P. Cau, C. Navarro, K. Harhouri, P. Roll, S. Sigaudy et al., Nuclear matrix, nuclear envelope and premature aging syndromes in a translational research perspective Cdna sequencing of nuclear lamins a and c reveals primary and secondary structural homology to intermediate filament proteins, Proc. Natl. Acad. Sci. USA 1986, pp.125-147

F. Lin and H. J. Worman, Structural organization of the human gene encoding nuclear lamin a and nuclear lamin c, J. Biol. Chem, vol.268, pp.16321-16326, 1993.

M. W. Hetzer and S. R. Wente, Border Control at the Nucleus: Biogenesis and Organization of the Nuclear Membrane and Pore Complexes, Developmental Cell, vol.17, issue.5, pp.606-616, 2009.
DOI : 10.1016/j.devcel.2009.10.007

K. Weber, U. Plessmann, and P. Traub, Maturation of nuclear lamin A involves a specific carboxy-terminal trimming, which removes the polyisoprenylation site from the precursor; implications for the structure of the nuclear lamina, FEBS Letters, vol.1008, issue.2, pp.411-414, 1989.
DOI : 10.1016/0167-4781(89)90179-6

I. Varela, S. Pereira, A. P. Ugalde, C. L. Navarro, M. F. Suarez et al., Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging, Nature Medicine, vol.154, issue.7, pp.767-772, 2008.
DOI : 10.1172/JCI200422087
URL : https://hal.archives-ouvertes.fr/inserm-00376425

D. Sandre-giovannoli, A. Bernard, R. Cau, P. Navarro, C. Amiel et al., Lamin A Truncation in Hutchinson-Gilford Progeria, Science, vol.300, issue.5628, p.2055, 2003.
DOI : 10.1126/science.1084125

T. Y. Moses and P. Berglund, Recurrent de novo point mutations in lamin a cause hutchinson-gilford progeria syndrome, Nature, vol.423, pp.293-298, 2003.

R. C. Hennekam, Hutchinson???Gilford progeria syndrome: Review of the phenotype, American Journal of Medical Genetics Part A, vol.81, issue.23, pp.2603-2624, 2006.
DOI : 10.1016/S1388-1981(02)00342-6

R. D. Goldman, D. K. Shumaker, M. R. Erdos, M. Eriksson, A. E. Goldman et al., Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome, Proc. Natl. Acad. Sci, pp.8963-8968, 2004.
DOI : 10.1016/0076-6879(91)00127-I

F. Barthelemy, C. Navarro, R. Fayek, N. Da-silva, P. Roll et al., Truncated prelamin A expression in HGPS-like patients: a transcriptional study, European Journal of Human Genetics, vol.23, issue.8, pp.1051-1061, 2015.
DOI : 10.1126/scitranslmed.3002847
URL : https://hal.archives-ouvertes.fr/hal-01597886

F. M. Hisama, D. Lessel, D. Leistritz, K. Friedrich, K. L. Mcbride et al., Coronary artery disease in a Werner syndrome-like form of progeria characterized by low levels of progerin, a splice variant of lamin A, American Journal of Medical Genetics Part A, vol.272, issue.12, pp.3002-3006, 2011.
DOI : 10.1126/science.272.5259.258

K. Fukuchi, T. Katsuya, K. Sugimoto, M. Kuremura, H. D. Kim et al., LMNA mutation in a 45 year old Japanese subject with Hutchinson-Gilford progeria syndrome, Journal of Medical Genetics, vol.41, issue.5, pp.41-67, 2004.
DOI : 10.1136/jmg.2003.014688

C. L. Moulson, L. G. Fong, J. M. Gardner, E. A. Farber, G. Go et al., mutations causes severe progeroid syndromes, Human Mutation, vol.281, issue.9, pp.882-889, 2007.
DOI : 10.1002/humu.20536

S. A. Shalev, A. De-sandre-giovannoli, A. A. Shani, and N. Levy, An association of Hutchinson???Gilford progeria and malignancy, American Journal of Medical Genetics Part A, vol.272, issue.16, pp.1821-1826, 2007.
DOI : 10.1016/0921-8734(95)00015-X

A. K. Agarwal, J. P. Fryns, R. J. Auchus, and A. Garg, Zinc metalloproteinase, ZMPSTE24, is mutated in mandibuloacral dysplasia, Human Molecular Genetics, vol.12, issue.16, 1995.
DOI : 10.1093/hmg/ddg213
URL : https://academic.oup.com/hmg/article-pdf/12/16/1995/6947753/ddg213.pdf

