2014
DOI: 10.18632/aging.100680
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Abstract: Lamin A is a key component of the nuclear lamina produced through post-translational processing of its precursor known as prelamin A. LMNA mutations leading to farnesylated prelamin A accumulation are known to cause lipodystrophy, progeroid and developmental diseases, including Mandibuloacral dysplasia, a mild progeroid syndrome with partial lipodystrophy and altered bone turnover. Thus, degradation of prelamin A is expected to improve the disease phenotype. Here, we show different susceptibilities of prelamin… Show more

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Cited by 27 publications
(44 citation statements)
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References 65 publications
(44 reference statements)
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“…Coimmunoprecipitation (IP) experiments showed in vivo binding of lamin A and HDAC2 (Figure 3a). The interplay was confirmed by in situ proximity ligation assay (PLA) (Cenni et al, 2014) showing that HDAC2‐lamin A/C complexes were formed in the nucleus of control skin fibroblasts, and PLA signals were enriched at the nuclear envelope in 47% of cells (Figure 3b). Signals were not observed in the absence of lamin A/C antibody (Figure 3c) nor after HDAC2 or lamin A/C knockdown (Figure 3c).…”
Section: Resultsmentioning
confidence: 72%
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“…Coimmunoprecipitation (IP) experiments showed in vivo binding of lamin A and HDAC2 (Figure 3a). The interplay was confirmed by in situ proximity ligation assay (PLA) (Cenni et al, 2014) showing that HDAC2‐lamin A/C complexes were formed in the nucleus of control skin fibroblasts, and PLA signals were enriched at the nuclear envelope in 47% of cells (Figure 3b). Signals were not observed in the absence of lamin A/C antibody (Figure 3c) nor after HDAC2 or lamin A/C knockdown (Figure 3c).…”
Section: Resultsmentioning
confidence: 72%
“…Anti‐lamin A/C and anti‐prelamin A antibodies used in this study have been previously characterized in control and HGPS cells (Cenni et al, 2014; Columbaro et al, 2005; Lattanzi et al, 2014). The class I HDAC inhibitor MS‐275 (entinostat) was applied 5 µM for 18 hr to fibroblasts cultures.…”
Section: Methodsmentioning
confidence: 99%
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“…101 In fact, treatment with rapamycin of MAD cells, which feature very low levels of the nicotine adenine dinucleotide (NAD)-dependent sirtuin SIRT1 in the nuclear matrix, restores SIRT1 localization and chromatin-marker distribution, elicits release of the transcription factor Oct1, and determines shortening of the prolonged S-phase. 101 …”
Section: Mandibuloacral Dysplasiamentioning
confidence: 99%
“…No curative treatment is currently available for any type of laminopathy. A number of preclinical studies have explored the therapeutic potential of different compounds that modulate the mTOR/AKT pathway [3,4], the mitogen-activated protein kinase cascade [5,6] and the epigenetic regulator NAT10 [7], among others. Gene therapy approaches are being studied as well.…”
Section: Introductionmentioning
confidence: 99%