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)
- The accumulation of mutant huntingtin (mHTT) aggregates drives the pathology of Huntington's disease (HD), yet therapies capable of distinguishing toxic species from wild-type proteins remain elusive. Here, a synthetic gene circuit, termed ARAA, was engineered to couple the preferential recognition of aggregated polyQ species to the on-demand activation of autophagy. Utilizing a repurposed bacterial NarX-NarL system fused with a conformation-sensitive intrabody, the circuit detects pathological polyQ conformers and triggers the transcriptional expression of the master autophagy regulator TFEB. To enable systemic application, the ARAA plasmid is encapsulated in CD98-targeted immunoliposomes (LIP-CD98) that facilitate efficient blood-brain barrier crossing via receptor-mediated transcytosis. In the R6/2 HD mouse model, ARAA treatment significantly reduces mHTT burden, attenuates neuroinflammation, and rescues synaptic deficits. This closed-loop intervention improves motor function and extends lifespan. Together, these findings provide proof-of-concept evidence that aggregate-responsive regulation of autophagy can mitigate disease-associated phenotypes in exon 1-based HD models. - Source: PubMed
Publication date: 2026/09/27
Zhu JieXie Xi-XiuLi LeiTian ChenWang Hao-TianWang Xiao-JieYu Xiao-LinZhang Gui-FengLiu Rui-Tian - Huntington's Disease is a neurodegenerative disorder that progresses over time and can be passed down from parent to child. In uncontrolled motor activities, behavioural problems come into play, as well as progressive mental decline. The CAG triplet in the HTT gene found on chromosome 4 undergoes changes, leading to the production of a mutant protein called huntingtin, which consists of a bigger-than-normal polyglutamine tract that then undergoes misfolding and produces toxic oligomers and fibrillar deposits that can cause dysfunction in normal cell functioning and therefore in nerve cells as well. Although early research linked the pathophysiology of Huntington's disease primarily to mHTT aggregation, more recent research indicates broad protein-protein interaction networks that affect several cellular pathways. Systems biology approaches using tools such as STRING, BioGRID, and Cytoscape have provided evidence of interconnected networks that promote proteostasis, mitochondrial dynamics, energy metabolism, neuroinflammation, synaptic transmission, and transcriptional and epigenetic regulation. Important protein hubs, including HSP70, DRP1, NLRP3, and TFEB, act as central controls that bind those pathways. mHTT-mediated defect in the function of the ubiquitin-proteasome system promotes mitochondrial oxidative stress, which triggers the NLRP3 inflammasome, leading to synaptic dysfunction and specific loss of striatal medium spiny neurons. Investigations using various experimental techniques, which involve R6/2 and YAC128 mouse models, neurons derived from human iPS cells, and multi-omics studies, reveal that faulty neuroplasticity develops before the formation of visible protein aggregates. As for therapeutics targeting central components of neuronal networks, they have all demonstrated certain neuroprotective effects. - Source: PubMed
Publication date: 2026/09/27
Panwar ChhaviGoel FalguniGarg Vipin Kumar - Dysregulated bone remodeling, attenuated endogenous osteogenic capacity, and the lack of bone-targeting capability in therapeutics constitute the core challenges in current clinical interventions for osteoporosis. In this study, a hybrid nanodelivery system integrating betaine-loaded metal-organic frameworks with engineered exosomes (BZ@Exos) is constructed to restore bone metabolic homeostasis and improve bone microstructure. The engineered exosomes co-overexpressing CXCR4 and CD47 proteins on the surface exhibit high bone tissue targeting efficiency and evade clearance by the mononuclear phagocyte system, while ZIF-8 enables stable encapsulation of betaine. Internalized betaine promotes nuclear translocation of TFEB via targeted binding to the 14-3-3 protein, enhances autophagic flux in senescent bone marrow mesenchymal stem cells (BMSCs), and thereby facilitates their osteogenic differentiation. In parallel, BZ@Exos significantly inhibits osteoclast-mediated bone resorption and restores bone metabolic homeostasis. In vivo assays demonstrate that intravenously administered BZ@Exos successfully reverses bone loss and alleviates senescence-related phenotypes in ovariectomized rat models of osteoporosis. This novel therapeutic system with integrated functions of bone homeostasis remodeling, regenerative potential restoration, and precise targeting provides a new perspective for osteoporosis treatment. - Source: PubMed
Publication date: 2026/09/27
Li XiaorongLi MengshaLi ZhenghaoGu JiayingMo LinzhenZhu YuetongChen YangZeng LeliPan YihangZhang ChaoSi Yunhui - Long-term exposure to polystyrene nanoplastics (PS-NPs) causes neurotoxicity, but the underlying mechanisms remain unclear. We combined network toxicology, molecular docking, and in vivo experiments to investigate the role of MTOR-TFEB-regulated autophagy in PS-NP-induced neurotoxicity. Potential targets related to PS-NPs and neurodegenerative diseases were screened from public databases. Enrichment analysis indicated involvement of neurodegenerative and autophagy pathways. Protein-protein interaction and docking simulations prioritized as a candidate target. Sprague-Dawley rats were gavaged with PS-NPs (0.15 or 1.5 mg/kg) for 60 days. Morris water maze tests showed impaired spatial learning and memory. Western blotting of hippocampal tissues revealed increased p-MTOR/MTOR ratios, decreased total cytoplasmic and nuclear TFEB, reduced lysosomal proteins (LAMP2, CTSD, and CTSB), elevated autophagy markers SQSTM1 and MAP1LC3B-II, and altered apoptosis regulators (BAX up and BCL2 down). Collectively, PS-NPs disrupt the MTOR-TFEB axis, impair lysosomal function and autophagic clearance, and promote apoptosis, leading to neurocognitive deficits. These findings provide mechanistic insights into the MTOR-TFEB axis and highlight it as a candidate pathway warranting further evaluation as a potential intervention target. - Source: PubMed
Publication date: 2026/09/09
Tang NaWang ChunZhang MengLi YajieLiang YongkangZhang JingjingNiu Qiang - Alzheimer's disease (AD) is a complex neurodegenerative disorder with multifaceted pathogenesis. Given the clinical need for multi-target interventions, this study elucidated the neuroprotective mechanisms of walnut ( L.) against AD-related cognitive impairment. Methods: We characterized 25 bioactive constituents (fatty acids and ellagitannins) and constructed a protein-protein interaction (PPI) network. GO/KEGG enrichment, integrated with Ingenuity Pathway Analysis (IPA), deciphered pharmacological pathways, followed by molecular docking to evaluate ligand-target binding thermodynamics. Network analysis revealed that walnut phytochemicals synergistically modulate the MAPK-mTORC1-TFEB-mediated endolysosomal homeostasis pathway. Molecular docking indicated that ellagitannins (strictinin, pedunculagin, tellimagrandin I) exhibit robust affinities for upstream RAS/RAF/MEK kinases, suppressing pro-pathogenic signaling. Concurrently, gallic acid targeted ABCA1 and TFEB, promoting TFEB activation and nuclear translocation to enhance beta-amyloid clearance and lysosomal biogenesis. This study provides evidence that walnut attenuates AD pathology through "multi-component" reinforcement of the endolysosomal defense system, establishing a mechanistic foundation for walnut as a promising functional food. - Source: PubMed
Publication date: 2026/09/17
Lin Chih-TingChen Kuan-TsoHung Yu-Chiang