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RAD6 is upregulated in response to chemotherapy and significantly correlated with expression of ovarian cancer (OC) stem cell signaling genes ALDH1A1 and SOX2 and poor prognosis of OC patients.
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These data deepen insights into the vital role of RAD6/translesion synthesis in platinum drug tolerance and reveal clinical benefits of targeting RAD6 with SMI#9 for managing chemoresistant cancers.
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These results point to an important role of the affinity between RNF4 and its cognate RAD6B or UBCH5B in governing the multiplicity of substrate ubiquitination.
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RAD6 promotes proteasome activity and nuclear translocation by enhancing the degradation of PSMF1 and the lamin B receptor.
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In conclusion, we reveal that miR-455-5p expression is regulated by the TGF-beta-dependent pathway, which subsequently leads to UBE2B down-regulation and contributes to oral cancer tumourigenesis.
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Data show that the ubiquitin-conjugating enzyme E2 RAD6A/B-MDM2 ubiquitin ligase machinery regulates anti-silencing function 1A protein (ASF1A) degradation.
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These findings show the importance of Rad6 in ovarian cancer and emphasize the need for further studies of Rad6 as a potential target for the treatment of ovarian cancer.
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A novel variant (Chr5.133706925 A > G) residing in the UBE2B gene promoter region confers a high risk for idiopathic azoospermia in a Chinese population.
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RAD6 physically interacts with heterochromatin protein 1alpha and ubiquitinates HP1alpha at residue K154, thereby promoting heterochromatin protein 1alpha degradation through the autophagy pathway
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UBE2B mRNA alterations are associated with severe oligozoospermia in infertile men.
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RNF168, in complex with RAD6A or RAD6B, is activated in the DNA-damage-induced protein ubiquitination cascade.
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UBE2B polymorphisms g.-293T>G, g.20016A>G and g.9157A>G are not associated with male infertility, and the GA haplotype is likely a protective factor for male fertility in Northeast Chinese men.
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beta-catenin and Rad6B interacting regions, were identified.
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Hydroquinone could upregulate the expression of Rad6B in L-02 hepatic cells.
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The Rad6-Rad18 enzyme plays an essential role in promoting replication through DNA lesions by translesion synthesis in mammalian cells.
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RAD6 can form a ternary complex with MDM2 and p53 that contributes to the degradation of p53.
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Data show that the homodimeric Rad18 RING domain can recruit two Rad6b E2 enzymes, whereas the full-length Rad18 homodimer binds only to a single Rad6b molecule.
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Ubc2/Rad6 ser(120) regulates ubiquitin-dependent N-end rule targeting by E3{alpha}/Ubr1
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Rad6B is a fundamental component of postreplication DNA repair and can be used as an independent marker for determining response to neoadjuvant chemotherapy.
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MCF10A cells stably transfected with antisense RAD6B display hypersensitivity to damage-inducing drugs.
