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
- High concentrations of free fatty acids (FFA) during early lactation cause metabolic stress and oxidative damage in bovine mammary epithelial cells. This study explored the protective mechanism of lycopene (LYC), a natural antioxidant, against FFA-induced injury in the MAC-T cells. We found that 1.2 mM FFA induced oxidative stress, reactive oxygen species (ROS) accumulation, apoptosis, and impaired autophagy. LYC dose-dependently alleviated FFA-induced oxidative damage, restored autophagy flux, upregulated ATG5 autophagy-related 5 (ATG5), LC3-II, and transcription factor EB (TFEB), and downregulated p62, ROS, and apoptosis. Inhibition of autophagy abolished the protective effects of the LYC. Overexpression of TFEB mitigated FFA-induced dysfunction, while TFEB knockdown aggravated cell injury. These results demonstrate that LYC protects mammary epithelial cells from FFA-induced oxidative damage via regulating TFEB-mediated autophagy, suggesting its potential use in alleviating metabolic stress in periparturient dairy cows. - Source: PubMed
Sun XinyuanJia HongdouChen YuanyuanWu YutongYan JiayiYu YueWang JingxinDing WenqiMa LiXu QiushiLoor Juan JXu ChuangSun Xudong - Hypervirulent Klebsiella pneumoniae (hvKp) is an emerging pathogen that causes severe community-acquired infections; however, the immune mechanisms controlling intracellular hvKp have yet to be clearly defined. In this study, we investigated the therapeutic potential of berberine against hvKp infection and elucidated the underlying molecular mechanisms using macrophage cell models and in vivo zebrafish models. Berberine significantly reduced intracellular hvKp survival in macrophages and improved survival in hvKp-infected zebrafish. Berberine markedly attenuated proinflammatory cytokine production and inhibited the c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) signaling pathways. Notably, we found that hvKp exploited host lipid droplets (LD) biosynthesis to support its intracellular survival, and berberine effectively suppressed LD accumulation. Mechanistically, berberine promoted the nuclear translocation of transcription factor EB (TFEB), thereby enhancing lipolysis. Although berberine upregulated autophagy-related gene expression during hvKp infection, it did not induce lipophagy, the selective autophagic degradation of LD. Collectively, these findings indicate that berberine has potential as a therapeutic agent against hvKp infection by modulating host lipid metabolism to restrict bacterial intracellular survival. - Source: PubMed
Publication date: 2026/08/31
Lee Ju YeongJung Hui-JungAsh AnweshaJeon SeunghyeonHyun MiriLee Ji YeonLee Sang-HeeKwon Hyuk NamBaek Won-KiJang JichanKim Hyun AhKim Jin Kyung - Folliculin (FLCN)-mutated renal tumors, in the setting of Birt-Hogg-Dubé (BHD) syndrome or sporadically, typically show low-grade eosinophilic morphology and follow an indolent clinical course; however, rare high-grade variants with more aggressive behavior remain poorly defined and underrecognized. To better characterize this unusual subset, we identified six high-grade renal cell carcinomas (RCCs) and performed integrated clinicopathologic, immunohistochemical, molecular, and clinical follow-up analyses. All tumors demonstrated infiltrative growth, extensive necrosis, variable desmoplastic stroma, and high-grade nuclear features. They exhibited papillary/tubulopapillary and solid growth patterns, mixed eosinophilic and clear cell cytology, focal biphasic morphology, and prominent nucleoli, overlapping morphologically with high-grade papillary RCC, FH-deficient RCC, and TFE3- or TFEB-rearranged RCC. Targeted DNA sequencing identified FLCN frameshift mutations in all cases, including four germline mutations, one likely germline mutation, and one somatic mutation, without additional alterations characteristic of other established RCC subtypes. In keeping with the FLCN-mutated phenotype, all tumors extensively and strongly expressed GPNMB. Clinically, three patients had features consistent with BHD syndrome; one additional patient lacked typical pulmonary and cutaneous findings but was confirmed to carry a germline mutation; another could not be