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Transcription factor that specifically recognizes and binds E-box sequences (3'-CANNTG-5'). Additionally we are shipping Transcription Factor EB Antibodies (153) and and many more products for this protein.
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Human TFEB Protein expressed in Escherichia coli (E. coli) - ABIN2733467
Song, Sun, Peluso, Zeng, Yu, Lu, Xu, Wang, Liu, Huang, Chen, Durairajan, Zhang, Zhou, Zhang, Lu, Ballabio, Medina, Guo, Li: A novel curcumin analog binds to and activates TFEB in vitro and in vivo independent of MTOR inhibition. in Autophagy 2016
Data suggest that transcription factor EB (TFEB) is a protective transcription factor against endothelial cell inflammation and a potential target for treating atherosclerosis and associated cardiovascular diseases.
Both Danon Disease and glycogen (show GYS1 Proteins) storage disease type II show accumulation and altered localization of VPS15 in autophagy-incompetent fibers. However, TFEB displays a different pattern between these two lysosomal storage diseases
Studies identified TFEB and TFE3 (show TFE3 Proteins) as master modulators of stress response notably in the lysosomal biogenesis and autophagy with capability to upregulate hundreds of genes involved in intracellular clearance, catabolism, metabolic processes, and cellular homeostasis.
Findings suggest that TFEB activation in tauopathy model mice stimulates the autophagy-lysosome pathway, resulting in the clearance of PHF-tau (show MAPT Proteins) and lipofuscins, which in turn may rescue loss of synapses, and learning and memory deficits.
Data suggest that PEG3 is required for TFEB induction and nuclear translocation in a VEGFR2 (show KDR Proteins)- and AMPK (show PRKAA1 Proteins)-dependent manner for decorin/decorin (show DCN Proteins) receptor-evoked autophagy. (PEG3 = paternally expressed 3 protein; TFEB = transcription factor EB; VEGFR2 (show KDR Proteins) = vascular endothelial growth factor receptor-2 (show KDR Proteins); AMPK (show PRKAA1 Proteins) = AMP-activated protein kinase (show PRKAA2 Proteins))
Results demonstrate that TFEB levels and subcellular distribution undergo distinct short-term and long-term control. These findings suggest that the rapid rheostatic response, mediated by mTOR (show FRAP1 Proteins), allows the cell to quickly adapt to metabolic changes, while the long-term, mTOR (show FRAP1 Proteins) independent homeostatic response controls the magnitude and duration of TFEB activation, and presumably limits excessive autophagy.
Consistent with reduced transcription factor EB (TFEB) activity, accumulation of phosphorylated TFEB in STUB1 (show STUB1 Proteins)-deficient cells resulted in reduced autophagy and reduced mitochondrial biogenesis. These studies reveal that the ubiquitin-proteasome pathway participates in regulating autophagy and lysosomal functions by regulating the activity of TFEB.
TFEB has attracted a lot of attention owing to its ability to induce the intracellular clearance of pathogenic factors in a variety of murine models of disease, such as Parkinson's and Alzheimer's, suggesting that novel therapeutic strategies could be based on the modulation of TFEB activity.
Amplification of chromosome 6p including the TFEB gene is a novel occurrence in renal cell carcinoma (show MOK Proteins), which seems to be associated with an often aggressive and infiltrative tubulopapillary growth pattern.
TFEB-amplified renal cell carcinomas represent a distinct molecular subtype of high-grade adult renal cell carcinomas associated with aggressive clinical behavior, variable morphology, and aberrant melanocytic marker expression
These results suggest that TFEB expression in the striatum of HDQ175/Q7 mice stimulates autophagy and lysosome activity.
A functional role for TFEB downregulation in impaired autophagy completion with JAK2 (show JAK2 Proteins) knockdown is implied by the coincident downregulation in TFEB-regulated genes and a restoration of autophagic flux and podocyte permselectivity by TFEB overexpression.
Tfe3 (show TFE3 Proteins) and Tfeb are required for the induced expression of Ppargamma2 (show PPARG Proteins) and subsequently for adipogenic genes.
our data indicate that PPAR-alpha (show PPARA Proteins) mediates antimicrobial responses to mycobacterial infection by inducing TFEB and lipid catabolism.
These findings identify TFEB as a critical mediator of the beneficial effects of exercise on metabolism.
Consistent with reduced mTOR (show FRAP1 Proteins) activity and increased TFEB levels, loss of C9orf72 (show C9ORF72 Proteins) enhances autophagic flux, suggesting that C9orf72 (show C9ORF72 Proteins) is a negative regulator of autophagy
these results uncover a potent role for TFEB-mediated autophagy in the pathogenesis of Cd-induced neurotoxicity, suggesting that control of the autophagic pathway by melatonin might provide an important clue for exploring potential targets for novel therapeutics of Cd-induced neurotoxicity.
TFEB mediated autophagy is crucial for protection against lipopolysaccharide induced myocardial injury particularly in aging senescent heart.
Acute and chronic ethanol administration affects TFEB localization in the liver and regulates hepatic autophagy.
The zebrafish genome contain two mitf (mitfa (show MITF Proteins) and mitfb (show MITF Proteins)), two tfe3 (show TFE3 Proteins) (tfe3a and tfe3b), and single tfeb and tfec (show TFEC Proteins) genes.
Transcription factor that specifically recognizes and binds E-box sequences (3'-CANNTG-5'). Efficient DNA-binding requires dimerization with itself or with another MiT/TFE family member such as TFE3 or MITF. In association with TFE3, activates the expression of CD40L in T-cells, thereby playing a role in T- cell-dependent antibody responses in activated CD4(+) T-cells and thymus-dependent humoral immunity. Specifically recognizes and binds the CLEAR-box sequence (5'-GTCACGTGAC-3') present in the regulatory region of many lysosomal genes, leading to activate their expression. It thereby plays a central role in expression of lysosomal genes. Specifically recognizes the gamma-E3 box, a subset of E-boxes, present in the heavy-chain immunoglobulin enhancer. Plays a role in the signal transduction processes required for normal vascularization of the placenta.
transcription factor EB
, transcription factor EB-like
, T-cell transcription factor EB
, class E basic helix-loop-helix protein 35