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)
- Lysosomes were once considered terminal degradative organelles responsible for disposing of cellular waste. However, recent studies have revealed that lysosomes serve as dynamic signalling and metabolic hubs at the center of diverse biological processes, including nutrient sensing, metabolic regulation, membrane trafficking, autophagy, inflammation, and cell death. To support this broad functional repertoire, lysosomes must possess robust mechanisms to maintain their integrity in the face of damage or stress. In response to lysosomal membrane damage, cells engage multilayered adaptive mechanisms that act in coordination-membrane repair (Repair), selective removal of damaged organelles (Removal), and de novo biogenesis of lysosomes (Regeneration). These processes are mediated by a range of molecular pathways, including the ESCRT complex, the PITT pathway, lysophagy, and TFEB-dependent lysosomal regeneration. Notably, recent findings highlight the noncanonical autophagy-like pathway known as ATG8ylation (conjugation of ATG8s on single membranes), which is activated via the STING-V-ATPase-ATG16L1 axis and functions as a critical hub connecting multiple arms of the lysosomal damage response. In this review, we systematically outline the molecular basis of lysosomal damage responses, including ATG8ylation, and explore how these networks are implicated in a broad spectrum of pathological conditions such as aging, neurodegeneration, cancer, obesity-related disorders, and immune dysfunction. Understanding these lysosomal quality control mechanisms not only sheds light on the fundamental principles of organelle homeostasis but also opens new avenues for therapeutic innovation. - Source: PubMed
Publication date: 2026/05/11
Minami SatoshiHamasaki Maho - Signaling mechanisms at the lysosome-mitochondria interface form a critical network that enables cancer cells to maintain mitochondrial quality control, adapt to metabolic stress, and survive therapy. However, the incomplete understanding of the mechanisms coordinating this network has limited the development of effective therapies, especially for triple-negative breast cancers (TNBC). Here, we identify TRPML1 as an important regulator of lysosome-mitochondrial communication in MDA-MB-231 TNBC cells. We find that TRPML1 knockdown (ML1-KD) impaired mitochondrial respiration, oxidative substrate utilization, ATP production and redox balance in MDA-MB-231 cells, whereas comparable changes were not observed in non-cancerous MCF10A cells. ML1-KD reduced lysosomal acidification and impaired autophagic flux and was accompanied by reduced TFEB nuclear localization, impaired mitophagy, and alterations in mitochondrial maintenance proteins. These changes were accompanied by organellar proximity remodelling, with increased mitochondria-ER proximity and reduced mitochondria-lysosome proximity, together with altered cytosolic/mitochondrial Ca responses, broad metabolic remodelling, G0/G1 arrest, and caspase-3/7-independent cell death. Importantly, ML1-KD cells showed enhanced responses to otherwise subeffective concentrations of doxorubicin and paclitaxel. Together, our findings support TRPML1-dependent lysosomal signaling as an important contributor to mitochondrial-metabolic resilience and chemotherapy responsiveness in MDA-MB-231 TNBC cells. - Source: PubMed
Publication date: 2026/09/22
Syeda Alia KAlmasi ShekoufehBenson Cory JKennedy Barry EYoast Ryan MEmrich Scott MDelima-Baril AmariSlade LoganPakkiriswami ShanmugasundaramVijayan Vishnu VSheela Unnikrishnan BGujar ShashiPulinilkunnil ThomasTrebak MohamedEl Hiani Yassine - [This corrects the article DOI: 10.3389/fcimb.2026.1835140.]. - Source: PubMed
Publication date: 2026/09/07
Rinkel SvenSchulze-Luehrmann JanKadavil Baburaj BhavyalakshmiWeber FionaLiebler-Tenorio Elisabeth MLührmann Anja - Chemoresistance, often driven by aberrant transcriptional and epigenetic mechanisms, remains a significant barrier to effective colon cancer therapy. This study introduces a dendrimer-based proteolysis-targeting chimera (PROTAC) system, JTP, generated by conjugation of polyamidoamine (PAMAM-G4) dendrimer with 4-hydroxythalidomide (an E3 ligase recruiter) and JQ1 carboxylic acid (a BRD4 inhibitor). The multivalent dendrimer scaffold increases local surface ligand density, promotes endocytic uptake and endosomal escape, and facilitates cytosolic engagement of BRD4 for proteasome-mediated degradation. In vitro, JTP effectively increased the chemosensitivity of CT26 colon cancer cells to chemotherapy, particularly to irinotecan, leading to enhanced DNA damage, cell cycle arrest in the S and G2/M phases, and apoptosis, as well as a synergistic reduction in oncoprotein expression. In vivo studies in orthotopic colon cancer-bearing mice demonstrated a prominent antitumor effect of JTP in combination with irinotecan, yielding marked inhibition of tumors and metastases and promoting long-term survival, with toxicity within a well-tolerated range. The in vivo studies also demonstrated the robust effects of JTP on reducing the expression of TFEB, c-Myc, β-catenin, Bcl-2, VEGFR2, IL-1β, TNF-α, HIF-1α, and vimentin by BRD4 elimination in tumor tissues. These findings demonstrate that combining JTP with epigenetic modulation offers an effective strategy to promote chemotherapeutic effects in colon cancer. - Source: PubMed
Publication date: 2026/09/17
Sharmila RamalingamIong Weng ChiLu I-LinSabu ArjunLo Chun-LiangShen Mina Ming-YinChiu Hsin-Cheng - Renal cell carcinoma (RCC) is traditionally considered a disease of older adults; however, its incidence among young individuals is steadily increasing. Despite this epidemiologic shift, early-onset RCC remains poorly characterized and is still largely managed according to evidence derived from older populations. Available retrospective series suggest that younger patients more frequently present with localized disease and experience improved cancer-specific and overall survival compared with older counterparts. Nevertheless, they also exhibit greater histologic and molecular heterogeneity, with an overrepresentation of rare and genetically defined subtypes, including TFE3-rearranged and TFEB-altered RCC, fumarate hydratase-deficient RCC, succinate dehydrogenase-deficient RCC and SMARCB1-deficient renal medullary carcinoma. These entities are frequently associated with hereditary cancer syndromes and distinct metabolic patterns. In parallel, von Hippel-Lindau-related RCC and the development of HIF-2α inhibitors such as belzutifan illustrate how targeting lineage-specific pathways can modify the natural history of early-onset disease and reduce the burden of repeated local interventions. Emerging evidence also suggests that immune checkpoint inhibitor (ICI)-based combinations, particularly those incorporating VEGFR-targeted tyrosine kinase inhibitors, may provide clinically meaningful activity across several rare RCC subtypes, whereas outcomes with monotherapy remain variable. This evidence remains promising but preliminary and is not specific to young adults. A deeper molecular characterization of early-onset RCC may enable earlier detection and more accurate risk stratification, ultimately guiding treatment selection. Dedicated prospective studies are urgently needed to define age-specific management strategies, including surveillance protocols, genetic counseling, and personalized therapeutic approaches for young patients with RCC. - Source: PubMed
Publication date: 2026/09/20
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