Transcription Factor E3 Proteins (TFE3)

Human Transcription Factor E3 (TFE3) interaction partners

1. TFE3 gene rearrangement is associated with Epithelioid Rich Perivascular Epithelioid Cell Neoplasm of the Bladder.

2. The data reveal that 4E-BP3 expression is controlled by the transcription factor TFE3 through a cis-regulatory element in the EIF4EBP3 gene promoter.

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

4. 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.

5. TFE3 may promote renal tumor growth by regulating cell cycle progression and activating the phosphatidylinositol 3kinase/AKT serine/threonine kinase 1/mTOR signaling pathway.

6. We report for the first time the presence of both TFE3 translocation and SDHB mutation in the same renal cell carcinoma tumor.

7. TFEB 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

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

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

10. results reveal that PRCC-TFE3 dual-fusion FISH probe is an efficient and concise technique for diagnosing PRCC-TFE3 RCC in paraffin-embedded tissue

11. Case Report: Melanotic Xp11 renal cell carcinoma with ARID1B-TFE3 gene fusion.

12. Studies identified TFEB 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.

13. Ovarian sclerosing stromal tumor strongly overexpress TFE3.

14. Describe the unusual morphology and expanded the morphologic spectrum of SFPQ/PSF-TFE3 renal cell carcinomas.

15. Despite TFE3 over expression, TFE3 genetic alterations are less likely to be a major molecular event driving tumorigenesis in hepatic angiolipomas.

16. we analyze 60 Xp11 translocation cancers by fluorescence in situ hybridization using custom bacterial artificial chromosome probes to establish their TFE3 fusion gene partner

17. These results show that ASPL-TFE3 regulates cell cycle progression and induces cellular senescence by up-regulating p21 expression.

18. RBM10-TFE3 is a recurrent gene fusion in Xp11 translocation renal cell carcinoma.

19. Case Report: melanotic PEComa of the sinonasal mucosa with NONO-TFE3 fusion.

20. Xp11 translocation renal cell carcinomas with RBM10-TFE3 gene fusion demonstrating melanotic features and overlapping morphology with t(6;11) RCC.

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

1. TFEB 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 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 are required for the induced expression of Ppargamma2 and subsequently for adipogenic genes.

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

6. TFEB 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-TFE3 from human alveolar soft part sarcoma (ASPS) 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); TFE3 appears to be regulated by diet; up-regulation of TFE3 may inhibit expression of lipolysis genes in WAT and thermogenesis genes in BAT.

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

11. Machinery regulating exit of embryonic stem cells from pluripotency is ill defined; Flcn with its interaction partners Fnip1 and Fnip2 drives differentiation by restricting nuclear localization and activity of the bHLH transcription factor Tfe3.

12. a major regulator of mast cell-mediated allergic response

13. TFE3 and Galpha(16) are up-regulated under pathologic conditions and are involved in a novel mechanism of transcriptional regulation via the relocalization and activation of Galpha(16).

14. FLCN tumor suppressor gene inactivation induces TFE3 transcriptional activity by increasing its nuclear localization

15. TFE3 and TFEB regulate E-cadherin and WT1 expression

16. IRS2, HK2 and INSIG1 are direct targets of TFE3

17. Maximum Cd40lg promoter activity and gene expression required TFE3 or TFEB.