ライフサイエンスコーパス: lamin

1 eus and nuclear blebbing, without perturbing lamins.

2 orders caused by mutations in genes encoding lamins.

3 etained at the NE by association with A-type lamins.

4 nal requirements of nucleoporins and nuclear lamins.

5 nuclear mechanics by using a system lacking lamins.

6 main structural proteins of the nucleus, the lamins.

7 cally interacts with A-type, but not B-type, lamins.

8 lation site to a conserved site in mammalian lamin A (LA), S268.

9 otein 1alpha, and localize in proximity with Lamin A and B1 accumulation, whereas in newborn mice and

10 Mutations in LMNA (lamin A/C), which encodes lamin A and C, typically cause age-dependent cardiac phe

11 of LAP2alpha, a protein that interacts with lamin A and chromatin, has no such effect on genome dyna

12 ssociated with an increased distance between lamin A and matrin-3.

13 n A tail, 17 (13%) were previously described lamin A binding partners.

14 oss of function of differentiation-dependent lamin A binding to the MIR335 locus.

15 on in LMNA, resulting in a truncated form of lamin A called progerin.

16 mutant form of the nuclear scaffold protein lamin A distorts nuclei and sequesters nuclear proteins.

17 Depleting normal lamin A or inducing mutant lamin A expression are each sufficient to drive nucleola

18 r, administration of the exon 11 ASO reduced lamin A expression in wild-type mice and progerin expres

19 matrix, cytoskeletal force dipoles, and the lamin A gene circuit illustrate the wide range of testab

20 mulation of progerin, an altered form of the Lamin A gene.

21 However, despite ubiquitous expression of lamin A in all differentiated cells, the HGPS mutation r

22 lecular regulation of chromatin diffusion by lamin A in the nuclear interior is critical for the main

23 ered biophysical properties and the matrin-3-lamin A interface is positioned to contribute to these d

24 nd decrease in cell fluidity with increasing lamin A levels.

25 The lamin A mutation further promotes spatial clustering of

26 Our results link a laminopathy-causing lamin A mutation to an unsuspected deregulation of chrom

27 atalytic activity is critical for processing lamin A on the inner nuclear membrane and clearing clogg

28 Depleting normal lamin A or inducing mutant lamin A expression are each s

29 We show in this study that the lamin A p.R482W hot spot mutation prevents adipogenic ge

30 actor 2 (SRSF2), and SRSF2 knockdown lowered lamin A production in cells and in murine tissues.

31 Lamin A protects nuclei from the impact of actomyosin ac

32 To gain insight about lamin A protein interactions, binding proteins associate

33 The nuclear structure protein lamin A provides one example, with protein and transcrip

34 Interestingly, depletion of lamin A strikingly alters genome dynamics, inducing a dr

35 0 nuclear proteins found associated with the lamin A tail, 17 (13%) were previously described lamin A

36 romosomal inter-chain interactions formed by lamin A throughout the nucleus contribute to chromatin d

37 te that this mutation impairs the ability of lamin A to repress the anti-adipogenic miR-335, providin

38 This mutation generates the lamin A variant progerin, which we show here leads to lo

39 binding proteins associated with the tail of lamin A were characterized.

40 s assessed using precursor accumulation (for lamin A) or a MAPLE3 photoconvertible tag (for lamin B1)

41 NA, lamin C and prelamin A (the precursor to lamin A), are produced in similar amounts in most tissue

42 s in the brain produce lamin C but almost no lamin A, a consequence of the removal of prelamin A tran

43 d that Nelfinavir impaired the maturation of lamin A, a structural component of the nuclear envelope,

44 the NE, visualized by fluorescently labeled lamin A, and of the chromatin globule surface (CGS) unde

45 ntibodies were found to co-immunoprecipitate lamin A, and the lamin-A binding domain was mapped to th

46 n-Gilford progeria syndrome caused by mutant lamin A, as well as cells from patients with the disease

47 aracterized the supramolecular structures of lamin A, C, B1, and B2 in mouse embryo fibroblast nuclei

48 Progerin, a mutated lamin A, causes the severe premature-aging syndrome Hutc

49 Mutations in LMNA, the gene encoding lamin A, lead to a diverse set of inherited conditions i

50 nt form of the nuclear architectural protein lamin A, leading, through unknown mechanisms, to diverse

51 Knockdown of YY1 or lamin A/C, but not lamin A, led to a loss of lamina association.

52 One protein not previously linked to lamin A, matrin-3, was selected for further study, becau

53 brane (INM) by comparative BioID analysis of lamin A, Sun2 and a minimal INM-targeting motif.

54 Three-dimensional mapping of the lamin A-matrin-3 interface showed that the LMNA truncati

55 ajor role in converting prelamin A to mature lamin A.

