TFEB EMSA Kit
- Known as:
- TFEB EMSA Kit
- Catalog number:
- AY1413
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- TFEB EMSA Kit
Related genes to: TFEB EMSA Kit
- 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
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- Histone deacetylase 6 (HDAC6) is a promising therapeutic target in cancer. However, its inhibitors show limited efficacy as monotherapies and are more effective in combination settings, suggesting a context-dependent mechanism that remains poorly defined. Here, we show that tubacin sensitizes cancer cells to ferroptosis under glutathione (GSH) depletion caused by buthionine sulfoximine (BSO). This effect was not observed with other HDAC6 inhibitors or with HDAC6 depletion, suggesting a mechanism not solely attributable to HDAC6 inhibition. Co-treatment with tubacin and BSO induced lipid peroxidation, which was abrogated by ferroptosis inhibitors, indicating ferroptosis as the predominant mode of cell death. Mechanistically, tubacin activated transcription factor EB (TFEB), leading to lysosomal acidification and expansion, accompanied by ferritin degradation and increased intracellular ferrous iron. These effects were reversed by TFEB silencing, lysosomal inhibition, or nuclear receptor coactivator 4 depletion, supporting a role for TFEB-dependent lysosomal ferritinophagy. However, iron accumulation driven by tubacin was insufficient to trigger ferroptosis, indicating a requirement for redox imbalance. Consistently, tubacin enhanced ferroptosis under GSH-glutathione peroxidase 4 (GPX4) axis disruption by imidazole ketone erastin or arsenic trioxide. Collectively, our findings identify TFEB-driven lysosomal activation and ferritinophagy as a critical determinant of ferroptotic sensitivity under redox imbalance and suggest that pharmacological modulation of TFEB-lysosomal function by tubacin may represent a potential strategy for enhancing ferroptosis-based cancer therapy. - Source: PubMed
Publication date: 2026/09/10
Kim GyeongmiJang Se-KyeongKim Do-GyeongKim HyunggeeLee Jae HoBae SeungheePark In-ChulJin Hyeon-Ok - In Anorexia Nervosa (AN), the combination of self-induced starvation and hyperactivity may initially recruit the autophagic machinery to sustain the function of energy-demanding brain regions; however, its dysregulation may ultimately contribute to impaired brain function. We therefore investigated the autophagic machinery in the dorsal hippocampus (dHip), a central hub for energy status modulation and for cognitive processing, in the activity-based anorexia (ABA) rat model, the gold standard in the field. To analyze autophagic markers in the dHip, adolescent female Sprague-Dawley rats were exposed to 2 h/day of food access + free wheel access (ABA induction) and were sacrificed when they reached the maximum body weight loss allowed concomitantly with an increase in the running activity (acute phase) or following a 7-day recovery period. Our results show that ABA induction persistently disrupts the regulation of the autophagic machinery. In the acute phase, the ABA condition increases the phosphorylation of mTOR/ULK1 while promoting TFEB-associated mechanisms, enhancing the expression of autophagic markers such as Becn1, Ctsb genes, Beclin-1, and LC3-II proteins. After weight recovery, TFEB-induced activation of Becn1, Ctsb, Beclin-1, and LC3-II remains elevated. In addition, the enhanced expression of autophagic markers is accompanied by an increase in p62 and Caspase3, pro-apoptotic signals. Our findings reveal a sustained activation of autophagy across different stages of the ABA protocol. Rather than functioning exclusively as a survival mechanism, this process could evolve into a driver of aberrant behaviors typical of individuals with AN, such as dieting behaviors and hippocampal-dependent deficits. - Source: PubMed
Rizzi BeatriceTarga GiorgiaTaddini SofiaParolaro SusannaRapini LetiziaFumagalli FabioCaffino LuciaMottarlini Francesca - Xiaobanxia decoction (XBXD), a classical Chinese antiemetic formula, has potential benefits for treating chemotherapy-induced nausea and vomiting (CINV). The present study investigates its antiemetic effect and explores the possible mechanisms. - Source: PubMed
Publication date: 2026/09/01
