Christopher J. Jones

发表

p53-Dependent growth arrest and altered p53-immunoreactivity following metabolic labelling with 32P ortho-phosphate in human fibroblasts

T. Hupp, K. Webley, A. Craig, 1999, Oncogene.

Does telomere shortening drive selection for p53 mutation in human cancer?

N. Colburn, H. Moses, E. Bresnick, 1995 .

Telomere erosion triggers growth arrest but not cell death in human cancer cells retaining wild-type p53: implications for antitelomerase therapy

Christopher J. Jones, D. Wynford‐Thomas, M. Haughton, 2004, Oncogene.

Telomerase activity and telomere length in thyroid neoplasia: biological and clinical implications

Christopher J. Jones, D. Wynford‐Thomas, J. Skinner, 2001, The Journal of pathology.

Direct evidence from siRNA-directed "knock down" that p16(INK4a) is required for human fibroblast senescence and for limiting ras-induced epithelial cell proliferation.

J. Bond, Christopher J. Jones, D. Wynford‐Thomas, 2004, Experimental cell research.

Posttranslational Modifications of p 53 in Replicative Senescence Overlapping but Distinct from Those Induced by DNA Damage

T. Hupp, J. Blaydes, K. Webley, 2000 .

Replicative senescence in sheep fibroblasts is a p53 dependent process

R. Faragher, Christopher J. Jones, J. Skinner, 2005, Experimental Gerontology.

Telomerase activity is a biomarker for high grade malignant peripheral nerve sheath tumors in neurofibromatosis type 1 individuals

A. Guha, L. Kluwe, Christopher J. Jones, 2008, Genes, chromosomes & cancer.

An analysis of replicative senescence in dermal fibroblasts derived from chronic leg wounds predicts that telomerase therapy would fail to reverse their disease-specific cellular and proteolytic phenotype.

F. Wyllie, Christopher J. Jones, J. Skinner, 2003, Experimental cell research.

Fibroblast clones from patients with Hutchinson–Gilford progeria can senesce despite the presence of telomerase

R. Faragher, Christopher J. Jones, D. Kipling, 2004, Experimental Gerontology.

Telomerase prevents the accelerated cell ageing of Werner syndrome fibroblasts

R. Faragher, F. Wyllie, Christopher J. Jones, 2000, Nature Genetics.

Telomere-based proliferative lifespan barriers in Werner-syndrome fibroblasts involve both p53-dependent and p53-independent mechanisms

R. Faragher, F. Wyllie, Christopher J. Jones, 2003, Journal of Cell Science.

Characterisation of novel mutations in Cockayne syndrome type A and xeroderma pigmentosum group C subjects

Christopher J. Jones, D. Wynford‐Thomas, A. Ridley, 2005, Journal of Human Genetics.

Posttranslational Modifications of p53 in Replicative Senescence Overlapping but Distinct from Those Induced by DNA Damage

T. Hupp, J. Blaydes, K. Webley, 2000, Molecular and Cellular Biology.

A P53-dependent, telomere-independent proliferative life span barrier in human astrocytes consistent with the molecular genetics of glioma development.

F. Wyllie, Christopher J. Jones, D. Wynford‐Thomas, 2003, Cancer research.

Prevention of Accelerated Cell Aging in the Werner Syndrome

Christopher J. Jones, M. Haughton, D. Kipling, 2006, Annals of the New York Academy of Sciences.

Normal telomere erosion rates at the single cell level in Werner syndrome fibroblast cells.

Christopher J. Jones, D. Kipling, T. Davis, 2004, Human molecular genetics.

Telomerase and cellular lifespan: Ending the debate?

R. Faragher, Christopher J. Jones, D. Kipling, 1998, Nature Biotechnology.

Prevention of accelerated cell aging in Werner syndrome using a p38 mitogen-activated protein kinase inhibitor.

Christopher J. Jones, M. Haughton, D. Kipling, 2005, The journals of gerontology. Series A, Biological sciences and medical sciences.

Investigation of the Signaling Pathways Involved in the Proliferative Life Span Barriers in Werner Syndrome Fibroblasts

R. Faragher, Christopher J. Jones, D. Kipling, 2004, Annals of the New York Academy of Sciences.

Tumor-environment biomimetics delay peritoneal metastasis formation by deceiving and redirecting disseminated cancer cells.

J. Remon, G. Berx, C. Vanhove, 2015, Biomaterials.