Log in

Relevant bibliographies by topics / Transcription factor EB (TFEB) / Journal articles

To see the other types of publications on this topic, follow the link: Transcription factor EB (TFEB).

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

Author: Grafiati

Published: 10 January 2024

Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Transcription factor EB (TFEB).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

2

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

3

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

4

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

5

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

6

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

7

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

8

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

10

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

11

Cesana, Marcella, Gennaro Tufano, Francesco Panariello, et al. "EGR1 drives cell proliferation by directly stimulating TFEB transcription in response to starvation." PLOS Biology 21, no. 3 (2023): e3002034. http://dx.doi.org/10.1371/journal.pbio.3002034.

Full text

Abstract:

The stress-responsive transcription factor EB (TFEB) is a master controller of lysosomal biogenesis and autophagy and plays a major role in several cancer-associated diseases. TFEB is regulated at the posttranslational level by the nutrient-sensitive kinase complex mTORC1. However, little is known about the regulation of TFEB transcription. Here, through integrative genomic approaches, we identify the immediate-early gene EGR1 as a positive transcriptional regulator of TFEB expression in human cells and demonstrate that, in the absence of EGR1, TFEB-mediated transcriptional response to starvat

APA, Harvard, Vancouver, ISO, and other styles

12

Wang, Shujun, Yanse Chen, Hongluan Wu, et al. "Role of Transcription Factor EB in Mitochondrial Dysfunction of Cisplatin-Induced Acute Kidney Injury." International Journal of Molecular Sciences 24, no. 3 (2023): 3028. http://dx.doi.org/10.3390/ijms24033028.

Full text

Abstract:

Cisplatin, a widely used anticancer agent, can cause nephrotoxicity, including both acute kidney injury (AKI) and chronic kidney diseases, by accumulating in renal tubular epithelial cells (TECs). Mitochondrial pathology plays an important role in the pathogenesis of AKI. Based on the regulatory role of transcription factor EB (TFEB) in mitochondria, we investigated whether TFEB is involved in cisplatin-induced TEC damage. The results show that the expression of TFEB decreased in a concentration-dependent manner in both mouse kidney tissue and HK-2 cells when treated with cisplatin. A knockdow

APA, Harvard, Vancouver, ISO, and other styles

13

Corà, Davide, Federico Bussolino, and Gabriella Doronzo. "TFEB Signalling-Related MicroRNAs and Autophagy." Biomolecules 11, no. 7 (2021): 985. http://dx.doi.org/10.3390/biom11070985.

Full text

Abstract:

The oncogenic Transcription Factor EB (TFEB), a member of MITF-TFE family, is known to be the most important regulator of the transcription of genes responsible for the control of lysosomal biogenesis and functions, autophagy, and vesicles flux. TFEB activation occurs in response to stress factors such as nutrient and growth factor deficiency, hypoxia, lysosomal stress, and mitochondrial damage. To reach the final functional status, TFEB is regulated in multimodal ways, including transcriptional rate, post-transcriptional regulation, and post-translational modifications. Post-transcriptional r

APA, Harvard, Vancouver, ISO, and other styles

14

Bartlett, Jordan J., Purvi C. Trivedi, Pollen Yeung, Petra C. Kienesberger, and Thomas Pulinilkunnil. "Doxorubicin impairs cardiomyocyte viability by suppressing transcription factor EB expression and disrupting autophagy." Biochemical Journal 473, no. 21 (2016): 3769–89. http://dx.doi.org/10.1042/bcj20160385.

Full text

Abstract:

Doxorubicin (DOX) is an effective anti-cancer agent. However, DOX treatment increases patient susceptibility to dilated cardiomyopathy. DOX predisposes cardiomyocytes to insult by suppressing mitochondrial energy metabolism, altering calcium flux, and disrupting proteolysis and proteostasis. Prior studies have assessed the role of macroautophagy in DOX cardiotoxicity; however, limited studies have examined whether DOX mediates cardiac injury through dysfunctions in inter- and/or intra-lysosomal signaling events. Lysosomal signaling and function is governed by transcription factor EB (TFEB). In

APA, Harvard, Vancouver, ISO, and other styles

15

Alcalde, Alejandra Diaz, Edoardo Vallariello, Elena Astanina, Emanuele Middonti, and Federico Bussolino. "Abstract 2355: Transcription factor EB modulates fibrotic response in pancreatic ductal adenocarcinoma." Cancer Research 83, no. 7_Supplement (2023): 2355. http://dx.doi.org/10.1158/1538-7445.am2023-2355.