definitively classified as having BHD and was considered suspected; and the remaining one had no clinical evidence of BHD and was considered likely sporadic. At last follow-up, three patients were free of recurrence or metastasis at 10, 25, and 7 months; the remaining three developed distant metastases, including two who died of disease at 17 and 26 months postoperatively and one who remained alive with metastatic disease at 85 months. Our findings expand the morphologic spectrum of FLCN-mutated renal tumors and the genetic landscape of papillary-patterned RCCs, raising awareness of this aggressive subset and supporting consideration of FLCN testing in morphologically overlapping high-grade papillary tumors. - Source: PubMed
Publication date: 2026/09/03
Wang Xiao-TongFang RuYe Sheng-BingWang XuanLi RuiHe YanZhang Ru-SongXia Qiu-YuanZhao MingRao Qiu - Mitochondrial quality control has traditionally been attributed to mitophagy. However, emerging evidence indicates that mitochondrial microautophagy represents a distinct quality control pathway. This pathway enables selective removal of damaged mitochondrial subdomains while preserving overall organelle integrity. Therefore, mitochondrial microautophagy can be viewed as a redox-adaptive, sub-organelle quality control system that responds to localized mitochondrial stress. In this review, we integrate recent mechanistic, imaging, and molecular studies to establish an updated framework of mitochondrial microautophagy. We describe this process as a sequential pathway involving damage sensing, mitochondria-lysosome contact formation, lysosomal membrane remodeling, selective degradation, and metabolic recycling. Localized reactive oxygen species (ROS) serve as important signals during this process. ROS define specific damage microdomains and facilitate selective mitochondrial component recognition. Subsequent cargo delivery and degradation are regulated by multiple molecular modules. These modules include the ubiquitin-autophagy-related protein 8 system, vacuolar-type H-ATPase-dependent membrane remodeling, Ras-related in brain-endosomal sorting complexes required for transport signaling, the spermatogenesis-associated 18/mitochondria-eating protein pathway, and the mechanistic target of rapamycin complex 1-transcription factor EB and nuclear factor erythroid 2-related factor 2 stress-response networks. Despite substantial progress, several fundamental questions remain unresolved. The mechanisms underlying cargo recognition require further clarification. The existence of specific redox-sensitive receptors remains to be determined. In addition, future technological advances will provide deeper insights into this pathway. Understanding mitochondrial microautophagy may reveal new therapeutic opportunities for mitochondrial dysfunction-associated disorders, including neurodegeneration, ischemic injury, metabolic disorders, and aging. 00, 000-000. - Source: PubMed
Publication date: 2026/09/02
Zhang HuijiaChen YingJiang JunjieDing YarongHu SiZhou ZhongzhiChen Li - Schizophrenia (SCZ) and bipolar disorder (BD) share genetic risk factors and cognitive impairments, yet the underlying mechanisms remain incompletely understood. Loss-of-function variants in AKAP11 (A-kinase anchoring protein 11) have recently emerged as major risk factors for both disorders. Our recent study demonstrates that AKAP11 deficiency in the mouse hippocampus causes cognitive deficits and synaptic dysfunction, accompanied by autophagy dysregulation. Mechanistically, AKAP11 interacts with PPP3CB (protein phosphatase 3 catalytic subunit beta) to promote TFEB (transcription factor EB) dephosphorylation and nuclear translocation, thereby sustaining autophagy-lysosomal gene expression. knockout cells display impaired autophagy initiation, reduced lysosomal activity, and compromised autophagic flux. Therapeutically, pharmacological activation of TFEB rescues cognitive deficits in -deficient mice. These findings position AKAP11 as a critical regulator of TFEB-mediated autophagy and suggest that enhancing autophagy-lysosomal function may represent a therapeutic strategy for SCZ and BD. - Source: PubMed
Publication date: 2026/09/01
Kan YuxuanYue ZhenyuLi MinDeng Zhiqiang