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1 ure dilated cardiomyopathy associated with a laminopathy.
2 mouse provides a novel model of human OM and laminopathy.
3 pathological abnormalities characteristic of laminopathy.
4  restrictive dermopathy as a lethal neonatal laminopathy.
5 ciated with FXTAS may represent a functional laminopathy.
6 and a subset of the disorder can be judged a laminopathy.
7  and broadens the phenotypic spectrum of the laminopathies.
8 understanding the mechanistic basis of human laminopathies.
9 s, including NL-associated diseases, such as laminopathies.
10 LEMD2 is a new player inthe disease group of laminopathies.
11  severe human diseases collectively known as laminopathies.
12 ined the putative role of phosphorylation in laminopathies.
13 ntial therapeutic target for striated muscle laminopathies.
14  (LMNA) cause abnormal nuclear structure and laminopathies.
15 s a promising therapeutic approach for human laminopathies.
16  a major cause of mortality and morbidity in laminopathies.
17         DCM is the leading cause of death in laminopathies.
18 coding LMNA (lamin A/C), are responsible for laminopathies.
19 nsights imply a role of meshwork topology in laminopathies.
20 ons contribute to the pathogenesis of DCM in laminopathies.
21 ork and cause tissue-specific pathologies in laminopathies.
22 issue-specific disorders collectively called laminopathies.
23 se a variety of diseases collectively called laminopathies.
24 s accelerate the pathological progression of laminopathies.
25 atform for studies of the molecular basis of laminopathies.
26 ne protein SUN1 drives pathology in multiple laminopathies.
27 nstrate that miRNA expression is affected in laminopathies.
28 tissue-specific degenerative diseases termed laminopathies.
29 s of other mutations causing a wide range of laminopathies.
30 C, causes a diverse group of diseases called laminopathies.
31 an A-type lamin gene lead to diseases called laminopathies.
32 ogy reminiscent of those observed in diverse laminopathies [14-16].
33              As our understanding of cardiac laminopathies advances, we may have new tools to predict
34 te to the disease development, especially in laminopathies affecting mechanically stressed tissue suc
35  suggest alternative strategies for treating laminopathies and aging.
36 3 axis as a responsible mechanism for DCM in laminopathies and as a potential intervention target.
37 dence that tauopathies are neurodegenerative laminopathies and identifies a new pathway mediating neu
38        A useful model for understanding both laminopathies and lamin A/C function is the Lmna(-/-) mo
39  is a major source of genomic instability in laminopathies and lamin A/C-deficient tumors.
40                          Here, we review the laminopathies and the long strange trip from basic cell
41 nce, MASLD should be considered as a type of laminopathy and approaches to restore ZMPSTE24 expressio
42 NE) rupture and repair have been observed in laminopathy and cancer cells and result in intermittent
43  retina with definable transitions to severe laminopathy and visual loss.
44 artmentalization is associated with cancers, laminopathies, and aging.
45 itical role in development, virus infection, laminopathies, and cancer.
46                                              Laminopathies are a collection of phenotypically diverse
47                                              Laminopathies are a diverse group of rare diseases with
48                                              Laminopathies are caused by >300 distinct mutations in t
49                                              Laminopathies are diseases caused by dominant mutations
50 emerin in cell polarization and suggest that laminopathies are not directly associated with cells' in
51 sis for the pronounced tissue specificity of laminopathies are poorly understood.
52                                              Laminopathies are rare diseases associated with mutation
53                        To understand how the laminopathies arise from different mutations in a single
54                                 One of these laminopathies associated with missense mutations in LMNA
55  other pathological features mimicking human laminopathy associated with the LMNA mutation.
56                                              Laminopathy-associated mutations predicted to reduce ZMP
57       However, the underlying mechanisms for laminopathy-associated osteoporosis remain largely uncle
58 L and hyperthick INL were features of severe laminopathy at further eccentricities into the transitio
59                                   Studies of laminopathy-based progeria offer insights into aging-ass
60 al progress in our understanding of not only laminopathies, but also the biological roles of nuclear
61 ht comprise a therapeutic target for certain laminopathies by preventing damage from endogenous cellu
62 eatures of this disorder are also present in laminopathies caused by mutant LMNA encoding nuclear lam
63 s indicate that RD is an autosomal recessive laminopathy caused by inactivating ZMPSTE24 mutations th
64 ery-Dreifuss muscular dystrophy 1 (EDMD1), a laminopathy caused by mutations in the EMD gene.
65                                              Laminopathies, caused by mutations in A-type nuclear lam
66                                              Laminopathies, caused by mutations in the LMNA gene enco
67                           Our results link a laminopathy-causing lamin A mutation to an unsuspected d
68 s appears at all stages of disease and inner laminopathy complicates the phenotype at later stages.