Full text

Abstract:

Abstract Pancreatic ductal adenocarcinoma (PDAC), which comprises 85% of all the pancreatic cancers, is one of the most aggressive and deadly tumor that exists today with less than 8% of survival 5 years after diagnosis. It is predicted to become the second cause of cancer death by 2030. A typical characteristic of this tumor is the presence of prominent stroma component mainly produced by Pancreatic Stellate Cells (PSCs) in response to soluble factors released by cancer cells. PSCs activation and differentiation into CAF (Cancer-associated fibroblasts) is a reversible process, which impacts o

APA, Harvard, Vancouver, ISO, and other styles

16

Ma, Xiucui, Haiyan Liu, John T. Murphy та ін. "Regulation of the Transcription Factor EB-PGC1α Axis by Beclin-1 Controls Mitochondrial Quality and Cardiomyocyte Death under Stress". Molecular and Cellular Biology 35, № 6 (2015): 956–76. http://dx.doi.org/10.1128/mcb.01091-14.

Full text

Abstract:

In cardiac ischemia-reperfusion injury, reactive oxygen species (ROS) generation and upregulation of the hypoxia-inducible protein BNIP3 result in mitochondrial permeabilization, but impairment in autophagic removal of damaged mitochondria provokes programmed cardiomyocyte death. BNIP3 expression and ROS generation result in upregulation of beclin-1, a protein associated with transcriptional suppression of autophagy-lysosome proteins and reduced activation of transcription factor EB (TFEB), a master regulator of the autophagy-lysosome machinery. Partial beclin-1 knockdown transcriptionally sti

APA, Harvard, Vancouver, ISO, and other styles

17

Peña, Karina A., and Kirill Kiselyov. "Transition metals activate TFEB in overexpressing cells." Biochemical Journal 470, no. 1 (2015): 65–76. http://dx.doi.org/10.1042/bj20140645.

Full text

Abstract:

Exposure of cells to micromolar Cu activates recombinant transcription factor EB (TFEB), leading to expression of the lysosomal network genes. Whereas TFEB overexpression has a cytoprotective effect under moderate Cu exposure, it enhances oxidative stress and mitochondrial damage caused by high levels of Cu.

APA, Harvard, Vancouver, ISO, and other styles

18

Fan, Yanbo, Haocheng Lu, Wenying Liang, et al. "Endothelial TFEB (Transcription Factor EB) Positively Regulates Postischemic Angiogenesis." Circulation Research 122, no. 7 (2018): 945–57. http://dx.doi.org/10.1161/circresaha.118.312672.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Chen, Mingyue, Yashuang Dai, Siyu Liu, Yuxin Fan, Zongxian Ding, and Dan Li. "TFEB Biology and Agonists at a Glance." Cells 10, no. 2 (2021): 333. http://dx.doi.org/10.3390/cells10020333.

Full text

Abstract:

Autophagy is a critical regulator of cellular survival, differentiation, development, and homeostasis, dysregulation of which is associated with diverse diseases including cancer and neurodegenerative diseases. Transcription factor EB (TFEB), a master transcriptional regulator of autophagy and lysosome, can enhance autophagic and lysosomal biogenesis and function. TFEB has attracted a lot of attention owing to its ability to induce the intracellular clearance of pathogenic factors in a variety of disease models, suggesting that novel therapeutic strategies could be based on the modulation of T

APA, Harvard, Vancouver, ISO, and other styles

20

Shi, Yan, Zhaoyu Mi, Wei Zhao, et al. "Melatonin Mitigates Acidosis-Induced Neuronal Damage by Up-Regulating Autophagy via the Transcription Factor EB." International Journal of Molecular Sciences 26, no. 3 (2025): 1170. https://doi.org/10.3390/ijms26031170.

