Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Silencing of Dicer1 temporally separates pro- and anti-apoptotic signaling and confers susceptibility to chemotherapy in p53 mutated cells.

Cell cycle (Georgetown, Tex.) - 1 Jan 2014

Nekova Tatyana S, Kneitz Susanne, Einsele Hermann, Stuhler Gernot

Abstract excerpt

miRNAs are critically implicated in the initiation process of and progression through cancerogenesis. The mechanisms, however, by which miRNAs interfere with the signalosomes of human cancer cells, are still obscure. We utilized the p53-mutated human keratinocyte cell line HACAT to investigate the biological significance and extent to which miRNAs regulate proliferation, cell growth, and apoptosis in transformed...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antimetabolites, Antineoplastic
Share to Cell Cycle Checkpoints

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to DEAD-box RNA Helicases

Share to Fluorouracil

Share to Gene Expression Regulation, Enzymologic

Share to Keratinocytes

Share to Ribonuclease III

Share to RNA Interference

Source

Open in PubMed Open full text

Identifiers

PMID: 24846461
DOI: 10.4161/cc.29216
PMCID: PMC4111674

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Silencing of Dicer1 temporally separates pro- and anti-apoptotic signaling and confers susceptibility to chemotherapy in p53 mutated cells.PMID 24846461Read ↗

Cell cycle checkpoint control: The cyclin G1/Mdm2/p53 axis emerges as a strategic target for broad‑spectrum cancer gene therapy - A review of molecular mechanisms for oncologistsSemantic proximity Read ↗

DNAJA1 controls the fate of misfolded mutant p53 through the mevalonate pathway.Semantic proximity Read ↗

Myc-Induced MicroRNAs Integrate Myc-Mediated Cell Proliferation and Cell FateSemantic proximity Read ↗

Systematic characterization of cell cycle phase-dependent protein dynamics and pathway activities by high-content microscopy-assisted cell cycle phenotyping.Semantic proximity Read ↗

Mutant p53 regulates Dicer through p63-dependent and -independent mechanisms to promote an invasive phenotype.Semantic proximity Read ↗

Nuclear accumulation of cyclin D1 during S phase inhibits Cul4-dependent Cdt1 proteolysis and triggers p53-dependent DNA rereplication.Semantic proximity Read ↗

Large-Scale Analysis of CRISPR/Cas9 Cell-Cycle Knockouts Reveals the Diversity of p53-Dependent Responses to Cell-Cycle Defects.Semantic proximity Read ↗

Cdk1 participates in BRCA1-dependent S phase checkpoint control in response to DNA damage.Semantic proximity Read ↗

Beclin‐1–p53 interaction is crucial for cell fate determination in embryonal carcinoma cellsSemantic proximity Read ↗

SIRT1 inhibition restores apoptotic sensitivity in p53-mutated human keratinocytes.Semantic proximity Read ↗

Overall Cdk activity modulates the DNA damage response in mammalian cells.Semantic proximity Read ↗

Targeting mitosis-regulating genes in cisplatin-sensitive and -resistant melanoma cells: A live-cell RNAi screen displays differential nucleus-derived phenotypes.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.