Relevant bibliographies by topics / Transcription factor EB (TFEB)

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Transcription factor EB (TFEB)'

Author: Grafiati
Published: 10 January 2024
Last updated: 31 July 2025

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Journal articles on the topic "Transcription factor EB (TFEB)"

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Nezich, Catherine L., Chunxin Wang, Adam I. Fogel, and Richard J. Youle. "MiT/TFE transcription factors are activated during mitophagy downstream of Parkin and Atg5." Journal of Cell Biology 210, no. 3 (2015): 435–50. http://dx.doi.org/10.1083/jcb.201501002.

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The kinase PINK1 and ubiquitin ligase Parkin can regulate the selective elimination of damaged mitochondria through autophagy (mitophagy). Because of the demand on lysosomal function by mitophagy, we investigated a role for the transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, in this process. We show that during mitophagy TFEB translocates to the nucleus and displays transcriptional activity in a PINK1- and Parkin-dependent manner. MITF and TFE3, homologues of TFEB belonging to the same microphthalmia/transcription factor E (MiT/TFE) family, are similarly regulated d
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Markby, Greg Robert, and Kei Sakamoto. "Transcription factor EB and TFE3: new metabolic coordinators mediating adaptive responses to exercise in skeletal muscle?" American Journal of Physiology-Endocrinology and Metabolism 319, no. 4 (2020): E763—E768. http://dx.doi.org/10.1152/ajpendo.00339.2020.

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In response to the increased energy demands of contractions, skeletal muscle adapts remarkably well through acutely regulating metabolic pathways to maintain energy balance and in the longer term by regulating metabolic reprogramming, such as remodeling and expanding the mitochondrial network. This long-term adaptive response involves modulation of gene expression at least partly through the regulation of specific transcription factors and transcriptional coactivators. The AMPK-peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) pathway has long been known to orchestrate contra
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Dang, Thao Thi, and Sung Hoon Back. "Translation Inhibitors Activate Autophagy Master Regulators TFEB and TFE3." International Journal of Molecular Sciences 22, no. 21 (2021): 12083. http://dx.doi.org/10.3390/ijms222112083.

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The autophagy-lysosome pathway is a major protein degradation pathway stimulated by multiple cellular stresses, including nutrient or growth factor deprivation, hypoxia, misfolded proteins, damaged organelles, and intracellular pathogens. Recent studies have revealed that transcription factor EB (TFEB) and transcription factor E3 (TFE3) play a pivotal role in the biogenesis and functions of autophagosome and lysosome. Here we report that three translation inhibitors (cycloheximide, lactimidomycin, and rocaglamide A) can facilitate the nuclear translocation of TFEB/TFE3 via dephosphorylation an
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Yan, Xin, Li Yang, Xiaolei Fu, et al. "Transcription factor EB, a promising therapeutic target in cardiovascular disease." PeerJ 12 (October 11, 2024): e18209. http://dx.doi.org/10.7717/peerj.18209.

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Cardiovascular disease (CVD) remains the major cause of morbidity and mortality around the world. Transcription factor EB (TFEB) is a master regulator of lysosome biogenesis and autophagy. Emerging studies revealed that TFEB also mediates cellular adaptation responses to various stimuli, such as mitochondrial dysfunction, pathogen infection and metabolic toxin. Based on its significant capability to modulate the autophagy-lysosome process (ALP), TFEB plays a critical role in the development of CVD. In this review, we briefly summarize that TFEB regulates cardiac dysfunction mainly through amel
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Wundersitz, Sebastian, Cristina Pablo Tortola, Sibylle Schmidt, et al. "The Transcription Factor EB (TFEB) Sensitizes the Heart to Chronic Pressure Overload." International Journal of Molecular Sciences 23, no. 11 (2022): 5943. http://dx.doi.org/10.3390/ijms23115943.