56 iched with the intermediate filament protein lamin A.

57 ress the GFP-tagged nuclear envelope protein lamin A.

58 e caused by mutations in the nuclear protein lamin A.

59 is frequently caused by an R482W mutation in lamin A.

60 are variants in two AD cardiomyopathy genes, lamin A/C (LMNA) and myosin binding protein C (MYBPC3).

61 Lamin A/C (LMNA) cardiomyopathy is a genetic disease wit

62 ical behavior of cardiomyocytes carrying the lamin A/C (LMNA) D192G mutation known to cause defective

63 Mutations in the Lamin A/C (LMNA) gene-encoding nuclear LMNA cause lamino

64 ined diseases associated with alterations in lamin A/C (LMNA) splicing.

65 A mutation in the gene encoding Lamin A/C (LMNAp.R331Q ) led to reduced maximal force de

66 nd the non-sarcomeric gene mutation encoding lamin A/C (LMNAp.R331Q ).

67 deformation was governed by restructuring of Lamin A/C and increased heterochromatin content.

68 e determined that progerin binds directly to lamin A/C and induces profound nuclear aberrations.

69 UPR or not, prevents the phosphorylation of lamin A/C and LFCD in maturing LFCs in vivo, as well as

70 stablish the separate roles of chromatin and lamin A/C and show that they determine two distinct mech

71 aused nuclear morphology defects and reduced lamin A/C and SUN2 staining at the NE.

72 as a model, we found that reduced levels of lamin A/C at the onset of differentiation led to an anti

73 h the ability to block pathological progerin-lamin A/C binding may represent a promising strategy for

74 4, and JH13) that efficiently block progerin-lamin A/C binding.

75 Collectively, our results indicate that lamin A/C can modulate transcription through the regulat

76 The LAP2alpha-lamin A/C complex negatively affects cell proliferation.

77 CIP deficiency combined with lamin A/C deletion resulted in severe dilated cardiomyop

78 Here, we show that lamin A/C expressing cells can form an actin cap to resi

79 uclear stiffness is decreased by suppressing lamin A/C expression.

80 cytoskeleton) complex proteins together with lamin A/C for nuclear aberrations induced by Cofilin/ADF

81 (Sad1p/UNC84)-domain containing proteins and lamin A/C form the LInker of Nucleoskeleton-and-Cytoskel

82 SUMO1-dependent complex protects both RB and Lamin A/C from proteasomal turnover.

83 Cardiomyopathy caused by lamin A/C gene (LMNA) mutations (hereafter referred as L

84 Cardiomyopathy caused by lamin A/C gene mutations (LMNA cardiomyopathy) is charac

85 ng the differential effects of chromatin and lamin A/C in cell nuclear mechanics and their alteration

86 method to profile the dynamic interactome of lamin A/C in multiple cell and tissue types under variou

87 Here, we show that lamin A/C is evolutionarily required for correct PcG pro

88 providing structure to the nuclear envelope, lamin A/C is involved in transcriptional regulation.

89 ere we show that SUMO1 conjugation of RB and Lamin A/C is modulated by the SUMO protease SENP1 and th

90 w algorithms for image analysis reveals that lamin A/C knock-down leads to PcG protein foci disassemb

91 In contrast, lamin A/C levels control nuclear strain stiffening at la

92 ons, or a transcriptional down-regulation of lamin A/C levels in the constrained and isotropic geomet

93 However, how nuclear lamin A/C mediates the ability of the actin cap to regul

94 We found that a dominant negative lamin A/C mutant complemented the replication defect of

95 rces from the cytoskeleton and rigidity from lamin A/C nucleoskeleton can together regulate nuclear a

96 These cells also showed decreased lamin A/C phosphorylation and metaphase arrest.

97 The suppression of lamin A/C phosphorylation and metaphase transition induc

98 nce that the nuclear lamina filament protein Lamin A/C protects RB from proteasomal degradation.

99 Mutations in LMNA (lamin A/C), which encodes lamin A and C, typically cause

100 on of the LMNA gene encoding lamins A and C (lamin A/C).

101 response required the presence of vimentin, lamin A/C, and SUN (Sad1p, UNC-84)-domain protein linkag

102 it chromatin-remodeling molecules, including lamin A/C, barrier-to-autointegration factor (BAF), and

103 Knockdown of YY1 or lamin A/C, but not lamin A, led to a loss of lamina asso

104 P53, plus the nuclear architecture proteins Lamin A/C, in three different human cell lines.

105 Finally, the mechanosensitive proteins YAP, Lamin A/C, Lamin B, MRTF-A, and MRTF-B were analyzed on

106 ctivity of pUL97 is to phosphorylate nuclear lamin A/C, resulting in altered nuclear morphology and i

107 ar envelope-associated components (Lamin B1, Lamin A/C, Sun1, Nesprin-3, Plectin) compared with contr

108 The finding of a mutation in lamin A/C, the cause of approximately 6% of idiopathic D

109 at endogenous loci appear to be dependent on lamin A/C, YY1, H3K27me3, and H3K9me2/3 for maintenance

110 These functions are abrogated in lamin A/C-deficient mouse embryonic fibroblasts that rec

111 This study reveals how the nuclear lamin A/C-mediated formation of the perinuclear apical a

112 7, -8, -9, poly (ADP-ribose) polymerase, and lamin A/C.

