Negative Regulation of the Acetyltransferase TIP60-p53 Interplay by UHRF1 (Ubiquitin-like with PHD and RING Finger Domains 1)

Dai, Chao; Shi, Dingding; Gu, Wei

doi:10.1074/jbc.m113.476606

Cited by 32 publications

(50 citation statements)

References 58 publications

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“…(g) Protein level of H3K14ac in pEGFP-N1, Ras G12V/T35S , si-MDM2, and si-NC transfected cells was determined using western blot assay. ERK1/2: extracellular signal-regulated protein kinases 1 and 2; H3K14ac: histone H3 acetylated on lysine 14; MDM2: murine double minute 2; TIP60: tat-interaction protein, 60 kDa It is generally known that TIP60 is a lysine acetyltransferase, which can mediate acetylation modification of numerous proteins, such as p53, ATM, H2AX, Rb, and E2F1 (Dai, Shi, & Gu, 2013;Squatrito, Gorrini, & Amati, 2006). The recent exciting reports demonstrate that TIP60 is involved in many important cellular physiological activities, including cell proliferation, cell apoptosis, cycle arrest, and DNA damage repair (M. S. Tang, Luo, Zhang, & Gu, 2006).…”

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confidence: 99%

Retracted: Ras–ERK1/2 signaling promotes the development of uveal melanoma by downregulating H3K14ac

Sun

et al. 2019

Journal Cellular Physiology

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Ras–extracellular signal‐regulated protein kinases 1 and 2 (ERK1/2) signaling has been proposed as the crucial regulators in the development of various cancers. Histone acetylation at H3 lysine 14 (H3K14ac) is closely associated with gene expression and DNA damage. However, whether H3K14ac participates in mediating Ras–ERK1/2‐induced cell proliferation and migration in uveal melanoma cells remains unknown. The purpose of this study is to investigate the effect of H3K14ac on Ras–ERK1/2 affected uveal melanoma cell phenotypes. MP65 cells were transfected with Ras WT and Ras G12V/T35S, the unloaded plasmid of pEGFP‐N1 served as a negative control. Protein levels of phosphorylated ERK1/2 Thr202 and H3K14ac were assessed by western blot assay. Cell viability, number of colonies, migration, and the downstream genes of ERK1/2 were analyzed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2‐H‐tetrazolium bromide, soft‐agar colony formation, transwell, and chromatin immunoprecipitation assays. HA‐tag vectors of CLR3 and TIP60 and the small interfering RNAs that specific for CLR3 and MDM2 were transfected into MP65 cells to uncover the effects of CLR3, TIP60, and MDM2 on Ras–ERK1/2 mediated H3K14ac expression and MP65 cell phenotypes. We found that, Ras–ERK1/2 decreased H3K14ac expression in MP65 cells, and H3K14ac significantly suppressed Ras–ERK1/2‐induced cell viability, colony formation, and migration in MP65 cells. Moreover, the transcription of CYR61, IGFBP3, WNT16B, NT5E, GDF15, and CARD16 was regulated by H3K14ac. Additionally, CLR3 silence recovered H3K14ac expression and reversed the effect of Ras–ERK1/2 on MP65 cell proliferation, migration and the mRNAs of ERK1/2 downstream genes. Besides, Ras–ERK1/2 decreased H3K14ac expression by MDM2‐mediated TIP60 degradation. In conclusion, Ras–ERK1/2 promoted uveal melanoma cells growth and migration by downregulating H3K14ac via MDM2‐mediated TIP60 degradation.

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confidence: 99%

Retracted: Ras–ERK1/2 signaling promotes the development of uveal melanoma by downregulating H3K14ac

Sun

et al. 2019

Journal Cellular Physiology

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“…Interestingly, a recent study demonstrated that UHRF1 can promote nondegradative ubiquitination of lysine acetyltransferase Tip60 [23]. Multiple ubiquitin E3 ligases had been reported to reduce p53 stability by targeting p53 for ubiquitin-dependent degradation.…”

Section: Discussionmentioning

confidence: 97%

Ubiquitin E3 ligase UHRF1 regulates p53 ubiquitination and p53-dependent cell apoptosis in clear cell Renal Cell Carcinoma

Peng

et al. 2015

Biochemical and Biophysical Research Communications

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“…UHRF1 is a newly identified suppressor of Tip60 and p53 whose depletion markedly increases p53/Tip60-dependent transactivation of both growthinhibitory and apoptotic target genes. 49 These questions are highly relevant to our understanding of p53 signaling and merit further investigation.…”

Section: Discussionmentioning

confidence: 99%

Nuclear interactor of ARF and Mdm2 regulates multiple pathways to activate p53

Reed¹,

Hagen²,

Tompkins³

et al. 2014

Cell Cycle

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Negative Regulation of the Acetyltransferase TIP60-p53 Interplay by UHRF1 (Ubiquitin-like with PHD and RING Finger Domains 1)

Cited by 32 publications

References 58 publications

Retracted: Ras–ERK1/2 signaling promotes the development of uveal melanoma by downregulating H3K14ac

Retracted: Ras–ERK1/2 signaling promotes the development of uveal melanoma by downregulating H3K14ac

Ubiquitin E3 ligase UHRF1 regulates p53 ubiquitination and p53-dependent cell apoptosis in clear cell Renal Cell Carcinoma

Nuclear interactor of ARF and Mdm2 regulates multiple pathways to activate p53

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