Chemical biology
Phen-DC3 probes that reveal G4 ligand localization
Open access · cc by · source: Europe PMC
A Phen-DC3 handle lets chemists add BODIPY or a cell-penetrating peptide without losing G4 selectivity, showing the parent ligand misses the nucleus.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
This library holds 8 empirical chemistry papers on chemical biology with isolated findings, rates or spectra rather than reviews.
Evidence for the claim as stated.
A Phen-DC3 handle lets chemists add BODIPY or a cell-penetrating peptide without losing G4 selectivity, showing the parent ligand misses the nucleus.
Evidence for the claim as stated.
A binding pose or a DC50 in one cell line is not a drug; off-target proteome labelling varies with the tag.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
A binding pose or a DC50 in one cell line is not a drug; off-target proteome labelling varies with the tag.
- Supports · PROTAC THNAN69 degrades LIMK2, not LIMK1
Study at a glance
- Design
- Animal / in-vitro — Phen-DC3 conjugate synthesis with G4 assays and live-cell imaging in HeLa cells
- N
- Cell-based probe study; no single primary analytic N
- Population
- HeLa cells and in-vitro G4 DNA assays
- Outcome
- G4 stabilization, cellular localization, and mtDNA copy-number effects of Phen-DC3 conjugates
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
Phen-DC3 probes that reveal G4 ligand localization
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
Only 20% cell death after 100 μM Phen-DC3 for 48 h in HeLa cells.
However, in HeLa cells, the effect of Phen-DC3 on cell viability is surprisingly mediocre, with only 20% cell death after 100 μM treatment for 48 h ().
Dicarboxylic acid 4 was obtained in 56% overall yield.
Compound 2 was next converted to dicarbaldehyde 3 by selenium mediated oxidation, which was further oxidized to the dicarboxylic acid derivative 4 in 56% overall yield.
Key findings
BODIPY–Phen-DC3 still stabilizes G4 DNA over dsDNA but barely kills cells because it fails to enter the nucleus and instead partially localizes to mitochondria, lowering mtDNA copy number. Peptide conjugation keeps G4 selectivity and strongly boosts cellular/nuclear effects.
Methodology
Authors built a Phen-DC3 derivative with a phenanthroline amine handle, conjugated BODIPY or a cell-penetrating peptide, and tested G4 stabilization (Taq stop, FRET, CD/NMR) plus live-cell imaging and mtDNA copy number in HeLa cells.
Limitations
The work does not map which mitochondrial G4 sequences are bound in cells, nor does it prove tissue-selective delivery; viability was measured in HeLa cultures, not in vivo tumors.
Related papers in this topic
Same topic cluster — not a recommendation engine.