Pluripotency re-centered around Esrrb

Papp, Bernadett; Plath, Kathrin

doi:10.1038/emboj.2012.285

Cited by 21 publications

(19 citation statements)

References 11 publications

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“…1,21 Adaptation to hypoxic environments is mediated primarily through a program that depends on hypoxia-inducible factor (HIF). ESRRB has been shown to interact with HIF and stimulate HIF-induced transcription, making ESRRB essential for HIF function.…”

mentioning

confidence: 99%

Significant association of full-thickness rotator cuff tears and estrogen-related receptor-β (ESRRB)

Teerlink

Cannon‐Albright

Tashjian

2015

Journal of Shoulder and Elbow Surgery

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mentioning

confidence: 99%

Significant association of full-thickness rotator cuff tears and estrogen-related receptor-β (ESRRB)

Teerlink

Cannon‐Albright

Tashjian

2015

Journal of Shoulder and Elbow Surgery

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“…In fact, this observation appears to support recent reports highlighting the importance of Esrrb in establishing pluripotency and self-renewal independent of Sox2. [34][35][36] Buganim et al 34 reported that combination of Esrrb, Nanog, Sall4 and Lin28 can efficiently support pluripotency with a quality higher than other factor combinations, including Oct4, Sox2, Klf4 and Myc. 34 Interestingly, in addition to Esrrb and Nanog, the expression levels of Lin28 and Sall4 also maintain at a higher expression level in U1 and U2 cells (Figure 6b).…”

Section: Resultsmentioning

confidence: 99%

Ube2s regulates Sox2 stability and mouse ES cell maintenance

et al. 2015

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Sox2 has a critical role in embryonic stem (ES) cell maintenance and differentiation. Interestingly, its activity is highly dosagedependent. Although transcriptional regulation of Sox2 has been extensively studied, the mechanisms orchestrating its degradation remain unclear. In this study, we identified ubiquitin-conjugating enzyme E2S (Ube2s) as a novel effector for Sox2 protein degradation. Ube2s mediates K11-linked polyubiquitin chain formation at the Sox2-K123 residue, thus marking it for proteasome-mediated degradation. Besides its role in fine-tuning the precise level of Sox2, Ube2s reinforces the self-renewing and pluripotent state of ES cells. Importantly, it also represses Sox2-mediated ES cell differentiation toward the neural ectodermal lineage.

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“…Estrogen-related receptors (ERRs) are orphan members of this protein family that have no known endogenous ligands, although their function can be modified by synthetic ligands [13–15] and the abundance of binding partners [16–19]. In mice, ERRβ (ESRRB/ERR2/ERRbeta/ESRL2/NR3B2) has emerged as a key reprogramming factor in embryonic and induced pluripotent stem cells [20–22], where it promotes a more permissive G1/S checkpoint [23, 24]. By contrast, exogenous expression of human ERRβ has tumor suppressive activities that activate the G1/S checkpoint through the induction of CDKN1A (p21) in prostate cancer cells [25].…”

Section: Introductionmentioning

confidence: 99%

Antimitotic activity of DY131 and the estrogen-related receptor beta 2 (ERRβ2) splice variant in breast cancer

et al. 2016

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Breast cancer remains a leading cause of cancer-related death in women, and triple negative breast cancer (TNBC) lacks clinically actionable therapeutic targets. Death in mitosis is a tumor suppressive mechanism that occurs in cancer cells experiencing a defective M phase. The orphan estrogen-related receptor beta (ERRβ) is a key reprogramming factor in murine embryonic and induced pluripotent stem cells. In primates, ERRβ is alternatively spliced to produce several receptor isoforms. In cellular models of glioblastoma, short form (ERRβsf) and beta2 (ERRβ2) splice variants differentially regulate cell cycle progression in response to the synthetic agonist DY131, with ERRβ2 driving arrest in G2/M.The goals of the present study are to determine the cellular function(s) of ligand-activated ERRβ splice variants in breast cancer and evaluate the potential of DY131 to serve as an antimitotic agent, particularly in TNBC. DY131 inhibits growth in a diverse panel of breast cancer cell lines, causing cell death that involves the p38 stress kinase pathway and a bimodal cell cycle arrest. ERRβ2 facilitates the block in G2/M, and DY131 delays progression from prophase to anaphase. Finally, ERRβ2 localizes to centrosomes and DY131 causes mitotic spindle defects. Targeting ERRβ2 may therefore be a promising therapeutic strategy in breast cancer.

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Pluripotency re-centered around Esrrb

Abstract: Recent studies established the oestrogen‐related receptor b (Esrrb) as pivotal Nanog‐target gene. This places Esrrb and its novel Ncoa3 co‐activator into the centre of pluripotency regulation.

Cited by 21 publications

References 11 publications

Significant association of full-thickness rotator cuff tears and estrogen-related receptor-β (ESRRB)

Significant association of full-thickness rotator cuff tears and estrogen-related receptor-β (ESRRB)

Ube2s regulates Sox2 stability and mouse ES cell maintenance

Antimitotic activity of DY131 and the estrogen-related receptor beta 2 (ERRβ2) splice variant in breast cancer

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