TFEB antibody - middle region (P100809_P050)
- Known as:
- TFEB (anti-) - middle region (P100809_P050)
- Catalog number:
- p100809_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TFEB antibody - middle region (P100809_P050)
Related genes to: TFEB antibody - middle region (P100809_P050)
- Gene:
- TFEB NIH gene
- Name:
- transcription factor EB
- Previous symbol:
- -
- Synonyms:
- TCFEB, bHLHe35
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-20
- Date modifiied:
- 2016-10-05
Related products to: TFEB antibody - middle region (P100809_P050)
Related articles to: TFEB antibody - middle region (P100809_P050)
- Extracellular vesicles (EVs) are emerging mediators of intercellular and interkingdom communication. While bacterial EVs directly modulate host health, whether exogenous vesicles can reprogram gut microbial vesiculation and bioactivity remains unclear. Using a defined conditioning system, ScEV exposure altered EV production by , generating ScEV-conditioned vesicles (ScEV-LrEVs). Comparative proteomics and lipidomics revealed extensive remodeling of vesicle cargo, including ~60-fold enrichment of hydroxylated ceramide Cer(t18:0/24:0(2OH)) in ScEV-LrEVs. Functionally, ScEV-LrEVs showed enhanced anti-inflammatory activity in LPS-stimulated macrophages, accompanied by improved lysosomal function and coordinated changes in mTOR-TFEB-related lysosome-autophagy markers. In a DSS-induced colitis model, ScEV-LrEVs alleviated mucosal injury, reduced immune-cell infiltration, and reinforced epithelial barrier integrity, accompanied by restoration of lysosomal function and coordinated changes in mTOR-TFEB-related markers. Ceramide-enriched EVs partially recapitulated the anti-inflammatory and lysosome-restorative activity of ScEV-LrEVs. Together, these findings uncover a cross-kingdom vesicle communication axis whereby fungal EV exposure remodels the molecular and functional properties of gut microbial vesicles, accompanied by enhanced lysosomal homeostasis and protection against intestinal inflammation. - Source: PubMed
Publication date: 2026/09/19
Ji ZhengmeiChen GuoliangHe XiaolongZhang XiangqianChen BinXiao HangGuo YurongHan Yanhui - Nobiletin (NOB), a naturally occurring polymethoxyflavone enriched in Citri Reticulatae Pericarpium-the dried peel of mature citrus fruit-has attracted increasing attention because of its multi-target pharmacological activities. This study explored the protective effects of NOB on diabetic nephropathy (DN), with a focus on TP53-associated PANoptosis and TFEB-related lysosomal and energy metabolic changes. - Source: PubMed
Publication date: 2026/09/04
Zhang BiweiLiu YiMa LeileiZhao YingjieDong YimingZhou ZhengqiTian ChunyuWang DongjunXu DingjieLa XiaojinChang HongHan RujieLi JiayuWu ChenxiLi Ji'an - Chemotherapy resistance is a key factor in tumor recurrence and mortality and a barrier to durable therapeutic effectiveness. Besides canonical mechanisms, including target alterations and drug efflux, tumor cells integrate chemotherapy-induced DNA damage, oxidative stress, and metabolic stress into persistent adaptive stress-response programs in which the autophagy-lysosomal pathway (ALP) plays a pivotal role. Transcription factor EB (TFEB), a master transcriptional regulator of the ALP, undergoes stress-responsive nuclear translocation under chemotherapeutic conditions through mechanistic target of rapamycin complex 1 (mTORC1) inhibition, lysosomal Ca-calcineurin-mediated dephosphorylation, and related signaling cascades. Nuclear TFEB activates the canonical coordinated lysosomal expression and regulation (CLEAR) network while also engaging broader context-dependent transcriptional programs. Within the autophagy-lysosomal system, CLEAR-dependent regulation promotes autophagosome biogenesis and maturation, autophagosome-lysosome fusion, and lysosomal biogenesis, resulting in enhanced autophagic flux. TFEB-driven enhancement of ALP flux generates multiple adaptive functional outputs, including clearance of damaged cellular substrates, buffering of reactive oxygen species (ROS), recycling of metabolic substrates to meet bioenergetic demands, modulation of cell death thresholds, and reduced effective intracellular drug exposure via lysosomal sequestration, storage, efflux, and intracellular redistribution. This review presents an integrated conceptual platform linking stress-induced TFEB activation, enhanced autophagic flux, downstream functional adaptations, and the emergence of chemotherapeutic resistance. By focusing on the TFEB-ALP axis, this review further identifies a stratified therapeutic intervention model comprising upstream suppression, intermediate pathway blockade, and downstream functional counteraction. These perspectives provide a more systematic and mechanistic understanding for developing precision strategies to overcome chemotherapy resistance by targeting the TFEB-ALP axis. - Source: PubMed
