Core Pluripotency Factors Directly Regulate Metabolism in Embryonic Stem Cell to Maintain Pluripotency. (Q52937723)

9 May 2018

title

Core Pluripotency Factors Directly Regulate Metabolism in Embryonic Stem Cell to Maintain Pluripotency. (English)

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author name string

Hyunsoo Kim

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Tae Wan Kim

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Byung-Hee Kang

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Sang Eun Lee

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Yoon Kyung Jeon

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Doo Hyun Chung

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Jinmi Choi

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Jihoon Shin

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Eun-Jung Cho

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Hong-Duk Youn

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publication date

8 June 2015

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published in

Stem Cells

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volume

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issue

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page(s)

2699-2711

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The transcriptional and signalling networks of pluripotency

cites work

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Pluripotency and cellular reprogramming: facts, hypotheses, unresolved issues

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Metabolic plasticity in stem cell homeostasis and differentiation

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Metabolic regulation in pluripotent stem cells during reprogramming and self-renewal

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Stem cell metabolism in tissue development and aging

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Metabolism strikes back: metabolic flux regulates cell signaling

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Metabolic regulation of epigenetics

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Energy metabolism in human pluripotent stem cells and their differentiated counterparts

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The senescence-related mitochondrial/oxidative stress pathway is repressed in human induced pluripotent stem cells

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Somatic oxidative bioenergetics transitions into pluripotency-dependent glycolysis to facilitate nuclear reprogramming.

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Hypoxia-inducible factors have distinct and stage-specific roles during reprogramming of human cells to pluripotency.

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O-GlcNAc regulates pluripotency and reprogramming by directly acting on core components of the pluripotency network

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Reprogramming of human primary somatic cells by OCT4 and chemical compounds

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The metabolome of induced pluripotent stem cells reveals metabolic changes occurring in somatic cell reprogramming

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Wdr5 mediates self-renewal and reprogramming via the embryonic stem cell core transcriptional network

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Connecting microRNA genes to the core transcriptional regulatory circuitry of embryonic stem cells

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Master transcription factors and mediator establish super-enhancers at key cell identity genes

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Pluripotency Factors in Embryonic Stem Cells Regulate Differentiation into Germ Layers

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Direct reprogramming of fibroblasts into epiblast stem cells

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Phenotypic complementation establishes requirements for specific POU domain and generic transactivation function of Oct-3/4 in embryonic stem cells.

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Quantitative expression of Oct-3/4 defines differentiation, dedifferentiation or self-renewal of ES cells

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HIF1α modulates cell fate reprogramming through early glycolytic shift and upregulation of PDK1-3 and PKM2.

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Cabin1 represses MEF2 transcriptional activity by association with a methyltransferase, SUV39H1.

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The ground state of embryonic stem cell self-renewal

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CTCF-mediated functional chromatin interactome in pluripotent cells

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Reconstitution of the mouse germ cell specification pathway in culture by pluripotent stem cells

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HIF1α induced switch from bivalent to exclusively glycolytic metabolism during ESC-to-EpiSC/hESC transition

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An extended transcriptional network for pluripotency of embryonic stem cells

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Metabolic oxidation regulates embryonic stem cell differentiation

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A unique Oct4 interface is crucial for reprogramming to pluripotency

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Pyruvate kinase isozyme type M2 (PKM2) interacts and cooperates with Oct-4 in regulating transcription

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Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human glioblastoma multiforme

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PKM2 contributes to cancer metabolism

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The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth

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Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer

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PKM2, a Central Point of Regulation in Cancer Metabolism

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Identifiers

DOI

10.1002/STEM.2073

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9 May 2018

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