Search results for "Lamin Type A"

showing 2 items of 12 documents

Epigenetic involvement in Hutchinson-Gilford progeria syndrome: a mini-review.

2013

Hutchinson-Gilford progeria syndrome (HGPS) is a rare human genetic disease that leads to a severe premature ageing phenotype, caused by mutations in the <i>LMNA</i> gene. The <i>LMNA</i> gene codes for lamin-A and lamin-C proteins, which are structural components of the nuclear lamina. HGPS is usually caused by a de novo <i>C1824T</i> mutation that leads to the accumulation of a dominant negative form of lamin-A called progerin. Progerin also accumulates physiologically in normal ageing cells as a rare splicing form of lamin-A transcripts. From this perspective, HGPS cells seem to be good candidates for the study of the physiological mechanisms of ageing…

congenital hereditary and neonatal diseases and abnormalitiesAgingEuchromatinSettore BIO/11 - Biologia MolecolarecernaBiologySettore MED/13 - EndocrinologiaEpigenesis GeneticLMNAHistonesAdenosine TriphosphateProgeriaHGPS Progeria; epigenetics; chromatin; cernamedicineHumansEpigeneticsProtein PrecursorsChildEpigenesisGeneticsCell NucleusProgeriaintegumentary systemnutritional and metabolic diseasesNuclear ProteinsDNA Methylationmedicine.diseaseProgerinChromatin Assembly and DisassemblyLamin Type AChromatinCell biologySettore BIO/18 - GeneticaMicroRNAsSettore MED/03 - Genetica MedicaMutationHGPS ProgeriachromatinNuclear laminaGeriatrics and GerontologyepigeneticMi-2 Nucleosome Remodeling and Deacetylase ComplexGerontology
researchProduct

Sp1 transcription factor interaction with accumulated prelamin a impairs adipose lineage differentiation in human mesenchymal stem cells: essential r…

2012

Abstract Lamin A (LMNA)-linked lipodystrophies may be either genetic (associated with LMNA mutations) or acquired (associated with the use of human immunodeficiency virus protease inhibitors [PIs]), and in both cases they share clinical features such as anomalous distribution of body fat or generalized loss of adipose tissue, metabolic alterations, and early cardiovascular complications. Both LMNA-linked lipodystrophies are characterized by the accumulation of the lamin A precursor prelamin A. The pathological mechanism by which prelamin A accumulation induces the lipodystrophy associated phenotypes remains unclear. Since the affected tissues in these disorders are of mesenchymal origin, we…

congenital hereditary and neonatal diseases and abnormalitiesLipodystrophySp1 Transcription FactorCellular differentiationAdipose tissueBiologyLMNAHumansProtein PrecursorsTranscription factorOriginal Articles and ReviewsAdipogenesisintegumentary systemSecretory VesiclesMesenchymal stem cellnutritional and metabolic diseasesNuclear ProteinsCell DifferentiationMesenchymal Stem CellsCell BiologyGeneral MedicineLamin Type ALipid MetabolismCell biologyExtracellular MatrixBiochemistryAdipose TissueGene Expression RegulationAdipogenesisDifferentiationMutationMesenchymal stem cellsTranscription factorStem cellExperimental modelsLaminDevelopmental BiologyStem cells translational medicine
researchProduct