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INSIG1 coordinated with another ligase, translocation in renal carcinoma chromosome 8 (TRC8), and promoted Gag degradation through the lysosome pathway.
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TRC8 and MARCH6 depletion altered the turnover of the tail-anchored protein heme oxygenase-1.
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Low RNF139 expression is associated with progression of tongue cancer.
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interaction with Bag1 then shifts hERG degradation to the membrane-anchored E3 ligase TRC8 and its E2-conjugating enzyme Ube2g2, as determined by siRNA screening
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TRC8 and TMEM129 are endoplasmic reticulum-associated degradation ubiquitin E3 ligases for viral and cellular targeting of MHC class I. (Review)
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TRC8 suppresses tumorigenesis through targeting heme oxygenase-1 for ubiquitination and degradation.
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TRC8 function may provide a regulatory link between the lipid and protein biosynthetic pathways.
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TRC8 modulation of sterol response element binding protein activity comprises a novel regulatory link between growth control and the cholesterol/lipid homeostasis pathway.
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The presence of diploid and tetraploid tumor cells with and without TRC8 deletions on the nontranslocated chromosome suggest that loss of the remaining normal allele of TRC8 may contribute to tumor development at later stages.
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TRC8 is a novel sterol-sensing endoplasmic reticulum membrane protein that hinders SREBP-2 processing through interaction with SREBP-2 and SCAP, regulating its own turnover rate by means of its E3 ubiquitin ligase activity
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Data show that the TRC8 E3 ligase is required for MHC I dislocation from the ER and identify a new complex associated with mammalian ERAD.