mTOR Is Essential for Growth and Proliferation in Early Mouse Embryos and Embryonic Stem Cells

By Mirei Murakami, T. Ichisaka, M. Maeda, N. Oshiro, K. Hara, F. Edenhofer, H. Kiyama, K. Yonezawa, S. Yamanaka. Molecular and Cellular Biology, 2004

641 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/bb664444c00efbfc4fc72ffabeba3d9bff3e1b0e

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In Molecular Biology

1. David M. Sabatini
2. Michael N. Hall
3. M. Laplante
4. R. Loewith
5. Roberto Zoncu
6. D. Guertin
7. C. Thoreen
8. M. C. Simon

Citations in the corpus

• The role of oxygen availability in embryonic development and stem cell function (2008, background): “Germline disruption of the gene encoding mTOR in mice causes embryonic lethality during blastocyst implantatio”
• mTOR signaling in growth control and disease (2012, positive): “An understanding of the role ofmTOR in regulatingmetabolism in vivo has been limitedby the fact thatwhole-body inactivation in mice of key components of the pathway causes embryonic lethality (Gangloff et al., 2004; Guertin et al., 2006; Jacinto et al., 2006; Murakami et al., 2004; Shiota et al., 20”
• TOR signaling in growth and metabolism. (2006, background): “Homozygous mTOR−/− embryos resemble embryos starved of amino acids ex vivo and die shortly after implantation due to impaired cell proliferation in both embryonic and extraembryonic compartments (Gangloff et al., 2004; Martin and Sutherland, 2001; Murakami et al., 2004).”
• mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “This is supported by the absolute requirement for mTORC1 in early embryonic developmen”
• Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1. (2006, background): “(E) Staining for actin, phospho-S6 (as a marker for mTORC1 activity), and a-tubulin in control, rictor2/2, and mLST82/2 MEFs. shortly after implantation (Gangloff et al., 2004; Murakami et al., 2004).”
• Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, background): “TSC2 null Embryonic lethality [127] mTOR null Embryonic lethality [128, 129 ]”
• Defining the role of mTOR in cancer. (2007, background): “Deleting the mtor gene results in embryonic lethality around the time of implantation, thus precluding the ability to measure AKT phosphorylation in mtor null tissues (Gangloff et al., 2004; Murakami et al., 2004).”
• Proliferation, survival and metabolism: the role of PI3K/AKT/mTOR signalling in pluripotency and cell fate determination (2016, background): “Given the key roles that mTOR complexes play in AKT activation, protein translation and nucleotide biosynthesis, it is perhaps unsurprising to find that knockout mice of various components of the complexes lead to embryonic lethality (Rennebeck et al., 1998; Murakami et al., 2004; Guertin et al., 20”