| scholarly article | Q13442814 |
| P2093 | author name string | Haoyue Zhang | |
| Kan Cao | |||
| Julia E. Kieckhaefer | |||
| P2860 | cites work | The mutant form of lamin A that causes Hutchinson-Gilford progeria is a biomarker of cellular aging in human skin | Q21144407 |
| Prelamin A acts to accelerate smooth muscle cell senescence and is a novel biomarker of human vascular aging | Q24311723 | ||
| Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome | Q24531946 | ||
| Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome | Q24539118 | ||
| Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome | Q24562621 | ||
| Lamin B1 is required for mouse development and nuclear integrity | Q24564213 | ||
| Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts | Q24634195 | ||
| A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model | Q24657266 | ||
| Loss of A-type lamin expression compromises nuclear envelope integrity leading to muscular dystrophy | Q24681029 | ||
| Lamin A-dependent nuclear defects in human aging | Q24681309 | ||
| Laminopathies and the long strange trip from basic cell biology to therapy | Q28251294 | ||
| Human laminopathies: nuclei gone genetically awry | Q28276671 | ||
| Conditional gene expression in the epidermis of transgenic mice using the tetracycline-regulated transactivators tTA and rTA linked to the keratin 5 promoter | Q28589439 | ||
| Decreased bone formation and osteopenia in lamin a/c-deficient mice | Q33890914 | ||
| The lethal phenotype of a homozygous nonsense mutation in the lamin A/C gene | Q63531193 | ||
| Pathology and nuclear abnormalities in hearts of transgenic mice expressing M371K lamin A encoded by an LMNA mutation causing Emery-Dreifuss muscular dystrophy | Q79851107 | ||
| Targeted transgenic expression of the mutation causing Hutchinson-Gilford progeria syndrome leads to proliferative and degenerative epidermal disease | Q80853720 | ||
| Stem cell depletion in Hutchinson-Gilford progeria syndrome | Q84916810 | ||
| Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation. | Q33895774 | ||
| An accumulation of non-farnesylated prelamin A causes cardiomyopathy but not progeria | Q33904465 | ||
| Direct synthesis of lamin A, bypassing prelamin a processing, causes misshapen nuclei in fibroblasts but no detectable pathology in mice | Q33966782 | ||
| Differential temporal and spatial progerin expression during closure of the ductus arteriosus in neonates | Q34018880 | ||
| Nuclear lamins: their structure, assembly, and interactions | Q34067345 | ||
| Nuclear lamins | Q34136884 | ||
| Functional Coupling between the Extracellular Matrix and Nuclear Lamina by Wnt Signaling in Progeria | Q34137401 | ||
| Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. | Q34191451 | ||
| Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in Hutchinson-Gilford progeria syndrome cells | Q34196369 | ||
| Cardiovascular pathology in Hutchinson-Gilford progeria: correlation with the vascular pathology of aging. | Q34248086 | ||
| The nuclear lamina comes of age. | Q34390408 | ||
| Prelamin A and lamin A appear to be dispensable in the nuclear lamina | Q34416396 | ||
| Absence of progeria-like disease phenotypes in knock-in mice expressing a non-farnesylated version of progerin | Q34470636 | ||
| Progressive vascular smooth muscle cell defects in a mouse model of Hutchinson-Gilford progeria syndrome | Q34480435 | ||
| A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeria. | Q34495371 | ||
| A mitotic lamin B matrix induced by RanGTP required for spindle assembly | Q34502865 | ||
| Nuclear lamins: major factors in the structural organization and function of the nucleus and chromatin | Q34766646 | ||
| A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation. | Q34803249 | ||
| The laminopathies: nuclear structure meets disease | Q35145852 | ||
| Post-natal myogenic and adipogenic developmental: defects and metabolic impairment upon loss of A-type lamins. | Q35146605 | ||
| A lamin A protein isoform overexpressed in Hutchinson-Gilford progeria syndrome interferes with mitosis in progeria and normal cells | Q35677842 | ||
| Regulation of prelamin A but not lamin C by miR-9, a brain-specific microRNA. | Q35787261 | ||
| Mouse B-type lamins are required for proper organogenesis but not by embryonic stem cells | Q35835899 | ||
| Automated image analysis of nuclear shape: what can we learn from a prematurely aged cell? | Q35857196 | ||
| Mouse models of the laminopathies. | Q35942479 | ||
| Rapamycin reverses elevated mTORC1 signaling in lamin A/C-deficient mice, rescues cardiac and skeletal muscle function, and extends survival. | Q36731585 | ||
| Progerin elicits disease phenotypes of progeria in mice whether or not it is farnesylated. | Q36852109 | ||
| Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin | Q37323331 | ||
