WeiAttiq Ur-RehmanGe Meng-WeiShen Lu-TingFeng RuiZhong KangGao Si-QiChen Hong-Lin - Mitochondrial translation is crucial for maintaining cellular respiration, energy balance, calcium signaling, apoptosis, immune surveillance, and the regulation of inflammatory responses. This specialized process, involving mitochondrial rRNAs, tRNAs, mitoribosomes, and nuclear-encoded translation factors, ensures the synthesis of mitochondrially encoded proteins that support oxidative phosphorylation. The mitochondrial translation cycle is tightly regulated by RNA-binding proteins, mitochondrial unfolded protein response, and stress-responsive pathways such as mTOR, particularly during metabolic shifts and immune activation. Emerging evidence highlights mitochondrial translation as a critical modulator of inflammation. In this review, we describe the alteration in mitochondrial-specific translation dynamics in immune cells, its adaptation to stress, and its interplay with organelle-wide signaling via mito-nuclear and mito-cytosolic communication. We focus on the alterations in mitochondrial translation machinery including mitoribosomal proteins, rRNA, tRNA synthetases or other regulatory factors linked to inflammatory diseases, including neurodegeneration, IBD, metabolic and cardiovascular disorders. We further examine how mitochondrial translation influences immune responses through mitochondrial DNA/RNA release, activation of mitochondrial damage-associated molecular patterns, and inflammasomes such as NLRP3. Collectively, mitochondrial translation functions as an immune centric-checkpoint that presents promising therapeutic target for intervention in inflammation-driven diseases. - Source: PubMed
Publication date: 2026/04/16
Basu SwarnaliKhan RuksharSharma ShivaPrajapati PriyankaAmmanathan VeenaRungta SumitLahiri Amit