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The transcription factor EB (TFEB) promotes protein degradation by the autophagy and lysosomal pathway (ALP) and overexpression of TFEB was suggested for the treatment of ALP-related diseases that often affect the heart. However, TFEB-mediated ALP induction may perturb cardiac stress response. We used adeno-associated viral vectors type 9 (AAV9) to overexpress TFEB (AAV9-Tfeb) or Luciferase-control (AAV9-Luc) in cardiomyocytes of 12-week-old male mice. Mice were subjected to transverse aortic constriction (TAC, 27G; AAV9-Luc: n = 9; AAV9-Tfeb: n = 14) or sham (AAV9-Luc: n = 9; AAV9-Tfeb: n = 9
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Gravina, Teresa, Francesco Favero, Stefania Rosano, et al. "Integrative Bioinformatics Analysis Reveals a Transcription Factor EB-Driven MicroRNA Regulatory Network in Endothelial Cells." International Journal of Molecular Sciences 25, no. 13 (2024): 7123. http://dx.doi.org/10.3390/ijms25137123.

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Various human diseases are triggered by molecular alterations influencing the fine-tuned expression and activity of transcription factors, usually due to imbalances in targets including protein-coding genes and non-coding RNAs, such as microRNAs (miRNAs). The transcription factor EB (TFEB) modulates human cellular networks, overseeing lysosomal biogenesis and function, plasma–membrane trafficking, autophagic flux, and cell cycle progression. In endothelial cells (ECs), TFEB is essential for the maintenance of endothelial integrity and function, ensuring vascular health. However, the comprehens
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Su, Qian, Bin Zheng, Chen-yao Wang, et al. "Oxidative Stress Induces Neuronal Apoptosis Through Suppressing Transcription Factor EB Phosphorylation at Ser467." Cellular Physiology and Biochemistry 46, no. 4 (2018): 1536–54. http://dx.doi.org/10.1159/000489198.

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Background/Aims: This study determined the role and mechanism of action of transcription factor EB (TFEB) in H2O2-induced neuronal apoptosis. Methods: SH-SY5Y cells were treated with Akt inhibitor/activator and different concentrations of H2O2. Cell apoptosis was detected by flow cytometric analysis. Akt and TFEB phosphorylation and PARP cleavage were determined by Western blotting. HEK293T cells were transfected with different truncated TFEB mutants and HA-Akt-WT; SH-SY5Y cells were transfected with Flag-vector, Flag-TFEB, Flag-TFEB-S467A or Flag-TFEB-S467D; and TFEB interaction with Akt was
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Chang, Jin-Zhe, Shu-Dong Chen, Hui Zheng, and Hua-Ping Zhang. "Downregulation of transcription factor EB inhibits the growth and metastasis of colorectal carcinomas." European Journal of Inflammation 16 (January 2018): 205873921880533. http://dx.doi.org/10.1177/2058739218805333.

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To determine the roles of transcription factor EB (TFEB) in colorectal cancer (CRC), we collected samples of tumor tissues and normal tissues from 40 patients with CRC. The expression of TFEB in these samples was analyzed by using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Furthermore, we explored the expression of TFEB mRNA in CCD-18Co normal cells and HT-29, HCT-8, C2BBe1 cancer cells. HT-29, HCT-8, and C2BBe1 cancer cells were transfected with a TFEB-specific small interference RNA (siRNA) and scrambled siRNA, then the TFEB expression was confirmed by Weste
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Argüello, Graciela, Elisa Balboa, Pablo J. Tapia, et al. "Genistein Activates Transcription Factor EB and Corrects Niemann–Pick C Phenotype." International Journal of Molecular Sciences 22, no. 8 (2021): 4220. http://dx.doi.org/10.3390/ijms22084220.

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Niemann–Pick type C disease (NPCD) is a lysosomal storage disease (LSD) characterized by abnormal cholesterol accumulation in lysosomes, impaired autophagy flux, and lysosomal dysfunction. The activation of transcription factor EB (TFEB), a master lysosomal function regulator, reduces the accumulation of lysosomal substrates in LSDs where the degradative capacity of the cells is compromised. Genistein can pass the blood–brain barrier and activate TFEB. Hence, we investigated the effect of TFEB activation by genistein toward correcting the NPC phenotype. We show that genistein promotes TFEB tra
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Soleimani, Milad, Mark Duchow, Ria Goyal, et al. "Transcription factor EB (TFEB) activity increases resistance of TNBC stem cells to metabolic stress." Life Science Alliance 8, no. 3 (2025): e202302259. https://doi.org/10.26508/lsa.202302259.

