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UCHL1 inhibits apoptotic process. 17 / 20
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"Particularly , UCH-L1 inhibition was reported to contribute to apoptosis through the stimulation of unfolded protein response [ 218 ] ."
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"However, several E3 ligases such as HectH9, Mdm2, TNF receptor‐associated factor 6 (TRAF6; tumour necrosis factor receptor‐associated factor 6), cIAP1/2 (cellular inhibitor of apoptosis protein 1/2), CHIP, Parkin, UCHL1, TRAF2, ITCH and NEDD4‐2 specifically catalyse the K63‐linked ubiquitination.17, 18, 19 Interestingly, HectH9, Mdm2, RNF8 (ring finger protein 8) and cIAP1/2 catalyse both K63‐ and K48‐linked ubiquitination."
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"Since suppression UCHL1 reduced apoptosis, we performed MTT assay to determine whether UCHL1 knockdown in ovarian cancer cells influences resistance to cisplatin, a common reagent used to treat ovarian cancer."
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"Results showed that UCH-L1 inhibited the growth of breast cancer cells and its action was dependent on the inducement of cell death, showing the typical characteristics of apoptosis but not necrosis."
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"Bheda et al. presented a series of genes regulated by UCH-L1 using microarray and quantitative real-time PCR analysis, and they found that the inhibition of UCH-L1 activated genes controlling apoptosi[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Restoring UCHL1 expression in silenced cell lines significantly inhibits their growth and colony formation ability, by inhibiting cell proliferation through cell cycle arrest in the G2/M phase and inducing apoptosis through the intrinsic caspase dependent pathway."
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"Here, we show that increased expression of h-IAPP (but not r-IAPP) decreased UCH-L1 levels and that loss of UCH-L1 expression and activity induced ER stress and apoptosis in beta-cells."
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"Restoring UCHL1 expression in silenced cell lines significantly inhibited their growth and colony formation ability by inhibiting cell proliferation, causing cell cycle arrest in G2/M phase and inducing apoptosis through the intrinsic caspase dependent pathway."
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"Moreover, UCHL1 knockdown in ovarian cancer cell lines had increased cell growth, decreased apoptosis, and increased cisplatin resistance [43]."
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"In contrast to H838 cells, our study reveals UCH-L1 knockdown causes no difference in morphology, apoptosis or proliferation in H157 cells but does reduce the capacity for cell migration."
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"Knockdown of UCHL1 in OC cell lines promoted cell proliferation and reduced cell apoptosis [XREF_BIBR] UCHL1 also promotes prostate cancer metastasis through EMT induction [XREF_BIBR]."
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"Moreover, SGES upregulated the expression of GDNF, p-Akt and PGP9.5 in the vagotomized rats and inhibited the apoptosis of enteric neurons."
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"Knockdown of UCHL1 also reduced cell apoptosis and contributed to cisplatin resistance."
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"Previous studies have shown that Uch-L1 can prevent apoptosis in cells treated with lysosomal protease inhibitors."
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"UCH-L1 may accelerate the development of lymphoma by either increasing proliferation or reducing apoptosis in lymphocytes or in the resulting tumors."