IndraLab

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UCHL1 activates Death. 6 / 6
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"Moreover, and identical to podocyte death caused by UCH-L1 overexpression, the addition of zVAD-fmk did not prevent TNF induced cell death, demonstrating that TNF indeed elicits necroptosis in podocytes, and that UCH-L1 represents a downstream mediator of the necroptotic signaling cascade of TNF also in podocytes."

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"Pathogenetic NH2-truncated Tau was also discovered in AD models, and it can trigger redundant mitophagy by promoting the excessive mitochondrial translocation of Parkin and UCHL-1, which finally cause[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In fact, estrogen treatment increases UCHL1 levels in endometrial cells [ 66 ], and induces germ cell death and downregulation of cyclin A1 and/or B1 in spermatogenic cells [ 23 , 24 ]."

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"We and others have previously observed this effect of zVAD-fmk in necroptosis [XREF_BIBR, XREF_BIBR, XREF_BIBR], excluding that de novo expression and thus increased UCH-L1 activity causes death of podocytes by apoptosis but rather pointing to programmed necrosis and necroptosis as the responsible suicide program."

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"No pathological data are currently available.It is not clear why mutations in alpha-synuclein, parkin or UCH-L1 genes cause nigral dopaminergic cell death in familial PD."

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"Since UCH-L1 clearly contributes to the non apoptotic death of podocytes, interference with the necroptotic properties of HtrA2 and Omi and UCH-L1 may prove beneficial for the treatment of patients, e.g. in kidney failure."