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Breast cancer stem cells (CSCs) are difficult to therapeutically target, but continued efforts are critical given their contribution to tumor heterogeneity and treatment resistance in triple-negative breast cancer. CSC properties are influenced by metabolic stress, but specific mechanisms are lacking for effective drug intervention. Our previous work on TFEB suggested a key function in CSC metabolism. Indeed, TFEB knockdown (KD) inhibited mammosphere formation in vitro and tumor initiation/growth in vivo. These phenotypic effects were accompanied by a decline in CD44high/CD24lowcells. Glycolys
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Dissertations / Theses on the topic "Transcription factor EB (TFEB)"

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Armani, Andrea. "Transcription factor EB controls metabolic flexibility during exercise." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3422410.

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Skeletal muscle is the most abundant tissue in the whole organism representing more than 40% of the total body mass. This organ is responsible for the 30% of metabolic rate in basal condition, suggesting its great relevance not only for locomotor activity, but also for the control of whole body metabolism. Indeed skeletal muscle is a highly dynamic tissue that modulates its metabolism and mass as a consequence of different physiopathological conditions. One stimulus that triggers major adaptations is exercise, which is also well known to activate autophagy (Grumati, Coletto, Schiavinato, et al
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BALDASSARI, Federica. "Involvement of transcription factor EB (TFEB) and c subunit of mitochondrial F1/FO ATP synthase in cellular homeostasis." Doctoral thesis, Università degli studi di Ferrara, 2015. http://hdl.handle.net/11392/2389104.

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Marchand, Benoît. "Rôle des Glycogène synthase kinases 3 (GSK3) dans la régulation de l’autophagie et du facteur de transcription EB (TFEB) dans les cellules pancréatiques tumorales humaines." Thèse, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/8185.

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Plusieurs études ont suggéré une implication des glycogène synthase kinases 3 (GSK3) dans la carcinogenèse, notamment du pancréas. Des études ont rapporté des résultats contradictoires quant à l’impact des GSK3 sur la survie cellulaire. Au niveau du pancréas, il a été observé que l’inhibition des GSK3 inhibe la croissance entre autres via la régulation de la voie JNK ou NFkB. Les inhibiteurs des GSK3 sont présentement à l’étude comme traitement de différentes pathologies, notamment pour le cancer pancréatique. Une meilleure compréhension des voies de signalisation régulées par les GSK3
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Alvarez, Valadez Karla. "Targeting intracellular cholesterol transport for inducing lysosomal damage and immunogenic cell death in cancer." Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL123.

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Les lysosomes jouent un rôle central dans la régulation des processus anaboliques et cataboliques, la signalisation cellulaire ainsi que dans la mise en œuvre des programmes transcriptionnels au sein des cellules. Ils favorisent l’adaptation des cellules cancéreuses lors des variations du microenvironnement en leur fournissant les métabolites essentiels et l’énergie nécessaire à leur survie et à leur prolifération. Un acteur majeur dans la réponse adaptative des lysosomes est le facteur de transcription EB (TFEB). TFEB coordonne l’expression de gènes associés à la fonction et à la biogenèse de
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Bois, Philipp Du. "Transcriptional regulation of MuRF1 in skeletal muscle atrophy." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2014. http://dx.doi.org/10.18452/17079.

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Die Komposition der Skelettmuskulatur resultiert aus der fein abgestimmten Balance von Proteinauf- und Abbaumechanismen. Die Skelettmuskelatrophie kann in verschiedenen Situationen entstehen bzw. von diversen Krankheiten ausgelöst werden (Altern, Hunger, Krebs, Nervenschädigung, Kachexie) und ist meist die Folge von gesteigertem Proteinabbau, der die Proteinsynthese überwiegt. Der Muskelabbau ist physiologisch teilweise sinnvoll und dient der Notversorgung von lebenswichtigen Organen mit Lipiden, Aminosäuren und Glukose. Insgesamt ist eine funktionsfähige Muskulatur sehr wichtig, sowohl für Ge
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Torra, i. Talavera Albert. "Transcription factor EB-mediated neurotrophic and neuroprotective effects: relevance to Parkinson’s disease." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667794.

