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  5. How Does Nature.com Make Money
  6. How Much Does Nature.com Make
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We are analyzing https://www.nature.com/articles/s41420-020-0265-4.

Title:
Regulation of TFEB activity and its potential as a therapeutic target against kidney diseases | Cell Death Discovery
Description:
The transcription factor EB (TFEB) regulates the expression of target genes bearing the Coordinated Lysosomal Expression and Regulation (CLEAR) motif, thereby modulating autophagy and lysosomal biogenesis. Furthermore, TFEB can bind to the promoter of autophagy-associated genes and induce the formation of autophagosomes, autophagosome–lysosome fusion, and lysosomal cargo degradation. An increasing number of studies have shown that TFEB stimulates the intracellular clearance of pathogenic factors by enhancing autophagy and lysosomal function in multiple kidney diseases, such as cystinosis, acute kidney injury, and diabetic nephropathy. Taken together, this highlights the importance of developing novel therapeutic strategies against kidney diseases based on TFEB regulation. In this review, we present an overview of the current data on TFEB and its implication in kidney disease.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is nature.com built with?

Custom-built

No common CMS systems were detected on Nature.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of nature.com audience?

🌆 Monumental Traffic: 20M - 50M visitors per month


Based on our best estimate, this website will receive around 42,554,915 visitors per month in the current month.

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How Does Nature.com Make Money? {💸}


Display Ads {🎯}


The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

Ads are managed by yourbow.com. Particular relationships are as follows:

Direct Advertisers (10)
google.com, pmc.com, doceree.com, yourbow.com, audienciad.com, onlinemediasolutions.com, advibe.media, aps.amazon.com, getmediamx.com, onomagic.com

Reseller Advertisers (38)
conversantmedia.com, rubiconproject.com, pubmatic.com, appnexus.com, openx.com, smartadserver.com, lijit.com, sharethrough.com, video.unrulymedia.com, google.com, yahoo.com, triplelift.com, onetag.com, sonobi.com, contextweb.com, 33across.com, indexexchange.com, media.net, themediagrid.com, adform.com, richaudience.com, sovrn.com, improvedigital.com, freewheel.tv, smaato.com, yieldmo.com, amxrtb.com, adyoulike.com, adpone.com, criteo.com, smilewanted.com, 152media.info, e-planning.net, smartyads.com, loopme.com, opera.com, mediafuse.com, betweendigital.com

How Much Does Nature.com Make? {💰}


Display Ads {🎯}

$536,300 per month
Our estimates place Nature.com's monthly online earnings from display ads at $357,503 to $983,134.

Keywords {🔍}

pubmed, tfeb, article, google, scholar, cas, autophagy, kidney, central, lysosomal, cell, injury, biogenesis, cells, mitochondrial, function, cystinosis, disease, renal, diabetic, transcription, activation, expression, acute, cellular, tubular, aki, therapeutic, regulates, diseases, patients, nature, mitophagy, activity, factor, genes, clearance, diabetes, biol, mol, target, nephropathy, mtorc, involved, content, regulation, promotes, intracellular, lysosomes, protein,

Topics {✒️}

nature portfolio basic helix–loop–helix-leucine-zipper nature 436 nature bhlh basic helix–loop–helix basic helix-loop-helix protein privacy policy advertising social media yanse chen & huafeng liu reprints advanced glycation end-products helix-loop-helix protein pgc-1α-dependent tubular protection short interfering rna-mediated pgc-1a rescues huntington hyperglycemia-induced podocyte injury ubiquitous ser/thr kinase angiotensin-receptor antagonist irbesartan urinary inflammatory cytokines/chemokines research status chaperone-mediated autophagy leads gln glutamine-rich region proton-cystine symporter responsible disrupted multi-factor interactions starvation-induced autoregulatory loop atypical ser/thr kinase pro proline-rich segment mit/tfe proteins include peroxisome proliferator-activated receptor mit/tfe transcription factors cisplatin-treated rptc cells important ser/thr kinase alpha-1-anti-trypsin deficiency renal ischemia/reperfusion injury ser serine-rich region llc-pk1 cells play stz-induced diabetic mice125 research original author disordered endo-lysosomal compartments sepsis-induced kidney injury folic acid-induced aki permissions transcription factor eb mtor-induced autophagic dysfunction mit/tfe transcriptional factors promote autophagy-lysosomal fitness renal ischaemia–reperfusion injury pgc-1α promotes recovery

Questions {❓}

  • Inhibition and restimulation by insulin of cellular autophagy in distal tubular cells of the kidney in early diabetic rats?
  • Mitochondrial quality control in AMD: does mitophagy play a pivotal role?

Schema {🗺️}

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         description:The transcription factor EB (TFEB) regulates the expression of target genes bearing the Coordinated Lysosomal Expression and Regulation (CLEAR) motif, thereby modulating autophagy and lysosomal biogenesis. Furthermore, TFEB can bind to the promoter of autophagy-associated genes and induce the formation of autophagosomes, autophagosome–lysosome fusion, and lysosomal cargo degradation. An increasing number of studies have shown that TFEB stimulates the intracellular clearance of pathogenic factors by enhancing autophagy and lysosomal function in multiple kidney diseases, such as cystinosis, acute kidney injury, and diabetic nephropathy. Taken together, this highlights the importance of developing novel therapeutic strategies against kidney diseases based on TFEB regulation. In this review, we present an overview of the current data on TFEB and its implication in kidney disease.
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      headline:Regulation of TFEB activity and its potential as a therapeutic target against kidney diseases
      description:The transcription factor EB (TFEB) regulates the expression of target genes bearing the Coordinated Lysosomal Expression and Regulation (CLEAR) motif, thereby modulating autophagy and lysosomal biogenesis. Furthermore, TFEB can bind to the promoter of autophagy-associated genes and induce the formation of autophagosomes, autophagosome–lysosome fusion, and lysosomal cargo degradation. An increasing number of studies have shown that TFEB stimulates the intracellular clearance of pathogenic factors by enhancing autophagy and lysosomal function in multiple kidney diseases, such as cystinosis, acute kidney injury, and diabetic nephropathy. Taken together, this highlights the importance of developing novel therapeutic strategies against kidney diseases based on TFEB regulation. In this review, we present an overview of the current data on TFEB and its implication in kidney disease.
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