IndraLab

Statements

PAN2 binds SLC7A11. 9 / 9
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"All the aforementioned findings regarding the regulation and underlying mechanism of the USP52‐xCT axis prompted us to further investigate whether USP52 is linked to BLCA progression and prognosis in clinical samples."
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"Altogether, these findings indicate that USP52 interacts with xCT and promotes its stability in an enzyme‐dependent manner."
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"Mechanistically, USP52 interacts with xCT and enzymatically cleaves the K48‐conjugated ubiquitin chains at K4 and K12, enhancing its protein stability."
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"These findings elucidate the role of the USP52‐xCT axis in BLCA and highlight the therapeutic potential of targeting USP52 and ferroptosis inducers in BLCA."
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"USP52 Physically Interacts with xCT and Maintains Its Stability."
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"Plasmids encoding Myc‐tagged USP52 and Flag‐tagged xCT were transfected into HEK293T cells, and co‐IP assays revealed an exogenous interaction between USP52 and xCT ( Figure   xref )."
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"To better understand the underlying mechanism of the USP52‐xCT axis in the regulation of BLCA progression, we further performed a series of coimmunoprecipitation (co‐IP) analyses."
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"Mechanistically, USP52 physically associated with xCT through its WD40 domain, leading to xCT K48‐conjugated deubiquitination at K4 and K12, which in turn promoted xCT protein stability."
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"Similarly, endogenous USP52 efficiently interacted with xCT in 5637 and T24 cells (Figure  xref )."
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