Full text

Abstract:

Acidosis, a common feature of cerebral ischemia and hypoxia, results in neuronal damage and death. This study aimed to investigate the protective effects and mechanisms of action of melatonin against acidosis-induced neuronal damage. SH-SY5Y cells were exposed to an acidic environment to simulate acidosis, and a photothrombotic (PT) infarction model was used to establish an animal model of cerebral ischemia of male C57/BL6J mice. Both in vivo and in vitro studies demonstrated that acidosis increased cytoplasmic transcription factor EB (TFEB) levels, reduced nuclear TFEB levels, and suppressed

APA, Harvard, Vancouver, ISO, and other styles

21

Wang, Hongjie, Ruizhi Wang, Shaohua Xu, and Madepalli K. Lakshmana. "Transcription Factor EB Is Selectively Reduced in the Nuclear Fractions of Alzheimer’s and Amyotrophic Lateral Sclerosis Brains." Neuroscience Journal 2016 (June 28, 2016): 1–8. http://dx.doi.org/10.1155/2016/4732837.

Full text

Abstract:

Multiple studies suggest that autophagy is strongly dysregulated in Alzheimer’s disease (AD) and amyotrophic lateral sclerosis (ALS), as evidenced by accumulation of numerous autophagosomes, lysosomes with discontinuous membranes, and aggregated proteins in the patients’ brains. Transcription factor EB (TFEB) was recently discovered to be a master regulator of lysosome biogenesis and autophagy. To examine whether aberrant autophagy in AD and ALS is due to alterations in TFEB expression, we systematically quantified the levels of TFEB in these brains by immunoblotting. Interestingly, cytoplasmi

APA, Harvard, Vancouver, ISO, and other styles

22

Wang, Shujun, Kaipeng Jing, Hongluan Wu, et al. "Activation of Transcription Factor EB Alleviates Tubular Epithelial Cell Injury via Restoring Lysosomal Homeostasis in Diabetic Nephropathy." Oxidative Medicine and Cellular Longevity 2022 (January 12, 2022): 1–24. http://dx.doi.org/10.1155/2022/2812493.

Full text

Abstract:

Disruption of lysosomal homeostasis contributes to the tubulopathy of diabetic nephropathy; however, its underlying mechanisms remain unclear. Herein, we report that decreased activity of transcription factor EB (TFEB) is responsible for the disturbed lysosome biogenesis and clearance in this pathological process. This was confirmed by the findings that insufficient lysosomal replenishment and damaged lysosomal clearance coincided with TFEB inactivation, which was mediated by mTOR hyperactivation in the renal tubular epithelial cells (TECs) of diabetic nephropathy. Furthermore, either TFEB ove

APA, Harvard, Vancouver, ISO, and other styles

23

Kim, Soyoung, Gahyeon Song, Taebok Lee та ін. "PARsylated transcription factor EB (TFEB) regulates the expression of a subset of Wnt target genes by forming a complex with β-catenin-TCF/LEF1". Cell Death & Differentiation 28, № 9 (2021): 2555–70. http://dx.doi.org/10.1038/s41418-021-00770-7.

Full text

Abstract:

AbstractWnt signaling is mainly transduced by β-catenin via regulation of the β-catenin destruction complex containing Axin, APC, and GSK3β. Transcription factor EB (TFEB) is a well-known master regulator of autophagy and lysosomal biogenesis processes. TFEB’s nuclear localization and transcriptional activity are also regulated by various upstream signals. In this study, we found that Wnt signaling induces the nuclear localization of TFEB and the expression of Wnt target genes is regulated by TFEB-β-catenin-TCF/LEF1 as well as β-catenin-TCF/LEF1 complexes. Our biochemical data revealed that TF

APA, Harvard, Vancouver, ISO, and other styles

24

Martina, Jose A., and Rosa Puertollano. "Rag GTPases mediate amino acid–dependent recruitment of TFEB and MITF to lysosomes." Journal of Cell Biology 200, no. 4 (2013): 475–91. http://dx.doi.org/10.1083/jcb.201209135.