69    Mutations in LMNA are associated with the laminopathies, congenital diseases affecting tissue rege
70 identified in patients with various types of laminopathy-containing diseases, which have features of
71 lity, with its dysregulation being linked to laminopathy diseases and cancer.
72    Fibroblasts from patients with the severe laminopathy diseases, restrictive dermopathy (RD) and Hu
73 LMNA, the gene encoding A-type lamins, cause laminopathies-diseases of striated muscle and other tiss
74 ption for individuals with HGPS and/or other laminopathies due to Zmpste24 processing defects.
75                                              Laminopathies encompass a wide array of human diseases a
76 tulate the defective nuclear organization of laminopathies, featuring disruption of the actin cap.
77                             The aetiology of laminopathies has been attributed to perturbation of chr
78 ectrum, prognosis, and clinical relevance of laminopathies in DCM are unknown.
79 A and C, cause a panoply of human diseases ("laminopathies"), including muscular dystrophy, cardiomyo
80 e several diseases belonging to the class of laminopathies, including muscular dystrophies.
81 g nuclear envelope-associated proteins cause laminopathies, including progeria, myopathy, and dystoni
82 ions lead to degenerative disorders known as laminopathies, including the premature aging disease Hut
83 atin organization associated with cancer and laminopathies, including the premature-aging disease Hut
84 , and they identify a potential mechanism of laminopathy involving a B-type lamin.
85 cellular consequence of lamin dysfunction in laminopathies is relaxation of heterochromatic DNA [1].
86               These disorders, often called "laminopathies," mainly affect mesenchymal tissues (e.g.,
87 fects of lamin A/C mutations observed in the laminopathies may arise from varying degrees of impaired
88 intriguing possibility that fat loss seen in laminopathies may be caused, at least in part, by reduce
89  mutations seen in many clinically disparate laminopathies may similarly alter Rb function, with rega
90 hanges at the lamina in aged hepatocytes and laminopathy models lead to redistribution of lamina-asso
91                               The Drosophila laminopathy models were used to determine if altering th
92                                              Laminopathy occurred first in more peripheral rod-rich r
93 e longer in the aorta, heart, and fat, where laminopathy pathology is apparent, than in the liver and
94                  Using skin fibroblasts from laminopathy patients and lamin A/C-deficient mouse embry
95 ects seen in animal nuclei and in some human laminopathy patients.
96 ese features resemble the pathology of human laminopathies, possibly revealing some profound patholog
97 s into possible disease mechanisms for human laminopathies, ranging from muscular dystrophy to accele
98 is and that HEM dysplasia and ichthyosis are laminopathies rather than inborn errors of cholesterol s
99  fork collapse and mislocalization of XPA in laminopathy-related progeroid syndromes.
100 ns to cellular viability can be gleaned from laminopathies, severe disorders caused by mutations in g
101 are, this risk prediction model for LTVTA in laminopathies significantly facilitated the choice of ca
102 Mutations in the lamin A/C gene (LMNA) cause laminopathies such as the premature aging Hutchinson Gil
103 PSTE24 lead to diseases of lamin processing (laminopathies), such as the premature aging disease prog
104 ns in a group of muscular dystrophies called laminopathies suggest that the shape and mechanical prop
105 1 mutant phenotypes are reminiscent of human laminopathies, suggesting that studies in Drosophila wil
106 n A/C protein turnover as a novel feature of laminopathy syndromes.
107                         LMNA mutations cause laminopathies that afflict the cardiovascular system and
108 in genes encoding LEM-D proteins cause human laminopathies that are associated with tissue-restricted
109          Human LMNA gene mutations result in laminopathies that include Emery-Dreifuss muscular dystr
110 s referred to as "nuclear envelopathies" or "laminopathies" that affect different tissues and organ s
111 in disparate diseases, known collectively as laminopathies, that affect distinct tissues, including s
112 A-type lamins, cause several diseases called laminopathies, the most common of which is dilated cardi
113 e out links between altered pRB function and laminopathies, they fail to support such an assertion.
114 NL) and autofluorescence of the RPE melanin; laminopathy was found in the scotomas.
115    Because of the dominant family history, a laminopathy was suspected and a mutation in exon 11 of t
116 phila melanogaster models of skeletal muscle laminopathies were developed to investigate the patholog
117 o a variety of degenerative disorders termed laminopathies, whereas changes in the expression of lami
118  aetiology for the cardiac phenotype in many laminopathies, whereby lamin A/C and emerin regulate gen
119 typically diverse genetic disorders known as laminopathies, which have symptoms that range from muscu
120  A/C (LMNA) gene-encoding nuclear LMNA cause laminopathies, which include partial lipodystrophies ass
121 LMNA) cause several disorders referred to as laminopathies, which include premature aging syndromes,
122 A gene, encoding A-type lamins, give rise to laminopathies, which include several types of muscular d
123 rgeting of phosphorylation in the context of laminopathies will likely require mutant- and kinase-spe

 
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