Transcription Factor E3 Proteins (TFE3)

Human Transcription Factor E3 (TFE3) interaction partners

1. Both SOX11 (show SOX11 Proteins) and TFE3 were overexpressed in solid-pseudopapillary neoplasms (SPNs) and may be involved in the pathogenesis.

2. A Potential G-quadruplex-forming Sequence (PQS) in the intron 2 of the TFE3 gene suggested by in silico studies was confirmed. Increased and decreased formation of G-quadruplex occurred in presence of pyridostatin and antisense oligonucleotide respectively. Stable G-quadruplex formation affected biological processes and TFE3 splicing. G-quadruplex is behind TFE3 induced oncogenesis via translocation and mRNA splicing.

3. TFE3 may promote renal tumor growth by regulating cell cycle progression and activating the phosphatidylinositol 3kinase/AKT (show AKT1 Proteins) serine/threonine kinase (show TLK2 Proteins) 1/mTOR (show FRAP1 Proteins) signaling pathway.

4. We report for the first time the presence of both TFE3 translocation and SDHB (show SDHB Proteins) mutation in the same renal cell carcinoma (show MOK Proteins) tumor.

5. TFEB (show TFEB Proteins) and TFE3 collaborate with each other in activated macrophages and microglia to promote efficient autophagy induction, increased lysosomal biogenesis, and transcriptional upregulation of numerous proinflammatory cytokines

6. Findings indicated that TFE3 was an important hypoxia-induced transcriptional factor in HNSCC.

7. Solid pseudopapillary neoplasms (SPNs) showed positive staining for SRY (show SRY Proteins)-related high-mobility group box (show SSRP1 Proteins) 11 (SOX-11 (show SOX11 Proteins)), transcription factor E3 (TFE3) and beta-catenin (show CTNNB1 Proteins) on cell blocks.

8. results reveal that PRCC (show PRCC Proteins)-TFE3 dual-fusion FISH probe is an efficient and concise technique for diagnosing PRCC (show PRCC Proteins)-TFE3 RCC (show XRCC1 Proteins) in paraffin-embedded tissue

9. Case Report: Melanotic Xp11 renal cell carcinoma (show MOK Proteins) with ARID1B-TFE3 gene fusion.

10. Studies identified TFEB (show TFEB Proteins) and TFE3 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.

Mouse (Murine) Transcription Factor E3 (TFE3) interaction partners

1. TFEB (show TFEB Proteins) and TFE3 collaborate with each other in activated macrophages and microglia to promote efficient autophagy induction, increased lysosomal biogenesis, and transcriptional upregulation of numerous proinflammatory cytokines

2. These data indicate that TFE3 and TFEB (show TFEB Proteins) play a cooperative, rather than redundant, role in the control of the adaptive response of whole-body metabolism to environmental cues such as diet and physical exercise.

3. Findings indicated that TFE3 was an important hypoxia-induced transcriptional factor in HNSCC.

4. Tfe3 and Tfeb (show TFEB Proteins) are required for the induced expression of Ppargamma2 (show PPARG Proteins) and subsequently for adipogenic genes.

5. Tfe3 overexpression in HSPCs impaired long-term hematopoietic reconstitution in vivo, recapitulating the Flcn (show FLCN Proteins) KO phenotype, and supporting the notion that abnormal activation of Tfe3 contributes to the Flcn (show FLCN Proteins) KO phenotype. Flcn (show FLCN Proteins) KO mice develop an acute histiocytic hyperplasia in multiple organs, suggesting a novel function for Flcn (show FLCN Proteins) in macrophage development

6. TFEB (show TFEB Proteins) and TFE3 are novel components of the integrated stress response

7. Tfe3 is a critical transcription factor that regulates Pgc-1alpha gene expression in myotubes

8. A conditional expression in mice of the fusion gene ASPSCR1 (show ASPSCR1 Proteins)-TFE3 from human alveolar soft part sarcoma (ASPS (show DARS Proteins)) generated a model that recapitulates the human tumor histologically and by expression profile.

9. Data from transgenic mice suggest Tfe3 controls lipid metabolism in adipose tissue (white, WAT; brown, BAT (show BAAT Proteins)); TFE3 appears to be regulated by diet; up-regulation of TFE3 may inhibit expression of lipolysis genes in WAT and thermogenesis genes in BAT (show BAAT Proteins).

10. These findings indicated that TFE3 has a regulatory role in myoblast differentiation, and that transcriptional suppression of myogenin (show MYOG Proteins) expression may be part of the mechanism of action.