Publication date: 2026/09/18
Lu YueWang YuewenSun DayingQiao ZhangweiWang ZhengchaoSong ShuliangHou Junfeng - Nephrolithiasis-induced lipotoxicity is a critical driver of tubular cell death and renal function decline, yet targeted pharmacological interventions remain a major unmet clinical need. While Fatty Acid-Binding Protein 1 (FABP1) is widely recognized as a passive injury biomarker, its active functional role in buffering lipotoxicity during nephrolithiasis remains uncharacterized. By integrating clinical specimens from nephrolithiasis patients, AAV9-mediated kidney-specific Fabp1 knockdown murine models, and HK-2 cell lines, we delineated the FABP1 regulatory landscape using transcriptomic and untargeted metabolomic profiling. Furthermore, the core mechanistic interactions were definitively validated via Co-Immunoprecipitation (Co-IP) and PPRE-driven dual-luciferase reporter assays. FABP1 is significantly upregulated in nephrolithiasis. Mechanistically, crystal-induced lysosomal stress triggers Ca efflux, which activates the calcineurin pathway to drive TFEB nuclear translocation and subsequent FABP1 transcription. Crucially, FABP1 functions as an indispensable nuclear chaperone, physically engaging PPARγ to sustain its core transcriptional activity. FABP1 deficiency dismantles this defense, impairing protective lipid droplet biogenesis to sequester free fatty acids. This failure precipitates excessive 4-HNE accumulation, marked lipid peroxidation, TCA cycle collapse, a pronounced NF-κB-driven inflammatory storm, and ultimate renal functional deterioration. Importantly, targeted pharmacological activation of PPARγ utilizing rosiglitazone circumvents FABP1 depletion, rewiring global lipid and energetic fluxes to rescue tubular cell injury. Our findings redefine FABP1 from a passive clinical biomarker to an active homeostatic buffer. This study delineates the Ca/calcineurin-TFEB-FABP1-PPARγ axis as a vital defense mechanism against lipotoxicity, providing a compelling translational rationale for PPARγ-targeted metabolic interventions to treat nephrolithiasis. - Source: PubMed
He QiushiSong ZiyanJiang ZhiweiPan JianshanHou BingbingHuang QingfengXu YuexianHao Zongyao - Ischemic stroke triggers a mitochondrial metabolic crisis that propagates secondary injury through neuroimmune and neuron-intrinsic mechanisms. Within minutes, collapse of oxidative phosphorylation (OXPHOS) drives succinate accumulation; upon reperfusion, rapid succinate re-oxidation generates a burst of mitochondrial reactive oxygen species (ROS) via reverse electron transport, triggering neuroinflammation, blood-brain barrier disruption, and regulated neuronal death. Intermittent theta burst stimulation (iTBS), a time-efficient repetitive transcranial magnetic stimulation protocol, targets this crisis at a systems level. Preclinical evidence indicates that iTBS restores neurovascular integrity, reprograms microglial activation by suppressing the succinate/hypoxia-inducible factor-1α (HIF-1α)-driven Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB)/ NLR family pyrin domain-containing 3 (NLRP3) inflammasome cascade, and promotes a reparative immune microenvironment. We further propose that restoration of microglial OXPHOS may couple inflammatory resolution to enhanced synthesis of brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1), forming a metabolic bridge between immune resolution and neuronal survival-a connection assembled from independently supported components but not yet tested as an integrated pathway in the iTBS context. At the neuron-intrinsic level, iTBS suppresses apoptosis via miR-34c-5p/p53/Bax signaling, attenuates ferroptosis by restoring iron homeostasis and antioxidant capacity, and reinforces mitochondrial quality control through transcription factor EB (TFEB)-mediated autophagy. We propose a mitochondria-centered framework wherein mitochondrial homeostasis serves as the central integrative hub linking microglial immunometabolic reprogramming to neuron-intrinsic survival programs. This framework is intended as a hypothesis-generating synthesis rather than a summary of established causal pathways; several of its central links, including the microglial succinate-itaconate axis and the OXPHOS-trophic bridge, remain to be tested directly in iTBS-treated tissue. Preliminary clinical studies report functional improvements across motor, cognitive, language, and swallowing domains, although sample sizes are limited and protocols heterogeneous. We discuss translational challenges including parameter heterogeneity, and note that peripheral markers such as plasma succinate and cell-free mitochondrial DNA warrant exploration as candidate pharmacodynamic indices rather than as a validated response-guided panel. - Source: PubMed
Publication date: 2026/09/17
Liu YueZhang YizhuoHuang YingyingBi Xia