CoChat
Sign Up
Cited by 361

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Amyloid-binding compounds maintain protein homeostasis during ageing and extend lifespan

Alavez, Silvestre, Vantipalli, Maithili C., Zucker, David J. S., Klang, Ida M., Lithgow, Gordon J.·2011·Nature
DOI 10.1038/nature09873PMC PMC3610427
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/nature09873

Cites

6 of 6 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Amyloid-binding components can maintain proteostasis during aging and extend lifespan.

    “Moreover, activation of the master regulator of the heat-shock response, the transcription factor HSF-1, increases longevity and thermotolerance in nematodes (Chiang et al., 2012; Hsu et al., 2003), while amyloid-binding components can maintain proteostasis during aging and extend lifespan (Alavez et al., 2011).”

    From The Hallmarks of Aging (2013) · cites this paper as Alavez et al., 2011

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 21

  1. Morimoto, R. I. Proteotoxic stress and inducible chaperone networks in neurodegenerative disease and aging. Genes Dev. 22, 1427–1438 (2008) · DOI · Paper page
  2. Balch, W. E., Morimoto, R. I., Dillin, A. & Kelly, J. W. Adapting proteostasis for disease intervention. Science 319, 916–919 (2008) · DOI · Paper page
  3. Porat, Y., Abramowitz, A. & Gazit, E. Inhibition of amyloid fibril formation by polyphenols: structural similarity and aromatic interactions as a common inhibition mechanism. Chem. Biol. Drug Des. 67, 27–37 (2006) · DOI
  4. Frid, P., Anisimov, S. V. & Popovic, N. Congo red and protein aggregation in neurodegenerative diseases. Brain Res. Brain Res. Rev. 53, 135–160 (2007) · DOI
  5. Tullet, J. M. et al. Direct inhibition of the longevity-promoting factor SKN-1 by insulin-like signaling in C. elegans . Cell 132, 1025–1038 (2008) · DOI · Paper page
  6. Morley, J. F. & Morimoto, R. I. Regulation of longevity in Caenorhabditis elegans by heat shock factor and molecular chaperones. Mol. Biol. Cell 15, 657–664 (2004) · DOI
  7. Cohen, E., Bieschke, J., Perciavalle, R. M., Kelly, J. W. & Dillin, A. Opposing activities protect against age-onset proteotoxicity. Science 313, 1604–1610 (2006) · DOI · Paper page
  8. Groenning, M. Binding mode of Thioflavin T and other molecular probes in the context of amyloid fibrils—current status. J. Chem. Biol. 3, 1–18 (2009) · DOI
  9. Drake, J., Link, C. D. & Butterfield, D. A. Oxidative stress precedes fibrillar deposition of Alzheimer’s disease amyloid β-peptide (1–42) in a transgenic Caenorhabditis elegans model. Neurobiol. Aging 24, 415–420 (2003) · DOI · Paper page
  10. McColl, G. et al. The Caenorhabditis elegans Aβ1–42 model of Alzheimer’s disease predominantly expresses Aβ3–42 . J. Biol. Chem. 284, 22697–22702 (2009) · DOI
  11. Temussi, P. A., Masino, L. & Pastore, A. From Alzheimer to Huntington: why is a structural understanding so difficult? EMBO J. 22, 355–361 (2003) · DOI
  12. Zengel, J. M. & Epstein, H. F. Identification of genetic elements associated with muscle structure in the nematode Caenorhabditis elegans . Cell Motil. 1, 73–97 (1980) · DOI
  13. Anderson, P. & Brenner, S. A selection for myosin heavy chain mutants in the nematode Caenorhabditis elegans . Proc. Natl Acad. Sci. USA 81, 4470–4474 (1984) · DOI
  14. Ben-Zvi, A., Miller, E. A. & Morimoto, R. I. Collapse of proteostasis represents an early molecular event in Caenorhabditis elegans aging. Proc. Natl Acad. Sci. USA 106, 14914–14919 (2009) · DOI · Paper page
  15. Lakowski, B. & Hekimi, S. The genetics of caloric restriction in Caenorhabditis elegans . Proc. Natl Acad. Sci. USA 95, 13091–13096 (1998) · DOI
  16. Murphy, C. T. et al. Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans . Nature 424, 277–283 (2003) · DOI · Paper page
  17. Walker, G. A. & Lithgow, G. J. Lifespan extension in C. elegans by a molecular chaperone dependent upon insulin-like signals. Aging Cell 2, 131–139 (2003) · DOI · Paper page
  18. Li, W., Gao, B., Lee, S. M., Bennett, K. & Fang, D. RLE-1, an E3 ubiquitin ligase, regulates C. elegans aging by catalyzing DAF-16 polyubiquitination. Dev. Cell 12, 235–246 (2007) · DOI
  19. Chen, D., Thomas, E. L. & Kapahi, P. HIF-1 modulates dietary restriction-mediated lifespan extension via IRE-1 in Caenorhabditis elegans . PLoS Genet. 5, e1000486 (2009) · DOI · Paper page
  20. Timmons, L., Court, D. L. & Fire, A. Ingestion of bacterially expressed dsRNAs can produce specific and potent genetic interference in Caenorhabditis elegans . Gene 263, 103–112 (2001) · DOI
  21. McColl, G. et al. Insulin-like signaling determines survival during stress via posttranscriptional mechanisms in C. elegans . Cell Metab. 12, 260–272 (2010) · DOI

Cited by

Sorted by citations

Metadata

Authors
Alavez, S., Vantipalli, M. C., Zucker, D. J. S., Klang, I. M., & Lithgow, G. J.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
2011-03-30
Volume
472
Issue
7342
Pages
226-229
ISSN
  • 0028-0836
  • 1476-4687
DOI
10.1038/nature09873
PMC
PMC3610427
Cited by
361
References
6
Language
en
Licence
www.springer.com/tdm (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review