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Alterations in DNA replication timing identify TP63 as a novel marker of progeroid diseases

ABSTRACT: Alterations in DNA replication timing identify TP63 as a novel marker of progeroid diseases

PROVIDER: PRJNA385178 | ENA |

REPOSITORIES: ENA

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Alterations in DNA replication timing identify TP63 as a novel marker of progeroid diseases [RepliSeq]

Project description:Progeroid syndromes are rare genetic disorders that phenotypically resemble natural aging. Despite identification of causal mutations, mechanisms that generate their clinical manifestations remain elusive. Here, we identified a DNA replication timing (RT) signature that distinguishes progeroid syndromes from normal aging and identifies TP63 gene as a new disease marker. Abnormal TP63 RT appears early during differentiation of progeroid iPSCs and is associated with altered gene variant expression. Our findings demonstrate the utility of RT signatures to identify novel biomarkers not detected by other methods, reveal abnormal TP63 RT as an early event in progeroid disease progression and offer TP63 gene regulation as a potential therapeutic target.

2017-11-16 | GSE98472 | GEO

Alterations in DNA replication timing identify TP63 as a novel marker of progeroid diseases [Chip]

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Alterations in DNA replication timing identify TP63 as a novel marker of progeroid diseases

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-11-16 | GSE98475 | GEO

Homo sapiens

Project description:Alterations in DNA replication timing identify TP63 as a novel marker of progeroid diseases [RepliSeq]

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Homo sapiens

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DNA replication timing alterations identify common markers between distinct progeroid diseases.

Project description: Not available

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DNA methylation in progeroid syndromes

Project description:DNA methylation in progeroid syndromes

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Transciptome analysis of TP63 regulated pathways in HNSCC

Project description:Purpose: To identify TP63 expression regulated pathways in HNSCC Methods: A recombinant lentivirus encoding either NS shRNA or TP63 shRNA was introduced into a HNSCC cell line, FaDu. SCCs were gene generated by implanting either FaDu-NS shRNA (n=3) or FaDu-TP63 shRNA into the tongue of athymic nude mice. Tongue SCCs harvested at the end of study were used for transcriptome analysis

2019-03-15 | GSE120689 | GEO

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