D. Glass
Molecular Biology · Nature Cell Biology · 2001–2014
A researcher in the Science corpus: 12 papers; trusts 7 researchers and is trusted by 25 researchers here, as inferred from the citation graph.
Subfields
- Molecular Biology — 72 citations into it; #1,633 of 17,773 by trust here, #1,698 by citations
- Physiology — 27 citations into it
- Cellular and Molecular Neuroscience — 25 citations into it; #519 of 2,998 by trust here, #1,099 by citations
Whom D. Glass trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
Who trusts D. Glass overall
- Vernon G. Coffey
- J. Hawley
- A. Serrano
- Christoph Handschin
- M. Sandri
- J. Sacheck
- David H. Gross
- S. Lecker
- B. Baeza-Raja
- A. Goldberg
Papers from D. Glass's perspective
Ordered by how strongly the researchers D. Glass trusts endorse each paper. Same corpus, a different order for every researcher.
- Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo (Nature Cell Biology)
- FoxO3 controls autophagy in skeletal muscle in vivo. (Cell Metabolism)
- Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy. (Cell)
- The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors. (Molecules and Cells)
- Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy (Science)
- The phosphatidylinositol 3-Kinase–AKT pathway in human cancer (Nature Reviews. Cancer)
- Transcriptional co-activator PGC-1 alpha drives the formation of slow-twitch muscle fibres. (Nature)
- Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression (The FASEB Journal)
- TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling (Nature Cell Biology)
- Autophagy in metazoans: cell survival in the land of plenty (Nature reviews. Molecular cell biology)
Their papers
- Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo (2001) — 2,782 citations
- Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways (2001) — 1,642 citations
- Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy (2001) — 3,522 citations
- The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors. (2004) — 1,965 citations
- The E3 Ligase MuRF1 degrades myosin heavy chain protein in dexamethasone-treated skeletal muscle. (2007) — 700 citations
- Skeletal muscle hypertrophy and atrophy signaling pathways. (2005) — 1,138 citations
- mTOR inhibition improves immune function in the elderly (2014) — 716 citations
- IKKbeta/NF-kappaB activation causes severe muscle wasting in mice. (2004) — 819 citations
- Myostatin reduces Akt/TORC1/p70S6K signaling, inhibiting myoblast differentiation and myotube size. (2009) — 780 citations
- During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation (2009) — 617 citations
- Signalling pathways that mediate skeletal muscle hypertrophy and atrophy (2003) — 717 citations
- Cancer cachexia: mediators, signaling, and metabolic pathways. (2012) — 1,139 citations