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Most AMLs are entirely negative for TFE3 and TFEB, which helps distinguish them from translocation RCCs.
demonstrated the key role of translocation factor EB (TFEB) in regulating the lipopolysaccharide induced inflammation, oxidative stress, autophagy, and apoptosis in the aged heart and postulated TFEB as drug target to ameliorate the myocardial tissue injury in aged subjects.
A fluorescence in situ hybridization (FISH) was performed, although TFE3 and TFEB showed no evidence of such gene rearrangements.
By using mouse and human cells upregulated or knocked-down for TFEB expression, the applicant will establish a role for TFEB in exosome biogenesis, cargo selectivity and secretion.
Both TFE3 and TFEB belong to the microphthalmia transcription factor (MiTF) subfamily.
TFEB overexpression in cultured cells significantly increases the number of autophagosomes and induces lysosomal biogenesis [9, 10].
1,2) These tumors have now been incorporated into the larger category of the microphthalmia transcription factor (MiT) family of translocation RCC, which includes TFE3, TFEB, TFC, and MiTF.
TFEB translocates to nucleus and regulates hundreds of genes which consist of Coordinated Lysosomal Expression and Regulation (CLEAR) network [9,10].
Molecular genetics and cellular features of TFE3 and TFEB fusion kidney cancers.
Hao, "Role of TFEB mediated autophagy, oxidative stress, inflammation, and cell death in endotoxin induced myocardial toxicity of young and aged mice," Oxidative Medicine and Cellular Longevity, vol.
21) Although immunohistochemistry may be useful as part of the initial workup, fluorescence in situ hybridization for TFE3 and/or TFEB rearrangements is the most sensitive and specific method to confirm the diagnosis of t-RCC.
Translocation-associated renal cell carcinoma (t-RCC) is a distinct subtype of renal cell carcinoma (RCC) harboring recurrent gene rearrangements of the TFE3 or TFEB loci.
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