S. Shackleton, D. T. Smallwood, P. Clayton, L. C. Wilson, A. K. Agarwal et al., Compound heterozygous ZMPSTE24 mutations reduce prelamin A processing and result in a severe progeroid phenotype, Journal of Medical Genetics, vol.42, issue.6, pp.42-78, 2005.
DOI : 10.1136/jmg.2004.029751

B. Yaou, R. Navarro, C. Quijano-roy, S. Bertrand, A. T. Massart et al., Type B mandibuloacral dysplasia with congenital myopathy due to homozygous ZMPSTE24 missense mutation, European Journal of Human Genetics, vol.140, issue.6, pp.647-654, 2011.
DOI : 10.1210/jc.2007-0116
URL : https://hal.archives-ouvertes.fr/hal-00611256

S. Blondel, A. L. Jaskowiak, A. L. Egesipe, A. Le-corf, C. Navarro et al., Induced Pluripotent Stem Cells Reveal Functional Differences Between Drugs Currently Investigated in Patients With Hutchinson-Gilford Progeria Syndrome, STEM CELLS Translational Medicine, vol.131, issue.4, pp.510-519
DOI : 10.1016/j.mad.2009.11.006

V. Cenni, C. Capanni, M. Columbaro, M. Ortolani, M. R. D-'apice et al., Autophagic degradation of farnesylated prelamin A as a therapeutic approach to lamin-linked progeria, Eur. J. Histochem, pp.55-91, 2011.

K. Cao, J. J. Graziotto, C. D. Blair, J. R. Mazzulli, M. R. Erdos et al., Rapamycin Reverses Cellular Phenotypes and Enhances Mutant Protein Clearance in Hutchinson-Gilford Progeria Syndrome Cells, Science Translational Medicine, vol.30, issue.11
DOI : 10.1161/ATVBAHA.110.209460

J. I. Toth, S. H. Yang, X. Qiao, A. P. Beigneux, M. H. Gelb et al., Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes, Proc. Natl. Acad. Sci. USA 2005, pp.12873-12878
DOI : 10.1007/s00223-004-0024-1

S. H. Yang, M. O. Bergo, J. I. Toth, X. Qiao, Y. Hu et al., Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation, Proc. Natl. Acad. Sci. USA 2005, pp.10291-10296
DOI : 10.1083/jcb.147.5.913

P. Scaffidi and T. Misteli, Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome, Nature Medicine, vol.22, issue.4, pp.440-445, 2005.
DOI : 10.1038/nbt964

M. K. Parra, S. Gee, N. Mohandas, and J. G. Conboy, Manipulation of Alternative Pre-mRNA Splicing Events Using Antisense Morpholinos in Mice, Journal of Biological Chemistry, vol.3, issue.8, pp.6033-6039, 2011.
DOI : 10.1038/nm1345

F. G. Osorio, C. Barcena, C. Soria-valles, A. J. Ramsay, F. De-carlos et al., Nuclear lamina defects cause ATM-dependent NF-??B activation and link accelerated aging to a systemic inflammatory response, Genes & Development, vol.26, issue.20, pp.2311-2324, 2012.
DOI : 10.1101/gad.197954.112

G. Marino, A. P. Ugalde, A. F. Fernandez, F. G. Osorio, A. Fueyo et al., Insulin-like growth factor 1 treatment extends longevity in a mouse model of human premature aging by restoring somatotroph axis function, Proc. Natl. Acad. Sci. USA 2010, pp.16268-16273
DOI : 10.1006/meth.2001.1262

N. Kubben, W. Zhang, L. Wang, T. C. Voss, J. Yang et al., Repression of the Antioxidant NRF2 Pathway in Premature Aging, Cell, vol.165, issue.6, pp.1361-1374, 2016.
DOI : 10.1016/j.cell.2016.05.017

D. Gabriel, D. Roedl, L. B. Gordon, and K. Djabali, Sulforaphane enhances progerin clearance in Hutchinson-Gilford progeria fibroblasts, Aging Cell, vol.281, issue.1, pp.78-91, 2015.
DOI : 10.1074/jbc.R600033200
URL : http://onlinelibrary.wiley.com/doi/10.1111/acel.12300/pdf

P. A. Morcos, Y. Li, and S. Jiang, Vivo-Morpholinos: A non-peptide transporter delivers Morpholinos into a wide array of mouse tissues, BioTechniques, vol.45, issue.6, pp.613-614, 2008.
DOI : 10.2144/000113005