Full text

Abstract:

The mTORC1 complex supports cell growth and proliferation in response to energy levels, growth factors, and nutrients. The Rag guanosine triphosphatases (GTPases) activate mTORC1 in response to amino acids by promoting its redistribution to lysosomes. In this paper, we identify a novel role for Rags in controlling activation of transcription factor EB (TFEB), a master regulator of autophagic and lysosomal gene expression. Interaction of TFEB with active Rag heterodimers promoted recruitment of TFEB to lysosomes, leading to mTORC1-dependent phosphorylation and inhibition of TFEB. The interactio

APA, Harvard, Vancouver, ISO, and other styles

25

Lee, Sun-Jae, Young-Ah Kim, and Kwan-Kyu Park. "Anti-Fibrotic Effect of Synthetic Noncoding Decoy ODNs for TFEB in an Animal Model of Chronic Kidney Disease." International Journal of Molecular Sciences 23, no. 15 (2022): 8138. http://dx.doi.org/10.3390/ijms23158138.

Full text

Abstract:

Despite emerging evidence suggesting that autophagy occurs during renal interstitial fibrosis, the role of autophagy activation in fibrosis and the mechanism by which autophagy influences fibrosis remain controversial. Transcription factor EB (TFEB) is a master regulator of autophagy-related gene transcription, lysosomal biogenesis, and autophagosome formation. In this study, we examined the preventive effects of TFEB suppression on renal fibrosis. We injected synthesized TFEB decoy oligonucleotides (ODNs) into the tail veins of unilateral ureteral obstruction (UUO) mice to explore the regulat

APA, Harvard, Vancouver, ISO, and other styles

26

Yan, Shengmin. "Role of TFEB in Autophagy and the Pathogenesis of Liver Diseases." Biomolecules 12, no. 5 (2022): 672. http://dx.doi.org/10.3390/biom12050672.

Full text

Abstract:

The transcription factor EB (TFEB) is a master regulator of lysosomal function and autophagy. Mechanistic target of rapamycin (mTOR)-mediated phosphorylation on TFEB is known to regulate TFEB subcellular localization and activity at the lysosomal surface. Recent studies have shown that TFEB also plays a critical role in physiological processes such as lipid metabolism, and dysfunction of TFEB has been observed in the pathogenesis of several diseases. Owing to its ability to improve disease status in murine models, TFEB has attracted attention as a therapeutic target for diseases. In this revie

APA, Harvard, Vancouver, ISO, and other styles

27

Kim, Ji Hye, Jinyoung Lee, Young-Ra Cho, et al. "TFEB Supports Pancreatic Cancer Growth through the Transcriptional Regulation of Glutaminase." Cancers 13, no. 3 (2021): 483. http://dx.doi.org/10.3390/cancers13030483.

Full text

Abstract:

Transcription factor EB (TFEB) is a master regulator of lysosomal function and autophagy. In addition, TFEB has various physiological roles such as nutrient sensing, cellular stress responses, and immune responses. However, the precise roles of TFEB in pancreatic cancer growth remain unclear. Here, we show that pancreatic cancer cells exhibit a significantly elevated TFEB expression compared with normal tissue samples and that the genetic inhibition of TFEB results in a significant inhibition in both glutamine and mitochondrial metabolism, which in turn suppresses the PDAC growth both in vitro

APA, Harvard, Vancouver, ISO, and other styles

28

Liu, Yan, Jing Li, Xianfeng Lu, Shuangping Zhen, and Jing Huo. "Toll-Like Receptor 4 Exacerbates Mycoplasma pneumoniaevia Promoting Transcription Factor EB-Mediated Autophagy." Contrast Media & Molecular Imaging 2022 (July 31, 2022): 1–9. http://dx.doi.org/10.1155/2022/3357694.

Full text

Abstract:

Mycoplasma pneumoniae (M. pneumoniae) is the most common cause of community-acquired pneumonia. Toll-like receptors (TLRs) play an essential role in pneumonia. The purpose of this study was to investigate the roles of TLR4 in M. pneumoniae. Mice were administrated with 100 μl (1 × 107 ccu/ml) of M. pneumoniae. HE staining was applied for histological analysis. The protein expression was determined by western blot. The cytokine level was detected by ELISA. The results showed that TLR4-deficient mice were protected from M. pneumoniae. However, downregulation of TLR4 inhibited inflammatory respon

APA, Harvard, Vancouver, ISO, and other styles

29

La Spina, Martina, Michele Azzolini, Andrea Salmaso, et al. "Multiple Mechanisms Converging on Transcription Factor EB Activation by the Natural Phenol Pterostilbene." Oxidative Medicine and Cellular Longevity 2021 (December 28, 2021): 1–19. http://dx.doi.org/10.1155/2021/7658501.

