(Q40715420)

English

Expression of human telomerase (hTERT) does not prevent stress-induced senescence in normal human fibroblasts but protects the cells from stress-induced apoptosis and necrosis

scientific article published on 24 July 2002

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

Expression of human telomerase (hTERT) does not prevent stress-induced senescence in normal human fibroblasts but protects the cells from stress-induced apoptosis and necrosis (English)

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

author name string

Vera Gorbunova

1

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

Andrei Seluanov

2

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

Olivia M Pereira-Smith

3

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

language of work or name

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publication date

24 July 2002

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

Journal of Biological Chemistry

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

277

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

41

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

38540-38549

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

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Regulation of cellular senescence by p53.

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Telomeres and telomerase: implications for cancer and aging

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Stress, DNA damage and ageing -- an integrative approach

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Extension of life-span by introduction of telomerase into normal human cells

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Cellular and molecular mechanisms of stress-induced premature senescence (SIPS) of human diploid fibroblasts and melanocytes

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DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts

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Induction of a senescence-like phenotype in bovine aortic endothelial cells by ionizing radiation

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Molecular analysis of H2O2-induced senescent-like growth arrest in normal human fibroblasts: p53 and Rb control G1 arrest but not cell replication

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Induction of replicative senescence biomarkers by sublethal oxidative stresses in normal human fibroblast

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Human fibroblast commitment to a senescence-like state in response to histone deacetylase inhibitors is cell cycle dependent

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Similar gene expression pattern in senescent and hyperoxic-treated fibroblasts.

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ATM-dependent telomere loss in aging human diploid fibroblasts and DNA damage lead to the post-translational activation of p53 protein involving poly(ADP-ribose) polymerase.

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Accumulation of single-strand breaks is the major cause of telomere shortening in human fibroblasts.

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Uncoupling the senescent phenotype from telomere shortening in hydrogen peroxide-treated fibroblasts

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Absence of cancer-associated changes in human fibroblasts immortalized with telomerase

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Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling

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Bypass of senescence after disruption of p21CIP1/WAF1 gene in normal diploid human fibroblasts

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Emerging roles for telomerase in regulating cell differentiation and survival: a neuroscientist's perspective

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hTERT can function with rabbit telomerase RNA: regulation of gene expression and attenuation of apoptosis

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Human endothelial cell life extension by telomerase expression

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Role of p14(ARF) in replicative and induced senescence of human fibroblasts

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22 Autoradiography

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Change of the death pathway in senescent human fibroblasts in response to DNA damage is caused by an inability to stabilize p53.

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Specific Association of Human Telomerase Activity with Immortal Cells and Cancer

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Cellular responses to DNA damage

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Cell cycle regulation in H(2)O(2)-induced premature senescence of human diploid fibroblasts and regulatory control exerted by the papilloma virus E6 and E7 proteins

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Senescence-like changes induced by hydroxyurea in human diploid fibroblasts

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Stringent sequence requirements for the formation of human telomeres

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Chromosome healing: spontaneous and programmed de novo telomere formation by telomerase

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Chromosome healing, telomere capture and mechanisms of radiation-induced chromosome breakage

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Genetic analysis of indefinite division in human cells: identification of four complementation groups

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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

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Senescence of human fibroblasts induced by oncogenic Raf.

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Regulation of a senescence checkpoint response by the E2F1 transcription factor and p14(ARF) tumor suppressor

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The oncogene and Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus

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Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions

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Identifiers

10.1074/JBC.M202671200

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

23 September 2017

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