L. Wegner, S. Anthonsen, J. Bork-jensen, L. Dalgaard, T. Hansen et al., rs4641 and the Muscle Lamin A and C Isoforms in Twins???Metabolic Implications and Transcriptional Regulation, The Journal of Clinical Endocrinology & Metabolism, vol.95, issue.8, pp.3884-3892, 2010.
DOI : 10.1210/jc.2009-2675

J. L. Mesa, R. J. Loos, P. W. Franks, K. K. Ong, J. Luan et al., Lamin A/C Polymorphisms, Type 2 Diabetes, and the Metabolic Syndrome: Case-Control and Quantitative Trait Studies, Diabetes, vol.56, issue.3, pp.884-889, 2007.
DOI : 10.2337/db06-1055

L. Wegner, G. Andersen, T. Sparso, N. Grarup, C. Glumer et al., Common Variation in LMNA Increases Susceptibility to Type 2 Diabetes and Associates With Elevated Fasting Glycemia and Estimates of Body Fat and Height in the General Population: Studies of 7,495 Danish Whites, Diabetes, vol.56, issue.3, pp.694-698, 2007.
DOI : 10.2337/db06-0927

M. A. Merideth, L. B. Gordon, S. Clauss, V. Sachdev, A. C. Smith et al., Phenotype and Course of Hutchinson???Gilford Progeria Syndrome, New England Journal of Medicine, vol.358, issue.6, pp.592-604, 2008.
DOI : 10.1056/NEJMoa0706898

J. M. Lee, C. Nobumori, Y. Tu, C. Choi, S. H. Yang et al., Modulation of LMNA splicing as a strategy to treat prelamin A diseases, Journal of Clinical Investigation, vol.126, issue.4, pp.1592-1602, 2016.
DOI : 10.1172/JCI85908DS1

X. Nissan, S. Blondel, C. Navarro, Y. Maury, C. Denis et al., Unique Preservation of Neural Cells in Hutchinson- Gilford Progeria Syndrome Is Due to the Expression of the Neural-Specific miR-9 MicroRNA, Cell Reports, vol.2, issue.1, pp.1-9, 2012.
DOI : 10.1016/j.celrep.2012.05.015

H. J. Jung, C. Coffinier, Y. Choe, A. P. Beigneux, B. S. Davies et al., Regulation of prelamin A but not lamin C by miR-9, a brain-specific microRNA, Proc. Natl. Acad. Sci. USA 2012, pp.423-431
DOI : 10.1172/JCI35876

L. G. Fong, J. K. Ng, J. Lammerding, T. A. Vickers, M. Meta et al., Prelamin A and lamin A appear to be dispensable in the nuclear lamina, Journal of Clinical Investigation, vol.116, issue.3, pp.743-752, 2006.
DOI : 10.1172/JCI27125

J. M. Freije, J. Stevenin, and A. De-sandre-giovannoli, A conserved splicing mechanism of the lmna gene controls premature aging, Hum. Mol. Genet, vol.20, pp.4540-4555, 2011.

C. Strandgren, H. A. Nasser, T. Mckenna, A. Koskela, J. Tuukkanen et al., Transgene silencing of the Hutchinson-Gilford progeria syndrome mutation results in a reversible bone phenotype, whereas resveratrol treatment does not show overall beneficial effects, The FASEB Journal, vol.20, issue.8, pp.3193-3205
DOI : 10.1016/j.mehy.2014.08.016

S. Majumdar and K. Reue, Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice, Proc. Natl. Acad. Sci. USA, pp.18111-18116, 2004.

A. Goyenvalle, G. Griffith, A. Babbs, S. Andaloussi, K. Ezzat et al., Functional correction in mouse models of muscular dystrophy using exon-skipping tricyclo-DNA oligomers, Nature Medicine, vol.18, issue.3, pp.270-275, 2015.
DOI : 10.1038/mt.2009.248
URL : https://hal.archives-ouvertes.fr/hal-01165556

J. R. Mendell, L. R. Rodino-klapac, Z. Sahenk, K. Roush, L. Bird et al., Eteplirsen for the treatment of Duchenne muscular dystrophy, Annals of Neurology, vol.74, issue.5, pp.637-647, 2013.
DOI : 10.1086/381039

Q. L. Lu, S. Cirak, and T. Partridge, What Can We Learn From Clinical Trials of Exon Skipping for DMD?, Molecular Therapy - Nucleic Acids, vol.3, issue.3
DOI : 10.1038/mtna.2014.6