IndraLab

Statements


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"Deubiquitinase UCHL1 promotes angiogenesis and blood-spinal cord barrier function recovery after spinal cord injury by stabilizing Sox17."

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"Mechanistically, UCHL1 facilitates KDM4B accumulation and depends on the KDM4B/VEGFA axis to promote RCC angiogenesis."

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"These findings suggest that UCHL1 promotes angiogenesis and enhances motor function recovery in mice by increasing Sox17 expression (Fig. 7M)."

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"Thus, a positive feedback loop between UCHL1, HIF-1alpha, and POSTN might be proposed where UCHL1 may promote angiogenesis directly via HIF-1alpha stabilization and indirectly via POSTN upregulation."

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"Lastly, KDM4B knockdown significantly suppressed UCHL1-induced ccRCC growth and angiogenesis in vivo, as evidenced by tumor volume curves and IHC intensity analysis (Fig. 4H–J)."

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"By generating UCHL1 conditional knockout mice and conducting rescue experiments, we further validated that the deubiquitinase UCHL1 promotes angiogenesis and restoration of BSCB function after injury by stabilizing Sox17."

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"Our study therefore uncovered a novel amplification mechanism of HIF-2α signaling mediated by KDM4B in RCC.Functionally, we found that UCHL1 promoted RCC proliferation, migration, and angiogenesis in vitro and in vivo."

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"Immunoblotting results showed that UCHL1 protein expression was reduced in CKO mice compared with that in UCHL1 mice, along with the reduced expression of Sox17 and CD31 proteins observed after injury (Fig. 6B, C), indicating that UCHL1 knockdown may inhibit angiogenesis in vivo."

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"These immunoprecipitation studies confirm that UCH-L1 deubiquitinates NOX4 in HUVECs, and suggest that UCH-L1 is involved in ROS mediated angiogenesis in HUVECs by modulating NOX4 activity via deubiqu[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"