Ask about this productRelated genes to: TFEB antibody
- 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
Related articles to: TFEB antibody
- Arecoline, the principal constituent of areca nut, triggers oxidative stress and inflammasome activation, leading to chronic inflammation and oral cancer development. The aim of this study was to investigate the antioxidant and anti-inflammatory role of bacosine, a triterpenoid isolated from Bacopa monnieri, to counteract arecoline-induced oxidative and inflammatory responses in oral cancer cells. Our study revealed that bacosine induces NRF2 signalling to inhibit arecoline-induced reactive oxygen species (ROS) generation and inflammasome activation in oral cancer. Initially, our study identified that inhibition of the NRF2 pathway and its downstream antioxidant signalling drives excessive ROS accumulation during arecoline exposure. Bacosine restored NRF2 antioxidant signalling, leading to reduced intracellular ROS levels in arecoline-exposed cells. Additionally, bacosine triggers autophagy by upregulating autophagic regulators, ATG5 and BECLIN1, thereby enhancing lysosomal activity and promoting autophagic flux. Moreover, bacosine induces TFEB activation, linking antioxidant defence to autophagy induction in oral cancer cells. Likely, pharmacological inhibition (ML-385) and genetic silencing (siNRF2) of NRF2 diminished TFEB-induced autophagy during bacosine treatment. Interestingly, bacosine failed to attenuate arecoline-induced inflammasome activation in autophagy and TFEB-deficient cells, signifying that bacosine suppresses inflammasome activation through NRF2-TFEB-mediated autophagy. These findings underline bacosine as a promising therapeutic target for mitigating arecoline-induced oral pathologies and oral cancer. - Source: PubMed
Publication date: 2026/05/22
Mishra PriyadarshiniKar Rakesh KumarMishra Soumya RanjanMaiti SwatilekhaSingh Vineet KumarNagini SiddavaramBhutia Sujit Kumar - PQ-loop repeat-containing 2 (PQLC2) is a lysosomal transporter for cationic amino acid that plays a critical role in regulating intracellular amino acid levels. However, its role in lysosomal biogenesis and autophagy remains poorly understood. Here, we investigate the impact of PQLC2 loss on lysosomal function and autophagic flux using PQLC2 knockdown and knockout cell models. PQLC2-deficient cells exhibited enhanced nuclear translocation of transcription factor EB (TFEB), a key regulator of lysosome, accompanied by increased expression of TFEB-lysosomal and autophagy target genes. In addition, genes related to mechanistic target of rapamycin complex 1 (mTORC1), a negative regulator of TFEB, were destabilized, leading to reduced lysosomal recruitment and impaired mTORC1 signaling. Loss of PQLC2 also resulted in lysosomal dysfunction, including defective lysosomal acidification, decreased cathepsin activity, and lysosomal enlargement. Furthermore, autophagosome maturation and autophagic flux were disrupted in PQLC2-deficient cells, as evidenced by p62 accumulation and decreased LC3-II levels. Collectively, our results highlight that PQLC2 is essential for regulating mTORC1-dependent lysosomal function and autophagy, underscoring its potential role in maintaining cellular homeostasis. - Source: PubMed
Publication date: 2026/05/19
Jeung Yun-JiJang MinsuAhn JiwonKwon Ok-SeonKim Seung-HyunKwon Jae-EunPark YunhoJang Seung PilRyu KajungChung Kyung-Sook - Atherosclerosis (AS) is a chronic inflammatory disease characterized by lipid accumulation within the arterial wall. The imbalance between cholesterol influx and efflux, coupled with persistent inflammation, drives the progression of plaque formation. Lipophagy, a selective form of autophagy, specifically targets lipid droplets for lysosomal degradation. Consequently, this process is a notable regulator of cellular lipid homeostasis. In the present review, the core regulatory networks of lipophagy were systematically summarized, including the mechanistic target of rapamycin complex 1/AMP‑activated protein kinase, transcription factor EB (TFEB) and farnesoid X receptor/cAMP response element‑binding protein signaling axes. The multidimensional roles of lipophagy in key cell types involved in AS are also discussed. For example, in macrophages, lipophagy stabilizes plaques by promoting cholesterol efflux and inhibiting foam cell formation; however, dysregulated lipophagy can exacerbate necrotic core formation. In vascular smooth muscle cells, lipophagy regulates phenotype switching and calcification and in endothelial cells, lipophagy mitigates oxidative stress and inflammation. Advances in therapeutic strategies targeting lipophagy were evaluated, ranging from pharmacological agents (such as statins and metformin) to natural compounds (such as berberine and geniposide) and Traditional Chinese Medicine formulas. In conclusion, targeting lipophagy represents a pivotal therapeutic frontier for stabilizing atherosclerotic plaques; however, the broad application of autophagy inducers lacks precision. Future strategies should transition from generalized modulation to cell‑type specific interventions that precisely calibrate the sirtuin 1‑TFEB‑lipophagy axis. Furthermore, elucidating the 'double‑edged' role of lipophagy in late‑stage plaque outcomes is required for developing safe, clinically translatable modulators. - Source: PubMed
Publication date: 2026/05/22
Nan SonghuaPeng ChaojieMeng XueJia JingnanZhao FangfangCui Yinglin - Older adults are highly vulnerable to infectious diseases, and vaccines are often less effective in this population because of diminished B and T cell memory responses driven by impaired autophagy, immunosenescence, and chronic low-grade inflammation. Spermidine has been shown to counteract immunosenescence and induce autophagy in preclinical models, and its levels decline with age in humans. We conducted a double-blind, randomised, placebo-controlled pilot study in 40 adults over 65 years of age following their third SARS-CoV-2 vaccine dose to assess the safety of Spermidine and its effects on vaccine-induced immunity. Daily oral supplementation (6 mg, 13 weeks) was well-tolerated. Vaccine non-responsiveness was common, and non-responders exhibited a distinct immune-senescence signature marked by elevated p16, mTOR signalling, and γ-H2AX+ DNA damage in lymphocytes. Spermidine reversed these features and significantly enhanced spike-specific IgG secretion, memory B cell recall responses and neutralising antibody activity, specifically in non-responders. Single-cell RNA-seq after treatment revealed increased expression of TFEB targets and autophagy-related genes in B cells, in line with elevated autophagic flux. These findings suggest that targeting immune cell senescence with Spermidine may improve vaccine responsiveness in older adults and highlight immune-senescence markers as potential predictors of vaccine failure in ageing populations. - Source: PubMed
Alsaleh GhadaAli MohammadKayvanjoo Amir HosseinLiu FengMoreau TanaïsBibi SagidaLuo LinGovender MelissaCarroll MilesHofer Sebastian JTobias EisenbergMagnes ChristophKell LorenChung ChristopherDeng YuBhandari AneeshaGarner LucyConrad ThomasChen LiyeKronsteiner-Dobramysl BarbaraDunachie SusieSpiller Owen BLambe TeresaKlenerman PaulJones Lucy CSimon A Katharina - Podocyte loss and death are pathological hallmarks of diabetic kidney disease (DKD), and PANoptosis (apoptosis, pyroptosis, and necroptosis) in podocytes is crucial to DKD progression. Regulated in development and DNA damage response 1 (REDD1) is a multifaceted regulator involved in metabolism, oxidative stress, autophagy, and cell fate. In this study, we aimed to investigate the effects and underlying mechanisms of REDD1 on podocyte PANoptosis and autophagy in DKD. - Source: PubMed
Publication date: 2026/05/21
Liu MengyuYuan ChenLi YueSong ShanMu LinBian YaweiLi XinranYu XiaoxueLi GuiyingShi Yonghong