Research Paper Volume 8, Issue 2 pp 366—381
Permanent farnesylation of lamin A mutants linked to progeria impairs its phosphorylation at serine 22 during interphase
Figure 5. Inhibition of endogenous progerin farnesylation controls its phosphorylation and levels in fibroblasts from progeria patients. (A) Immunoblots for lamin A/C and phosphoserine 22 lamin A in fibroblasts from HGPS patients. (B) Normalizing phosphoserine 22 lamin A levels to progerin levels using the data in (A). (C) Immunofluorescence for lamin A/C in BJ young fibroblasts and HGPS fibroblasts after treatment with 3 μM FTI-277 or vehicle. (D) Immunofluorescence for lamin A/C and phospho serine 22 lamin A in HGPS fibroblasts after treatment with 3 μM FTI-277 or vehicle. (E) Immunofluorescence for phosphoserine 22 lamin A in HGPS fibroblasts after treatment with 3 μM FTI-277 and/or 60 nM flavopiridol or 1μM PD0332991 (PD).