ArticleFrontiers in oncology2026
Loss of RanBP9 cooperates with p53 deficiency to promote sarcomagenesis.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Ubiquitination is a major regulatory process that is often dysregulated in carcinogenesis. The C-terminal to LisH (CTLH) complex is a multi-subunit E3 ubiquitin ligase that has been shown to exert tumor-promoting and tumor-suppressing functions. Its core scaffolding subunit, RanBP9, has been implicated in regulating oncogenic signaling, but it remains unclear whether RanBP9 loss promotes tumorigenesis Objectives: This study aimed to evaluate the functional consequence of RanBP9 loss, alone or in combination with p53 deficiency, in mice. Methods: Mice with single or combined germline deletion of Results: Biallelic deletion of Discussion: Loss of RanBP9 induces deregulation of signaling cascades, and combined with p53 deficiency, further promotes sarcoma development in mice. This mouse model provides a valuable platform to further study pathways and candidates regulated by the CTLH complex in sarcoma biology.
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