IndraLab

Statements

TBX3 binds USP15. 11 / 11
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"Biochemical interaction partner screening and deubiquitylation analysis supports the USP15-TBX3 axis through different physiological and pathological contexts including PTC development."
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"Translationally, the findings shed light on targeting strategies for USP15-TBX3 axis related developmental and oncogenic diseases and provide more thoughts for BRAF/MAPK related therapy designs."
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"Dosage of USP15-TBX3 defines physiological differentiation and pathological de-differentiation."
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"Interaction between TBX3 and USP15 was further confirmed by Co-IP experiments, where HA-tagged USP15 was efficiently pulled-down by Flag-tagged TBX3 in HEK293T cell extracts, and vice versa (Fig.  xref )."
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"USP15 interacts with and stabilizes TBX3."
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"Interaction between TBX3 and USP15 was further confirmed by Co-IP experiments, where HA-tagged USP15 was efficiently pulled-down by Flag-tagged TBX3 in HEK293T cell extracts, and vice versa (Fig. 1b)."
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"Tissue specific knockout models of Erks will be ideal in the future to further testify the functional correlation between BRAF/MAPK activation and USP15-TBX3 axis in the future."
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"Domain mapping experiments suggest that the activation domain is most important for the physical interaction with USP15, since its deletion [ΔA and Δ(A + R1) TBX3 variants] inhibited TBX3-USP15 interaction (Fig.  xref )."
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"USP15-TBX3 axis mediates BRAF V600E -induced tumorigenesis."
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"The USP15-TBX3 axis is reactivated during tumorigenesis, and Usp15 knockout prohibits BRAF V600E -driven tumor development in a Tbx3-dependent manner."
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"As we have mentioned, BRAF V600E is the prevalent oncogenic mutation and correlates with dedifferentiation and poor prognosis in PTC, furthermore, USP15-TBX3 axis functions as indispensable downstream effectors of activated BRAF/MPAK pathway."
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