Full text

Abstract:

Pterostilbene (Pt) is a potentially beneficial plant phenol. In contrast to many other natural compounds (including the more celebrated resveratrol), Pt concentrations producing significant effects in vitro can also be reached with relative ease in vivo. Here we focus on some of the mechanisms underlying its activity, those involved in the activation of transcription factor EB (TFEB). A set of processes leading to this outcome starts with the generation of ROS, attributed to the interaction of Pt with complex I of the mitochondrial respiratory chain, and spreads to involve Ca2+ mobilization fr

APA, Harvard, Vancouver, ISO, and other styles

30

Gao, Xing, Ziying Liang, Yanan Yuan, and Wenbo Liu. "Silencing PDCD4 Mediates Transcription Factor EB Overexpression Promoting Proliferation, Migration, and Invasion of Cervical Cancer Hela Cells." Science of Advanced Materials 16, no. 8 (2024): 916–22. http://dx.doi.org/10.1166/sam.2024.4636.

Full text

Abstract:

Cervical cancer is a common gynecologic malignant tumor, the occurrence and development of which are related to multiple genetic and environmental factors. Recent studies have shown that Programmed Cell Death 4 (PDCD4) plays a crucial role in cervical cancer, and that silencing PDCD4 mediates Transcription Factor EB (TFEB) overexpression, promoting cell proliferation, migration, and invasion in this disease. This study utilized the Hela cell line as a cervical cancer model to investigate the changes in TFEB expression levels and the proliferation, migration, invasion, and EMT processes of cerv

APA, Harvard, Vancouver, ISO, and other styles

31

Wang, Yun-Ting, Jiajie Chen, Xiang Li, et al. "Contribution of transcription factor EB to adipoRon-induced inhibition of arterial smooth muscle cell proliferation and migration." American Journal of Physiology-Cell Physiology 317, no. 5 (2019): C1034—C1047. http://dx.doi.org/10.1152/ajpcell.00294.2019.

Full text

Abstract:

Abnormal vascular smooth muscle cell (SMC) dedifferentiation with increased proliferation and migration during pathological vascular remodeling is associated with vascular disorders, such as atherosclerosis and in-stent restenosis. AdipoRon, a selective agonist of adiponectin receptor, has been shown to protect against vascular remodeling by preventing SMC dedifferentiation. However, the molecular mechanisms that mediate adipoRon-induced SMC differentiation are not well understood. The present study aimed to elucidate the role of transcription factor EB (TFEB), a master regulator of autophagy,

APA, Harvard, Vancouver, ISO, and other styles

32

Li, Zhenyu, Guangqian Ding, Yudi Wang, Zelong Zheng, and Jianping Lv. "Safety profile of the transcription factor EB (TFEB)-based gene therapy through intracranial injection in mice." Translational Neuroscience 11, no. 1 (2020): 241–50. http://dx.doi.org/10.1515/tnsci-2020-0132.

Full text

Abstract:

AbstractTranscription factor EB (TFEB)-based gene therapy is a promising therapeutic strategy in treating neurodegenerative diseases by promoting autophagy/lysosome-mediated degradation and clearance of misfolded proteins that contribute to the pathogenesis of these diseases. However, recent findings have shown that TFEB has proinflammatory properties, raising the safety concerns about its clinical application. To investigate whether TFEB induces significant inflammatory responses in the brain, male C57BL/6 mice were injected with phosphate-buffered saline (PBS), adeno-associated virus serotyp

APA, Harvard, Vancouver, ISO, and other styles

33

Franco-Juárez, Berenice, Cristina Coronel-Cruz, Beatriz Hernández-Ochoa, et al. "TFEB; Beyond Its Role as an Autophagy and Lysosomes Regulator." Cells 11, no. 19 (2022): 3153. http://dx.doi.org/10.3390/cells11193153.

