LAMIN - Lamin-genome interactions in the development of Familial Partial Lipodystrophy

We hypothesize that in adipose progenitors, the LMNA p.R482W mutation causing FPLD2 alters lamin-genome contacts and reorganizes chromatin, mis-positioning developmental genes, deregulating transcription, and leading to defects in adipogenesis. This proposal aims to determine the role of the LMNA p.R482W mutation on the formation of lamina-associated domains (LADs) and subsequent impact on adipogenic commitment of progenitor cells:

TSD

  • Ja

Biobank

Godkjenninger

NSD - Ikke behov

Prosjektleder / prosjektansvarlig ved UiO

Philippe Collas

Ansvarlig enhet

Seksjon for Biokjemi

Forskere

Helsefaglig forskning

  • Ja

Personopplysninger

  • Ikke besvart

Tidsperiode

  • Start: 2013
  • Slutt: desember 2018