Associated Papers
Overview of cellular homeostasis-associated nuclear envelope lamins and associated input signals.
Kim HJ et al.
Frontiers in Cell and Developmental Biology, 2023
DNA repair-related genes and adipogenesis: Lessons from congenital lipodystrophies.
Campos JTAM et al.
Genetics and Molecular Biology, 2022
Clinical impact of exome sequencing in the setting of a general pediatric ward for hospitalized children with suspected genetic disorders.
Kagan M et al.
Frontiers in Genetics, 2022
Most myopathic lamin variants aggregate: a functional genomics approach for assessing variants of uncertain significance.
Anderson CL et al.
Npj Genomic Medicine, 2021
34862408 (PubMed )
Supplement: 41525_2021_265_MOESM1_ESM.pdf
Endoplasmic reticulum stress and muscle dysfunction in congenital lipodystrophies.
Araújo de Melo Campos JT et al.
Biochimica Et Biophysica Acta. Molecular Basis of Disease, 2021
Laminopathies' Treatments Systematic Review: A Contribution Towards a 'Treatabolome'.
Atalaia A et al.
Journal of Neuromuscular Diseases, 2021
Cardiometabolic assessment of lamin A/C gene mutation carriers: a phenotype-genotype correlation.
Kwapich M et al.
Diabetes & Metabolism, 2019
MicroRNAs in hereditary and sporadic premature aging syndromes and other laminopathies.
Frankel D et al.
Aging Cell, 2018
Bone imaging findings in genetic and acquired lipodystrophic syndromes: an imaging study of 24 cases.
Teboul-Coré S et al.
Skeletal Radiology, 2016
LMNA missense mutations causing familial partial lipodystrophy do not lead to an accumulation of prelamin A.
Tu Y et al.
Nucleus (austin, Tex.), 2016
LMNA mutations resulting in lipodystrophy and HIV protease inhibitors trigger vascular smooth muscle cell senescence and calcification: Role of ZMPSTE24 downregulation.
Afonso P et al.
Atherosclerosis, 2016
Nuclear lamins and oxidative stress in cell proliferation and longevity.
Shimi T et al.
Advances in Experimental Medicine and Biology, 2014
Human lipodystrophies linked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence.
Caron M et al.
Cell Death and Differentiation, 2007
Hutchinson-Gilford Syndrome (Progeria) with Heterozygous Mutation in the LMNA Gene-ENST00000368300.9 Presenting with Mandibuloacral Dysplasia and Acrogeroid Features-Overlap of Premature Aging Syndromes.
Muralidharan S et al.
Indian Dermatology Online Journal, 0
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