| B-type lamins and their elusive roles in metazoan cell proliferation and senescence | Q42223376 | ||
| Reversible phenotype in a mouse model of Hutchinson-Gilford progeria syndrome | Q43870213 | ||
| Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice. | Q52046408 | ||
| A progeroid syndrome in mice is caused by defects in A-type lamins | Q52105480 | ||
| Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice. | Q52545724 | ||
| Splicing-Directed Therapy in a New Mouse Model of Human Accelerated Aging | Q57082619 | ||
| Lamin A/C deficiency is associated with fat infiltration of muscle and bone | Q57086315 | ||
| Mouse model carrying H222P- Lmna mutation develops muscular dystrophy and dilated cardiomyopathy similar to human striated muscle laminopathies | Q60535383 | ||
| P433 | issue | 1 | |
| P407 | language of work or name | English | Q1860 |
| P304 | page(s) | 2-10 | |
| P577 | publication date | 2013-02-01 | |
| P1433 | published in | Aging Cell | Q2221073 |
| P1476 | title | Mouse models of laminopathies | |
| P478 | volume | 12 |
| Q41422120 | A Tissue Engineered Blood Vessel Model of Hutchinson-Gilford Progeria Syndrome Using Human iPSC-derived Smooth Muscle Cells |
| Q54971907 | Alternative mRNA Splicing in the Pathogenesis of Obesity. |
| Q40634162 | An inhibitory role of progerin in the gene induction network of adipocyte differentiation from iPS cells |
| Q57165494 | Cardiac ageing: extrinsic and intrinsic factors in cellular renewal and senescence |
| Q37469701 | Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations |
| Q34614178 | Cellular mechanosensing: getting to the nucleus of it all. |
| Q36580567 | Correlated alterations in genome organization, histone methylation, and DNA-lamin A/C interactions in Hutchinson-Gilford progeria syndrome |
| Q34480944 | DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome. |
| Q89999227 | Diminished Canonical β-Catenin Signaling During Osteoblast Differentiation Contributes to Osteopenia in Progeria |
| Q33855932 | Distinct Fiber Type Signature in Mouse Muscles Expressing a Mutant Lamin A Responsible for Congenital Muscular Dystrophy in a Patient. |
| Q64074438 | Generation and characterization of a novel knockin minipig model of Hutchinson-Gilford progeria syndrome |
| Q89965056 | High Fidelity of Mouse Models Mimicking Human Genetic Skeletal Disorders |
| Q38578682 | Hutchinson-Gilford progeria syndrome as a model for vascular aging |
| Q38087992 | Implications of multipotent mesenchymal stromal cell aging |
| Q51731708 | Increasing autophagy and blocking Nrf2 suppress laminopathy-induced age-dependent cardiac dysfunction and shortened lifespan. |
| Q39072434 | Lamin A Δexon9 mutation leads to telomere and chromatin defects but not genomic instability. |
| Q34547899 | Lamin A/C depletion enhances DNA damage-induced stalled replication fork arrest |
| Q54945496 | Lamins and bone disorders: current understanding and perspectives. |
| Q33551452 | Linker of nucleoskeleton and cytoskeleton complex proteins in cardiac structure, function, and disease |
| Q36210071 | Loss of H3K9me3 Correlates with ATM Activation and Histone H2AX Phosphorylation Deficiencies in Hutchinson-Gilford Progeria Syndrome |
| Q35218759 | Low levels of the reverse transactivator fail to induce target transgene expression in vascular smooth muscle cells |
| Q34338745 | Nuclear lamina builds tissues from the stem cell niche |
| Q33638752 | Nuclear localization signal deletion mutants of lamin A and progerin reveal insights into lamin A processing and emerin targeting |
| Q41457647 | Phenotype-Dependent Coexpression Gene Clusters: Application to Normal and Premature Ageing |
| Q51281097 | Rapamycin Reverses Metabolic Deficits in Lamin A/C-Deficient Mice. |
| Q55400232 | SMAD6 overexpression leads to accelerated myogenic differentiation of LMNA mutated cells. |
| Q91141600 | Single molecule analysis of lamin dynamics |
| Q36931652 | Targeting Mitogen-Activated Protein Kinase Signaling in Mouse Models of Cardiomyopathy Caused by Lamin A/C Gene Mutations |
| Q64051766 | The K219T-Lamin mutation induces conduction defects through epigenetic inhibition of SCN5A in human cardiac laminopathy |
| Q53080649 | The clinicopathological significance of lamin A/C, lamin B1 and lamin B receptor mRNA expression in human breast cancer. |
| Q42434438 | The decision-making process and criteria in selecting candidate drugs for progeria clinical trials |
| Q42017705 | Transgenic mice overexpressing glia maturation factor-β, an oxidative stress inducible gene, show premature aging due to Zmpste24 down-regulation |
| Q90393795 | Vascular Smooth Muscle Cell-Specific Progerin Expression Provokes Contractile Impairment in a Mouse Model of Hutchinson-Gilford Progeria Syndrome that Is Ameliorated by Nitrite Treatment |
| Q26827624 | When lamins go bad: nuclear structure and disease |
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