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La malaltia de Parkinson (MP) és un trastorn neurodegeneratiu crònic que es caracteritza per una pèrdua progressiva de les neurones dopaminèrgiques de la substància nigra pars compacta (SNpc). Tot i que s’han dut a terme diverses estratègies per intentar aturar la progressió de la MP, cap d’elles ha demostrat ser de suficient eficàcia. El possible paper del factor de transcripció EB (TFEB) com a diana terapèutica en la MP va guanyar importància quan es va descobrir que el TFEB controla la biogènesi lisosomal i l’autofàgia, i que la seva activació podria contrarestar el defecte lisosomal i l’ag
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Bécot, Anaïs. "Les APP-CTFs au cœur du processus pathologique de la maladie d’Alzheimer : contribution du système lysosomal-autophagique et de la sécrétion exosomale." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://theses.univ-cotedazur.fr/2019AZUR6039.

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La maladie d’Alzheimer (MA) se caractérise par l’accumulation dans le cerveau d’agrégats extracellulaires et intraneuronaux (Aβ et Tau). Dans la cellule, la principale voie de dégradation des protéines agrégées est la voie lysosomale-autophagique, qui est altérée de façon précoce chez les patients Alzheimer. Des études récentes de mon laboratoire ont montré que ce dysfonctionnement serait à la fois la cause et la conséquence de l’accumulation du précurseur direct de l’Aβ, appelé C99 ou APP-CTFβ. De par sa toxicité, le C99 semble donc jouer un rôle crucial dans l’étiologie de la maladie. Son ac
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La, Spina Martina. "Pharmacology, biochemistry and biomedical applications of plant stilbenes." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3423240.

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This thesis reports the research I conducted on aspects of the pharmacology and biological activities of two natural stilbenes, Resveratrol (Rv) and Pterostilbene (Pt), major polyphenolic components of grapevines and blueberries respectively. Over the years, these two molecules have drawn attention from the scientific community thanks to their beneficial bioactivities, relevant for many areas of health care. Numerous papers describe their protective roles against the metabolic syndrome, cancer development and neurodegeneration. These striking effects nowadays are not exclusively attribu
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Hsieh, Cheng-Wei, and 謝正偉. "Lysosome-responsive Transcription Factor EB Activation upon Mitophagy Degradation Stress." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/66573960627460377270.

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博士<br>國立清華大學<br>化學系<br>104<br>Except of the simplified view of lysosomes as the final compartments of degradation process, lysosomes are increasingly regarded as upstream organelles in the control of cell functions. Therefore, lysosome homeostasis should be tightly regulated to match the catabolic needs as well as to maintain lysosomal pathways. Here we use light-induced mitophagy substrates to disturb lysosome homeostatsis and reveal how lysosome biogenesis responses quantitatively to different levels of degradation stress. We observed that TFEB-mediated lysosomal genes activation is upregula
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Nidhiry, Anna S. "The role of the lysosome and transcription factor EB in tuberous sclerosis complex." Thesis, 2020. https://hdl.handle.net/2144/41147.

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Tuberous Sclerosis Complex (TSC) is a rare, autosomal dominant genetic disease that results from the loss-of-function mutations of either the TSC1 or TSC2 genes. It is a multisystemic disorder with manifestations in several organs including the lungs, kidneys, brain, skin, and heart. Loss of either TSC1 or TSC2 causes hyperactivation of the mechanistic target of rapamycin complex 1 (mTORC1) pathway resulting in cell proliferation and the continuous activation of multiple anabolic pathways that lead to tumor growth. Transcription factor EB (TFEB) is one of the many downstream targets of the
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Book chapters on the topic "Transcription factor EB (TFEB)"

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Gonçalves, João, Helena Soares, Norman L. Eberhardt, et al. "TFEB/Transcription Factor EB (AGS12)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101354.

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Li, Wei, Yang Liu, Min Hao, et al. "Expression of Transcription Factor EB (TFEB) Promotes Cancer Cell Proliferation, Migration and Invasion." In Lecture Notes in Electrical Engineering. Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4801-2_77.

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"TFEB/Transcription Factor EB (AGS12)." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_103808.

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Conference papers on the topic "Transcription factor EB (TFEB)"

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Marchand, Benoît, Alexandre Raymond-Fleury, and Marie-Josée Boucher. "Abstract 315: Regulation of the transcription factor TFEB and the autophagic/lysosomal network by GSK3 in pancreatic cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-315.

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