Full text

Abstract:

Transcription factor EB (TFEB) is considered the master transcriptional regulator of autophagy and lysosomal biogenesis, which regulates target gene expression through binding to CLEAR motifs. TFEB dysregulation has been linked to the development of numerous pathological conditions; however, several other lines of evidence show that TFEB might be a point of convergence of diverse signaling pathways and might therefore modulate other important biological processes such as cellular senescence, DNA repair, ER stress, carbohydrates, and lipid metabolism and WNT signaling-related processes. The reg

APA, Harvard, Vancouver, ISO, and other styles

34

Erlich, Avigail T., Diane M. Brownlee, Kaitlyn Beyfuss та David A. Hood. "Exercise induces TFEB expression and activity in skeletal muscle in a PGC-1α-dependent manner". American Journal of Physiology-Cell Physiology 314, № 1 (2018): C62—C72. http://dx.doi.org/10.1152/ajpcell.00162.2017.

Full text

Abstract:

The mitochondrial network in muscle is controlled by the opposing processes of mitochondrial biogenesis and mitophagy. The coactivator peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) regulates biogenesis, while the transcription of mitophagy-related genes is controlled by transcription factor EB (TFEB). PGC-1α activation is induced by exercise; however, the effect of exercise on TFEB is not fully known. We investigated the interplay between PGC-1α and TFEB on mitochondria in response to acute contractile activity in C2C12 myotubes and following exercise in wild-type and PG

APA, Harvard, Vancouver, ISO, and other styles

35

Huang, Yi, Yan Chen, Amanda Marie Shaw, Howard Goldfine, Junqiang Tian, and Jiyang Cai. "Enhancing TFEB-Mediated Cellular Degradation Pathways by the mTORC1 Inhibitor Quercetin." Oxidative Medicine and Cellular Longevity 2018 (October 28, 2018): 1–9. http://dx.doi.org/10.1155/2018/5073420.

Full text

Abstract:

Signaling pathways mediated by the mechanistic target of rapamycin (mTOR) play key roles in aging and age-related diseases. As a downstream protein of mTOR, transcription factor EB (TFEB) controls lysosome biogenesis and cellular trafficking, processes that are essential for the functions of phagocytic cells like the retinal pigment epithelium (RPE). In the current study, we show that a naturally occurring polyphenolic compound, quercetin, promoted TFEB nuclear translocation and enhanced its transcriptional activity in cultured RPE cells. Activated TFEB facilitated degradation of phagocytosed

APA, Harvard, Vancouver, ISO, and other styles

36

Jeong, Seokmin, Jun-Kyu Byun, Sung Cho, et al. "Transcription Factor Eb Is Required for Macropinocytosis-Mediated Growth Recovery of Nutrient-Deprived Kras-Mutant Cells." Nutrients 10, no. 11 (2018): 1638. http://dx.doi.org/10.3390/nu10111638.

Full text

Abstract:

Macropinocytosis is a regulated form of endocytosis that mediates the nonselective uptake of nutrients to support growth under nutrient-deprived conditions. KRAS-mutant cancer cells upregulate macropinocytosis to import extracellular proteins, which subsequently undergo proteolytic degradation in the lysosome. Although transcription factor EB (TFEB) is a master regulator of lysosomal biogenesis and function, its role in the degradation of extracellular protein from macropinocytosis in KRAS-mutant cells has not previously been elucidated. In this study, we investigated the role of TFEB in the r

APA, Harvard, Vancouver, ISO, and other styles

37

Liu, Cong, Dawang Zhou, Qiang Zhang та ін. "Transcription factor EB (TFEB) improves ventricular remodeling after myocardial infarction by inhibiting Wnt/β-catenin signaling pathway". PeerJ 11 (18 серпня 2023): e15841. http://dx.doi.org/10.7717/peerj.15841.

Full text

Abstract:

Background Adverse left ventricular remodeling after myocardial infarction (MI) compromises cardiac function and increases heart failure risk. Until now, comprehension of the role transcription factor EB (TFEB) plays after MI is limited. Objectives The purpose of this study was to describe the effects of TFEB on fibroblasts differentiation and extracellular matrix expression after MI. Methods AAV9 (adeno-associated virus) mediated up- and down-regulated TFEB expressions were generated in C57BL/6 mice two weeks before the MI modeling. Echocardiography, Masson, Sirius red staining immunofluoresc

APA, Harvard, Vancouver, ISO, and other styles

38

Wang, Ziying, Chuanbin Yang, Jia Liu, et al. "A Curcumin Derivative Activates TFEB and Protects Against Parkinsonian Neurotoxicity in Vitro." International Journal of Molecular Sciences 21, no. 4 (2020): 1515. http://dx.doi.org/10.3390/ijms21041515.

