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LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 1
2016 pubmed 17 citations

Antimicrobial peptide LL-37 participates in the transcriptional regulation of melanoma cells.

Muñoz. Mindy M; Craske. Madeleine M; Severino. Patricia P; de Lima. Thais Martins TM; Labhart. Paul P; Chammas. Roger R; Velasco. Irineu Tadeu IT; Machado. Marcel Cerqueira César MC; Egan. Brian B; Nakaya. Helder I HI; Pinheiro da Silva. Fabiano F

Key Findings

  • LL‑37 can migrate to the nucleus and bind gene promoter regions in melanoma cells
  • Silencing LL‑37 changes the transcription of genes involved in histones, metabolism, cellular stress, ubiquitination, and mitochondria
  • The observations were made in A375 melanoma cell lines, not in normal or whole‑body contexts

Practical Outcomes

  • At present there’s no actionable advice for biohackers—no dosage, supplement form, or protocol is suggested. The work is basic research that may inform future studies on LL‑37’s role in cell biology, but it doesn’t offer immediate health or performance benefits.

Summary

Scientists discovered that the antimicrobial peptide LL‑37 can move into the nucleus of melanoma cells and directly bind to DNA regions that control gene activity, reshaping the cells' gene expression patterns. This effect was seen in lab-grown cancer cells and doesn’t translate into any clear health‑boosting protocol for everyday use.

Abstract

Antimicrobial peptides are an ancient family of molecules that emerged millions of years ago and have been strongly conserved during the evolutionary process of living organisms. Recently, our group described that the human antimicrobial peptide LL-37 migrates to the nucleus, raising the possibility that LL-37 could directly modulate transcription under certain conditions. Here, we showed evidence that LL-37 binds to gene promoter regions, and LL-37 gene silencing changed the transcriptional program of melanoma A375 cells genes associated with histone, metabolism, cellular stress, ubiquitination and mitochondria.

Study Information

Provider

pubmed

Year

2016

Date

2016-11-26T00:00:00.000Z

DOI

10.7150/jca.16947

Citations

17

References

30