Feng LeiZhai Ya-RongLiang WanKan Shao-JunNie Ke - Spiro-benzylisoquinoline alkaloids (spiroBIAs) have sparked substantial interest due to their unique structures and biological significance. Phytochemical investigations on the whole plants of Hypecoum erectum guided by an integrated non-targeted metabolomics workflow led to the isolation of seven novel spiroBIAs erectumines A-G (1-7), one unusual spiroBIA erectumine H (8), and one rare BIA hypeisoxazole B (9), involving five intriguing skeletal types. Their structures were determined via extensive spectroscopic and spectrometric analyses, X-ray crystallography, and computational methods. Compound 1 features a distinctive spiro [1,2-dihydronaphthalene-isoindolinone] ring system; compounds 2-5 possess an undescribed spiro [2,3-dihydroisoquinoline-1,4-dione-1,2,3,4-tetrahydroisoquinoline] skeleton; compounds 6 and 7 bear a unique spiro [2,3,4,5-tetrahydro-1H-benzo[d]azepin-1-one-1,3-dihydroisobenzofuran] framework; compound 8 possesses an uncommon spiro [benzofuranone-benzazepine] structural architecture, and compound 9 has a diindeno[2,1-c:2',1'-d]isoxazole scaffold. The plausible biosynthetic pathways for 1-8 are proposed. Compound 9 is a potent hepatoprotective agent that exerts synergistic effects by activating TFEB-mediated autophagy and mitochondrial biogenesis. - Source: PubMed
Publication date: 2026/09/05
Liu YunGao GaiNiu YingSun Pan-TingZhang Meng-YaoSun Jia-XinLiu HuiFeng Wei-ShengWang DongdongAlilou MostafaXie Zhi-ShenChen Hui - To investigate the clinicopathological features, immunophenotypic characteristics, molecular genetic profiles for an accurate diagnosis of renal tumors associated with Birt-Hogg-Dubé (BHD) syndrome. Clinicopathological data from 10 patients with BHD syndrome-associated renal tumors were collected from Ningbo Clinical Pathology Diagnosis Center (4 cases) and Ruijin Hospital, Shanghai Jiaotong University School of Medicine (5 in-house cases and 1 consultation case) from January 2015 to December 2025. Their clinical characteristics and histological features were studied and analyzed. Immunohistochemical staining and next-generation sequencing (NGS) were performed. Follow-up data were obtained and relevant literature was reviewed. All 10 patients were adults, including 6 males and 4 females, with an age 57 (54, 67) years old. Seven patients had pulmonary bullae/pneumothorax and one patient had a right anterior chest wall fibroma. For the patients with renal tumor, 6 cases presented with a unilateral single tumor, 1 case with unilateral multiple tumors and 3 cases with bilateral multiple tumors (totaling 16 renal tumors). Four cases of the renal tumor were associated with multiple renal cysts. Histologically, among the 16 tumors, 10 were hybrid oncocytic/chromophobe tumors (HOCT) with the typical "mosaic" pattern, 4 with chromophobe renal cell carcinoma-like morphology, 1 with predominantly sarcomatoid morphology and focal areas of low-grade oncocytic renal tumor, and 1 renal angiomyolipoma. The immunophenotype of BHD-associated renal tumors was not specific. Immunohistochemistry revealed diffuse positive for GPNMB in all epithelial-derived renal tumors (15/15). CK7 and CD117 were focally expressed in 7/15 cases each, CD10 was focally expressed in 6/15 cases, and carbonic anhydrase Ⅸ (CAⅨ) was negative in all tumors (0/15). ALK, TFE3 and TFEB were negative. No loss of SDHB or FH expression was identified. DNA next-generation sequencing identified FLCN mutations in all cases, including 7 cases with germline FLCN mutations and 3 cases with somatic FLCN mutations. During a 9-120 months follow-up, the patient with sarcomatoid differentiation passed away 6 months after renal tumor identified, and another patient experienced relapse in the left kidney 6 years after bilateral nephron-sparing surgery. No relapse or metastasis was identified in the remaining 8 patients. Morphologically, BHD syndrome-associated renal tumors can mimic various low-grade oncocytic renal tumors. In addition to the classic HOCT morphology, they may also present with high-grade sarcomatoid differentiation. GPNMB is a highly sensitive marker for BHD-associated renal tumors. Molecular genetic analysis to detect FLCN mutation is the gold standard for definitive diagnosis. BHD syndrome-associated renal tumors typically show indolent biological behavior, with sarcomatoid differentiation as a morphological feature of poor prognosis. - Source: PubMed
Cheng XZhan YWang Y JYang X QZhang H Z