Connection

LAWRENCE DONEHOWER to DNA Damage

This is a "connection" page, showing publications LAWRENCE DONEHOWER has written about DNA Damage.
Connection Strength

1.774
  1. Altered senescence, apoptosis, and DNA damage response in a mutant p53 model of accelerated aging. Mech Ageing Dev. 2009 Apr; 130(4):262-71.
    View in: PubMed
    Score: 0.257
  2. The type 2C phosphatase Wip1: an oncogenic regulator of tumor suppressor and DNA damage response pathways. Cancer Metastasis Rev. 2008 Jun; 27(2):123-35.
    View in: PubMed
    Score: 0.242
  3. How does suppression of IGF-1 signaling by DNA damage affect aging and longevity? Mech Ageing Dev. 2008 May; 129(5):243-53.
    View in: PubMed
    Score: 0.237
  4. Augmented cancer resistance and DNA damage response phenotypes in PPM1D null mice. Mol Carcinog. 2006 Aug; 45(8):594-604.
    View in: PubMed
    Score: 0.213
  5. Reversal of the ATM/ATR-mediated DNA damage response by the oncogenic phosphatase PPM1D. Cell Cycle. 2005 Aug; 4(8):1060-4.
    View in: PubMed
    Score: 0.200
  6. Activation of WIP1 phosphatase by HTLV-1 Tax mitigates the cellular response to DNA damage. PLoS One. 2013; 8(2):e55989.
    View in: PubMed
    Score: 0.084
  7. Absence of Wip1 partially rescues Atm deficiency phenotypes in mice. Oncogene. 2012 Mar 01; 31(9):1155-65.
    View in: PubMed
    Score: 0.075
  8. The oncogenic phosphatase WIP1 negatively regulates nucleotide excision repair. DNA Repair (Amst). 2010 Jul 01; 9(7):813-23.
    View in: PubMed
    Score: 0.069
  9. The Wip1 phosphatase and Mdm2: cracking the "Wip" on p53 stability. Cell Cycle. 2008 Jan 15; 7(2):164-8.
    View in: PubMed
    Score: 0.059
  10. Decline and fall of the tumor suppressor. Proc Natl Acad Sci U S A. 2007 Nov 20; 104(47):18347-8.
    View in: PubMed
    Score: 0.058
  11. The Wip1 Phosphatase acts as a gatekeeper in the p53-Mdm2 autoregulatory loop. Cancer Cell. 2007 Oct; 12(4):342-54.
    View in: PubMed
    Score: 0.058
  12. PPM1D dephosphorylates Chk1 and p53 and abrogates cell cycle checkpoints. Genes Dev. 2005 May 15; 19(10):1162-74.
    View in: PubMed
    Score: 0.049
  13. Homeostatic regulation of base excision repair by a p53-induced phosphatase: linking stress response pathways with DNA repair proteins. Cell Cycle. 2004 Nov; 3(11):1363-6.
    View in: PubMed
    Score: 0.047
  14. Genomic and Molecular Landscape of DNA Damage Repair Deficiency across The Cancer Genome Atlas. Cell Rep. 2018 04 03; 23(1):239-254.e6.
    View in: PubMed
    Score: 0.030
  15. Genetic instability in animal tumorigenesis models. Cancer Surv. 1997; 29:329-52.
    View in: PubMed
    Score: 0.027
  16. Impact papers on aging in 2009. Aging (Albany NY). 2010 Mar; 2(3):111-21.
    View in: PubMed
    Score: 0.017
  17. 53BP1 oligomerization is independent of its methylation by PRMT1. Cell Cycle. 2005 Dec; 4(12):1854-61.
    View in: PubMed
    Score: 0.013
  18. Loss of heterozygosity occurs via mitotic recombination in Trp53+/- mice and associates with mammary tumor susceptibility of the BALB/c strain. Cancer Res. 2004 Aug 01; 64(15):5140-7.
    View in: PubMed
    Score: 0.012
  19. Chk1 is an essential kinase that is regulated by Atr and required for the G(2)/M DNA damage checkpoint. Genes Dev. 2000 Jun 15; 14(12):1448-59.
    View in: PubMed
    Score: 0.009
  20. Androgen suppressed apoptosis is modified in p53 deficient mice. Oncogene. 1995 Apr 06; 10(7):1269-74.
    View in: PubMed
    Score: 0.006
  21. Susceptibility to radiation-carcinogenesis and accumulation of chromosomal breakage in p53 deficient mice. Oncogene. 1994 Dec; 9(12):3731-6.
    View in: PubMed
    Score: 0.006
  22. Evidence that p53 and bcl-2 are regulators of a common cell death pathway important for in vivo lymphomagenesis. Oncogene. 1994 Nov; 9(11):3107-12.
    View in: PubMed
    Score: 0.006
Connection Strength

The connection strength for concepts is the sum of the scores for each matching publication.

Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.