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Millipore total p53 antibody
Total P53 Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 7. Schematics diagram showing the role of CERK driven sphingolipid metabolic reprogramming in modulating tamoxifen resistance in ER+ breast cancer. In wild type breast cancer cells, tamoxifen treatment can prohibit acid ceramidase-driven ceramide hydrolysis to increase ceramide level, which in turn prohibits PI3K/ AKT-dependent cell proliferation while activating <t>p53/caspase-3</t> driven apoptosis. In tamoxifen resistant cells, up-regulation of the EHF expression transcriptionally increases CERK expression and its mediated conversion of ceramide to ceramide-1-phosphate, which overruns the regulatory effect of tamoxifen on ceramide level, leading to increased PI3K/AKT dependent cell proliferation and reduced p53/caspase-3 dependent apoptosis.
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Fig. 7. Schematics diagram showing the role of CERK driven sphingolipid metabolic reprogramming in modulating tamoxifen resistance in ER+ breast cancer. In wild type breast cancer cells, tamoxifen treatment can prohibit acid ceramidase-driven ceramide hydrolysis to increase ceramide level, which in turn prohibits PI3K/ AKT-dependent cell proliferation while activating p53/caspase-3 driven apoptosis. In tamoxifen resistant cells, up-regulation of the EHF expression transcriptionally increases CERK expression and its mediated conversion of ceramide to ceramide-1-phosphate, which overruns the regulatory effect of tamoxifen on ceramide level, leading to increased PI3K/AKT dependent cell proliferation and reduced p53/caspase-3 dependent apoptosis.

Journal: Pharmacological research

Article Title: Ceramide kinase confers tamoxifen resistance in estrogen receptor-positive breast cancer by altering sphingolipid metabolism.

doi: 10.1016/j.phrs.2022.106558

Figure Lengend Snippet: Fig. 7. Schematics diagram showing the role of CERK driven sphingolipid metabolic reprogramming in modulating tamoxifen resistance in ER+ breast cancer. In wild type breast cancer cells, tamoxifen treatment can prohibit acid ceramidase-driven ceramide hydrolysis to increase ceramide level, which in turn prohibits PI3K/ AKT-dependent cell proliferation while activating p53/caspase-3 driven apoptosis. In tamoxifen resistant cells, up-regulation of the EHF expression transcriptionally increases CERK expression and its mediated conversion of ceramide to ceramide-1-phosphate, which overruns the regulatory effect of tamoxifen on ceramide level, leading to increased PI3K/AKT dependent cell proliferation and reduced p53/caspase-3 dependent apoptosis.

Article Snippet: The primary antibodies employed in this work included: anti-EHF (Cat#ab220113, Abcam), anti-CERK (Cat#PA1–16963, Invitrogen), anti-β-actin (Cat#sc-47778, Santa Cruz), anti-total AKT (Cat# 4691 S, Cell signaling technology), anti-p-AKT (Cat#4060 S, Cell signaling technology), anti-p-PI3K (Cat#AF3242–50,Affinity), anti-total PI3K (Cat#556399, BD Biosciences), anti-cleaved caspase-3 (Cat#9661 S, Cell signaling technology), anti-p-p53 (Cat# 9284 S, Cell signaling technology), anti-total p53 (Cat# sc-126, Santa Cruz).

Techniques: Expressing