Ell3 stabilizes p53 following CDDP treatment via its effects on ubiquitin-dependent and -independent proteasomal degradation pathways in breast cancer cells

The tumor suppressor protein p53 is unstable in quiescent cells and undergoes proteosomal degradation. Under conditions of cellular stress, p53 is rapidly stabilized by post-translational modification, thereby escaping degradation and translocating to the nucleus where it activates genes related to...

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Veröffentlicht in:	Oncotarget 2015-12, Vol.6 (42), p.44523-44537
Hauptverfasser:	Ahn, Hee-Jin, Kim, Kwang-Soo, Shin, Kyung-Won, Lim, Kee-Hwan, Kim, Jin-Ock, Lee, Je-Yong, Kim, Jiewan, Park, Ji-Hoon, Yang, Kyung-Min, Baek, Kwang-Hyun, Ko, Jeong-Jae, Park, Kyung-Soon
Format:	Artikel
Sprache:	eng
Schlagworte:	Antineoplastic Agents - pharmacology Apoptosis - drug effects Breast Neoplasms - drug therapy Breast Neoplasms - enzymology Breast Neoplasms - genetics Breast Neoplasms - pathology Cisplatin - pharmacology Extracellular Signal-Regulated MAP Kinases - metabolism Female Gene Expression Regulation, Neoplastic Humans Interleukins - genetics Interleukins - metabolism MCF-7 Cells NAD(P)H Dehydrogenase (Quinone) - genetics NAD(P)H Dehydrogenase (Quinone) - metabolism Proteasome Endopeptidase Complex - metabolism Protein Stability Proteolysis Research Paper RNA Interference Signal Transduction - drug effects Time Factors Transcriptional Elongation Factors - genetics Transcriptional Elongation Factors - metabolism Transfection Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Ubiquitination Up-Regulation
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