C. Schmitt
Physiology · Cell · 2002–2022
A researcher in the Science corpus: 5 papers; trusts 1 researcher and is trusted by 2 researchers here, as inferred from the citation graph.
Subfields
- Physiology — 94 citations into it; #2,087 of 2,276 by trust here, #676 by citations
- Molecular Biology — 90 citations into it
Whom C. Schmitt trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
Who trusts C. Schmitt overall
- A. Gudkov
- Scott W. Lowe
- V. Krizhanovsky
- J. Campisi
- E. Komarova
- J. Fridman
- Jiandong Chen
- G. Barrera
- R. Hoffman
- C. Sherr
Papers from C. Schmitt's perspective
Ordered by how strongly the researchers C. Schmitt trusts endorse each paper. Same corpus, a different order for every researcher.
- Senescence of activated stellate cells limits liver fibrosis (Cell)
- Tumour biology: Senescence in premalignant tumours (Nature)
- Identification of HSP90 inhibitors as a novel class of senolytics (Nature Communications)
- Living on a break: cellular senescence as a DNA-damage response (Nature Reviews. Cancer)
- Feedback between p21 and reactive oxygen production is necessary for cell senescence (Molecular Systems Biology)
- Senescence is a developmental mechanism that contributes to embryonic growth and patterning. (Cell)
- Autophagy mediates degradation of nuclear lamina (Nature)
- An Oncogene-Induced DNA Damage Model for Cancer Development (Science)
- Cellular senescence as a tumor-suppressor mechanism. (Trends in Cell Biology)
- Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. (The journals of gerontology. Series A, Biological sciences and medical sciences)
Their papers
- Oncogene-induced senescence as an initial barrier in lymphoma development (2005) — 1,269 citations
- Senescence-associated reprogramming promotes cancer stemness (2017) — 957 citations
- Senescence and cancer — role and therapeutic opportunities (2022) — 632 citations
- Cellular Senescence: Defining a Path Forward. (2019) — 2,621 citations
- A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy. (2002) — 1,074 citations