IndraLab
Statements
USP14 activates apoptotic process. 53 / 54
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53
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"Together, it was suggested that SPAG5‐AS1 stabilized SPAG5 protein through interacting with USP14 in HG‐treated HPCs, and that USP14 and AKT/mTOR formed a positive feedback loop.3.7
SPAG5-AS1 promoted apoptosis and attenuated autophagy in HG-treated HPCs through SPAG5/AKT/mTOR pathway."
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"Consistent with previous study, our study demonstrated that USP14 knockdown attenuated OGD/R treatment mediated the enhancement effect on SK-N-SH cell inflammation, apoptosis, and ferroptosis, indicating that USP14 accelerates the progression of stroke.Ferroptosis is a mechanism of cell death after ischemia in many organs, such as the kidney and heart."
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"Therefore, our current research may allow targeting UCHL5 and USP14 in 19S regulatory particle for anti-cancer drug development.b-AP15 was reported to inhibit tumor cell growth and induce cell apoptosis, and displays anti-tumor role in multiple tumor cell models without inhibiting 26S proteasomes proteolytic activities."
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"Selective USP14 and UCHL5 inhibitor b-AP15, induced apoptosis in MM cell lines and in primary MM cells via downregulation of cell division cycle 25C (CDC25C), CDC2, and cyclin-B1, as well as the activation of caspases and unfolded protein response pathways (p-IREalpha, p-eIF2alpha, and CHOP)."
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"Our recent study exemplifies the feasibility of such an approach : specifically, we showed that blockade of 19S associated DUBs USP14 and UCHL5 with a small-molecule inhibitor (bAP15 and VLX1570) induces apoptosis in MM cells and overcome bortezomib resistance, with a favorable toxicity profile."
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"Moreover, the expression of several S100 isoforms (including S100a4, S100a6, S100a8, and S100a9) has increased pro-inflammatory and pro-fibrotic activities [20] in all endothelial cell subtypes under TGT stimulation.3.4
TGT treatment caused marked inflammatory response, apoptosis, and fatty acid metabolism dysfunction in hepatocytes."
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"The expression of ER stress-associated proteins including ATF6, BiP, p-IRE1, XBP1s and CHOP, as well as apoptosis-associated cleaved caspase-3 and cleaved PARP1 proteins, was significantly upregulated by TGT treatment in osteosarcoma 143B cells, suggesting that TGT might promote the apoptosis of osteosarcoma 143B cells through the IRE1/CHOP pathway."