Full text

Abstract:

TFEB (transcription factor EB), which is a master regulator of autophagy and lysosome biogenesis, is considered to be a new therapeutic target for Parkinson’s disease (PD). However, only several small-molecule TFEB activators have been discovered and their neuroprotective effects in PD are unclear. In this study, a curcumin derivative, named E4, was identified as a potent TFEB activator. Compound E4 promoted the translocation of TFEB from cytoplasm into nucleus, accompanied by enhanced autophagy and lysosomal biogenesis. Moreover, TFEB knockdown effectively attenuated E4-induced autophagy and

APA, Harvard, Vancouver, ISO, and other styles

39

Zhang, Li, Haiying Ma, Xiaobing Zhang, et al. "Feasibility of transcription factor EB as a serological metric of poor prognosis following moderate–severe traumatic brain injury: A prospective cohort study." Medicine 104, no. 18 (2025): e42271. https://doi.org/10.1097/md.0000000000042271.

Full text

Abstract:

Transcription factor EB (TFEB) is an endogenous protective factor. Here, we sought to discern the possibility of serum TFEB as a prognostic biomarker of moderate–severe traumatic brain injury (msTBI). Serum TFEB levels of 141 patients with msTBI and 70 controls were quantified in this prospective cohort study. Rotterdam computed tomography (CT) classification and Glasgow coma scale (GCS) were considered as the severity metrics. Glasgow outcome scale (GOS) scores of 1 to 3 at 6 months after trauma meant a poor prognosis. The results were analyzed using multivariate analysis. Patients versus con

APA, Harvard, Vancouver, ISO, and other styles

40

Nakamura, Shuhei, Shiori Akayama, and Tamotsu Yoshimori. "Non-canonical roles of ATG8 for TFEB activation." Biochemical Society Transactions 50, no. 1 (2022): 47–54. http://dx.doi.org/10.1042/bst20210813.

Full text

Abstract:

Autophagy is an evolutionally conserved cytoplasmic degradation pathway in which the double membrane structure, autophagosome sequesters cytoplasmic material and delivers them to lysosomes for degradation. Many autophagy related (ATG) proteins participate in the regulation of the several steps of autophagic process. Among ATGs, ubiquitin-like protein, ATG8 plays a pivotal role in autophagy. ATG8 is directly conjugated on lipid in autophagosome membrane upon induction of autophagy thus providing a good marker to monitor and analyze autophagy process. However, recent discoveries suggest that ATG

APA, Harvard, Vancouver, ISO, and other styles

41

Ma, Shumin, Zijun Fang, Wenwen Luo, et al. "The C-ETS2-TFEB Axis Promotes Neuron Survival under Oxidative Stress by Regulating Lysosome Activity." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/4693703.

Full text

Abstract:

Excessive reactive oxygen species/reactive nitrogen species (ROS/RNS) produced as a result of ageing causes damage to macromolecules and organelles or leads to interference of cell signalling pathways, which in turn results in oxidative stress. Oxidative stress occurs in many neurodegenerative diseases (e.g., Parkinson’s disease) and contributes to progressive neuronal loss. In this study, we show that cell apoptosis is induced by oxidative stress and that lysosomes play an important role in cell survival under oxidative stress. As a compensatory response to this stress, lysosomal genes were u

APA, Harvard, Vancouver, ISO, and other styles

42

Moskot, Marta, Sandro Montefusco, Joanna Jakóbkiewicz-Banecka, et al. "The Phytoestrogen Genistein Modulates Lysosomal Metabolism and Transcription Factor EB (TFEB) Activation." Journal of Biological Chemistry 289, no. 24 (2014): 17054–69. http://dx.doi.org/10.1074/jbc.m114.555300.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Li, Yuting, Xiang Ye, Xiaodong Zheng, and Wei Chen. "Transcription factor EB (TFEB)-mediated autophagy protects against ethyl carbamate-induced cytotoxicity." Journal of Hazardous Materials 364 (February 2019): 281–92. http://dx.doi.org/10.1016/j.jhazmat.2018.10.037.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Spampanato, Carmine, Erin Feeney, Lishu Li, et al. "Transcription factor EB (TFEB) is a new therapeutic target for Pompe disease." EMBO Molecular Medicine 5, no. 5 (2013): 691–706. http://dx.doi.org/10.1002/emmm.201202176.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Kuiper, RP. "TFEB (transcription factor EB)." Atlas of Genetics and Cytogenetics in Oncology and Haematology, no. 3 (February 2011). http://dx.doi.org/10.4267/2042/38098.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

