Life without geminin

Karamitros, Dimitris; Kotantaki, Panoraia; Lygerou, Zoi; Veiga-Fernandes, Henrique; Pachnis, Vassilis; Kioussis, Dimitris; Taraviras, Stavros

doi:10.4161/cc.9.16.12554

Cited by 17 publications

(14 citation statements)

References 51 publications

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“…Our results showed that in the absence of Geminin, DNA damage or apoptosis were not induced. This is in agreement with recent in vivo studies [23,24] showing that Geminin depletion in progenitor T-cells also did not lead to DNA damage or apoptosis, and suggests that alternative mechanisms may safeguard genomic stability in the absence of Geminin. In this study, we report that Geminin has an important role in regulating proliferation and differentiation decisions of neural progenitors, contributing to the correct progenitor cell number and neuronal output in the developing cortex.…”

Section: Discussionsupporting

confidence: 92%

“…Geminin interacts with and regulates the function of crucial transcription and patterning factors during embryonic development, like the transcription factor Six3 and the Hox and Polycomb repressive complexes [20,21]. Geminin was also found to be implicated in the homeostasis of the hematopoietic system, as it has been shown to regulate hematopoietic stem cell maintenance and mature T-cell proliferation [22][23][24].…”

Section: Introductionmentioning

confidence: 99%

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Geminin Regulates Cortical Progenitor Proliferation and Differentiation

et al. 2011

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During cortical development, coordination of proliferation and differentiation ensures the timely generation of different neural progenitor lineages that will give rise to mature neurons and glia. Geminin is an inhibitor of DNA replication and it has been proposed to regulate cell proliferation and fate determination during neurogenesis via interactions with transcription factors and chromatin remodeling complexes. To investigate the in vivo role of Geminin in the maintenance and differentiation of cortical neural progenitors, we have generated mice that lack Geminin expression in the developing cortex. Our results show that loss of Geminin leads to the expansion of neural progenitor cells located at the ventricular and subventricular zones of the developing cortex. Early cortical progenitors lacking Geminin exhibit a longer S-phase and a reduced ability to generate early born neurons, consistent with a preference on self-renewing divisions. Overexpression of Geminin in progenitor cells of the cortex reduces the number of neural progenitor cells, promotes cell cycle exit and subsequent neuronal differentiation. Our study suggests that Geminin has an important role during cortical development in regulating progenitor number and ultimately neuron generation.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Geminin Regulates Cortical Progenitor Proliferation and Differentiation

et al. 2011

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“…Geminin is known as a DNA rereplication inhibitor that is expressed in the G2, S, and M phases but not in the G0 and G1 phases. 37,38 DNA replication begins with assembly of prereplication complexes (preRCs) at multiple sites throughout the genome as cells exit metaphase. 39 preRCs are then assembled into preinitiation complexes that are subsequently activated by protein kinases to begin DNA synthesis (S phase).…”

Section: Discussionmentioning

confidence: 99%

Contrast-enhanced intraoperative ultrasonography for vascular imaging of hepatocellular carcinoma: Clinical and biological significance

et al. 2013

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Abnormal tumor vascularity is one of the typical features of hepatocellular carcinoma (HCC). In this study, the significance of contrast-enhanced intraoperative ultrasonography (CEIOUS) images of HCC vasculature was evaluated by clinicopathological and gene expression analyses. We enrolled 82 patients who underwent curative hepatic resection for HCC with CEIOUS. Clinicopathological and gene expression analyses were performed according to CEIOUS vasculature patterns. CEIOUS images of HCC vasculatures were classified as reticular HCC or thunderbolt HCC. Thunderbolt HCC was significantly correlated with higher alpha-fetoprotein levels, tumor size, histological differentiation, portal vein invasion, and tumor-node-metastasis stage, and these patients demonstrated a significantly poorer prognosis for both recurrence-free survival (P 5 0.0193) and overall survival (P 5 0.0362) compared with patients who had reticular HCC. Gene expression analysis revealed that a rereplication inhibitor geminin was significantly overexpressed in thunderbolt HCCs (P 5 0.00326). In vitro knockdown of geminin gene reduced significantly the proliferation of human HCC cells. Immunohistochemical analysis confirmed overexpression of geminin protein in thunderbolt HCC (P < 0.0001). Multivariate analysis revealed geminin expression to be an independent factor in predicting poor survival in HCC patients (P 5 0.0170). Conclusion: CEIOUS vascular patterns were distinctly identifiable by gene expression profiling associated with cellular proliferation of HCC and were significantly related to HCC progression and poor prognosis. These findings might be clinically useful as a determinant factor in the postoperative treatment of HCC.

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“…Besides its role in cell cycle regulation [5], Geminin was initially characterized by its ability to expand neural plate in Xenopus embryos, when overexpressed [32]. During corticogenesis, Geminin is important for the regulation of self-renewal and differentiation decisions of neural progenitor cells [33], while T cell development in thymus remains unaffected by the absence of Geminin [34,35]. Furthermore, during chick development, it participates in axial patterning establishment through Polycomb mediated regulation of Hox gene expression [36].…”

Section: Developmental Roles Of Pre Rc Componentsmentioning

confidence: 99%

Licensing of DNA replication, cancer, pluripotency and differentiation: An interlinked world?

Tsaniras

Kanellakis

Symeonidou

et al. 2014

Seminars in Cell & Developmental Biology

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Recent findings provide evidence for a functional interplay between DNA replication and the seemingly distinct areas of cancer, development and pluripotency. Protein complexes participating in DNA replication origin licensing are now known to have roles in development, while their deregulation can lead to cancer. Moreover, transcription factors implicated in the maintenance of or reversal to the pluripotent state have links to the pre-replicative machinery. Several studies have shown that overexpression of these factors is associated to cancer.

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Life without geminin

Cited by 17 publications

References 51 publications

Geminin Regulates Cortical Progenitor Proliferation and Differentiation

Geminin Regulates Cortical Progenitor Proliferation and Differentiation

Contrast-enhanced intraoperative ultrasonography for vascular imaging of hepatocellular carcinoma: Clinical and biological significance

Licensing of DNA replication, cancer, pluripotency and differentiation: An interlinked world?

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