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Article

Co-Regulation of p16INK4a and Migratory Genes in Culture Conditions that Lead to Premature Senescence in Human Keratinocytes

24 Aug 2005

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Source

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 16117791
DOI: 10.1111/j.0022-202x.2005.23844.x

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Related research

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Co-Regulation of p16INK4a and Migratory Genes in Culture Conditions that Lead to Premature Senescence in Human KeratinocytesPMID 16117791Read ↗

The Role of p16INK4a Pathway in Human Epidermal Stem Cell Self-Renewal, Aging and CancerSemantic proximity Read ↗

The molecular balancing act of p16(INK4a) in cancer and aging.Semantic proximity Read ↗

A Transcriptional Roadmap to the Senescence and Differentiation of Human Oral KeratinocytesSemantic proximity Read ↗

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Tumor suppressor p16 <sup>INK4A</sup> is necessary for survival of cervical carcinoma cell linesSemantic proximity Read ↗

Downregulation of the tumour suppressor p16INK4A contributes to the polarisation of human macrophages toward an adipose tissue macrophage (ATM)-like phenotypeSemantic proximity Read ↗

p16 INK4A is a robust in vivo biomarker of cellular aging in human skinSemantic proximity Read ↗

Increased p16 expression with first senescence arrest in human mammary epithelial cells and extended growth capacity with p16 inactivationSemantic proximity Read ↗

The interplay of p16INK4a and non-coding RNAs: bridging cellular senescence, aging, and cancerSemantic proximity Read ↗

Activation of a cAMP Pathway and Induction of Melanogenesis Correlate with Association of p16INK4 and p27KIP1 to CDKs, Loss of E2F-Binding Activity, and Premature Senescence of Human MelanocytesSemantic proximity Read ↗

A two-stage, p16(INK4A)- and p53-dependent keratinocyte senescence mechanism that limits replicative potential independent of telomere status.Semantic proximity Read ↗

Senescence-associated genes in normal human oral keratinocytesSemantic proximity Read ↗

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