"Transcription factor EB (TFEB)." Science-Business eXchange 6, no. 18 (2013): 440. http://dx.doi.org/10.1038/scibx.2013.440.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Doronzo, Gabriella, Elena Astanina, and Federico Bussolino. "The Oncogene Transcription Factor EB Regulates Vascular Functions." Frontiers in Physiology 12 (April 12, 2021). http://dx.doi.org/10.3389/fphys.2021.640061.

Full text

Abstract:

Transcription factor EB (TFEB) represents an emerging player in vascular biology. It belongs to the bHLH-leucine zipper transcription factor microphthalmia family, which includes microphthalmia-associated transcription factor, transcription factor E3 and transcription factor EC, and is known to be deregulated in cancer. The canonical transcriptional pathway orchestrated by TFEB adapts cells to stress in all kinds of tissues by supporting lysosomal and autophagosome biogenesis. However, emerging findings highlight that TFEB activates other genetic programs involved in cell proliferation, metabo

APA, Harvard, Vancouver, ISO, and other styles

48

Pasquier, Adrien, Nunzia Pastore, Luca D'Orsi, et al. "TFEB and TFE3 control glucose homeostasis by regulating insulin gene expression." EMBO Journal, September 15, 2023. http://dx.doi.org/10.15252/embj.2023113928.

Full text

Abstract:

AbstractTo fulfill their function, pancreatic beta cells require precise nutrient‐sensing mechanisms that control insulin production. Transcription factor EB (TFEB) and its homolog TFE3 have emerged as crucial regulators of the adaptive response of cell metabolism to environmental cues. Here, we show that TFEB and TFE3 regulate beta‐cell function and insulin gene expression in response to variations in nutrient availability. We found that nutrient deprivation in beta cells promoted TFEB/TFE3 activation, which resulted in suppression of insulin gene expression. TFEB overexpression was sufficien

APA, Harvard, Vancouver, ISO, and other styles

49

Yin, Xiang, Li Cui, Jie Shao, Yue Lang, and Manqiu Ding. "Transcription Factor EB: A Promising Therapeutic Target for Ischemic Stroke." Current Neuropharmacology 21 (July 24, 2023). http://dx.doi.org/10.2174/1570159x21666230724095558.

Full text

Abstract:

Abstract: Transcription factor EB (TFEB) is an important endogenous defensive protein that responds to ischemic stimuli. Acute ischemic stroke is a growing concern due to its high morbidity and mortality. Most survivors suffer from disabilities such as numbness or weakness in an arm or leg, facial droop, difficulty speaking or understanding speech, confusion, impaired balance or coordination, or loss of vision. Although TFEB plays a neuroprotective role, its potential effect on ischemic stroke remains unclear. This article describes the basic structure, regulation of transcriptional activity,

APA, Harvard, Vancouver, ISO, and other styles

50

Killips, Brigham, Emily J. Bremer Heaton, Leonardo Augusto, Anders Omsland, and Stacey D. Gilk. "Coxiella burnetii inhibits nuclear translocation of TFEB, the master transcription factor for lysosomal biogenesis." Journal of Bacteriology, July 26, 2024. http://dx.doi.org/10.1128/jb.00150-24.

Full text

Abstract:

ABSTRACT Coxiella burnetii is a highly infectious, Gram-negative, obligate intracellular bacterium and the causative agent of human Q fever. The Coxiella Containing Vacuole (CCV) is a modified phagolysosome that forms through fusion with host endosomes and lysosomes. While an initial acidic pH < 4.7 is essential to activate Coxiella metabolism, the mature, growth-permissive CCV has a luminal pH of ~5.2 that remains stable throughout infection. Inducing CCV acidification to a lysosomal pH (~4.7) causes Coxiella degradation, suggesting that Coxiella regulates CCV pH. Supporting this hypothesi

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!