113 induce phosphorylation and reorganization of lamin A/C.

114 Lamin B and primary human erythroblasts only Lamin A/C.

115 a silent mutation of the LMNA gene encoding lamins A and C (lamin A/C).

116 Lamins A/C are encoded by LMNA, a single heterozygous mu

117 ibroblasts null for the expression of either lamins A/C or lamin B1, the remaining lamin meshworks ar

118 leads to loss of LAP2alpha and nucleoplasmic lamins A/C, impaired proliferation, and down-regulation

119 n to its cell cycle-inhibiting function with lamins A/C, LAP2alpha can also regulate extracellular ma

120 acellular matrix components independently of lamins A/C, which may help explain the proliferation-pro

121 pression but not the levels of nucleoplasmic lamins A/C.

122 teomics-detected targets of mechanosensitive lamin-A and retinoids underscore the convergent synergy

123 gonist to increase or maintain expression of lamin-A as well as for RARG-agonist to repress expressio

124 und to co-immunoprecipitate lamin A, and the lamin-A binding domain was mapped to the carboxy-termina

125 both actomyosin assembly and nucleoskeletal lamin-A increase.

126 Expression of lamin-A is known to be controlled by retinoic acid recep

127 A progerin allele of lamin-A is regulated in the same manner in iPSC-derived

128 Applying our system to lamin-A overexpressing fibrosarcoma cells, we found a ma

129 polarize quickly, increasing nucleoskeletal lamin-A yet expressing the 'scar marker' smooth muscle a

130 ntractility thus tenses the nucleus to favor lamin-A,C accumulation and suppress soft tissue phenotyp

131 enesis (a soft lineage) indeed increases LBR:lamin-A,C protein stoichiometry in MSCs versus osteogene

132 y diverse tissues and MSCs further show that lamin-A,C's increase with tissue or matrix stiffness ant

133 ss resulting from increases in myosin-II and lamin-A,C.

134 traction force microscopy and from increased lamin-A,C.

135 markers, and RARG-antagonist strongly drives lamin-A-dependent osteogenesis on rigid substrates, with

136 lpha and the mechanosensitive nuclear marker lamin-A.

137 nuclear deformations after transmigration in lamin-A/C-deficient cells, whereas the wild-type cells s

138 Hepatocyte nuclear lamin aggregation is a sensitive marker for PP-IX-mediat

139 A small fraction of lamins also localize throughout the nucleoplasm.

140 ope (NE) budding [4, 5] that requires A-type lamin, an inner nuclear membrane-associated protein, to

141 Nuclear blebs are associated with both lamin and chromatin alterations.

142 The functional integrity of lamin and nesprin-1 is thus required to modulate the FHO

143 te filament (IF) proteins, including nuclear lamins and cytoplasmic IF proteins, are essential cytosk

144 ental contexts, a direct link between B-type lamins and developmental gene expression in an in vivo s

145 L interactions, is important to the study of lamins and other NL proteins.

146 s are separated by endoplasmic reticulum and Lamin, and disappear following polar body extrusion.

147 scaling factors, including import proteins, lamins, and reticulons.

148 B-type lamins are major constituents of the nuclear lamina in a

149 ent combinations or all lamins, we show that lamins are required to prevent the aggregation of NPCs i

150 ibre appearance and shows that A- and B-type lamins assemble into tetrameric filaments of 3.5 nm thic

151 Lands model demarcates the previously mapped lamin-associated chromatin domains (LADs) into two HiLan

152 ) but negatively correlated with H3K9me2 and lamin-associated domains (LADs).

153 uclear lamina protein lamin B1, and binds to lamin-associated domains on chromatin.

154 primary mouse erythroblasts expressing only Lamin B and primary human erythroblasts only Lamin A/C.

155 opic expression of a caspase-3 non-cleavable lamin B mutant blocks nuclear opening formation, histone

156 Lamin B receptor (LBR) is a polytopic membrane protein r

157 sed that an interaction between Xist RNA and Lamin B receptor (LBR) is necessary and sufficient for X

158 factors in regulating the gene encoding the lamin B receptor (LBR), an inner nuclear membrane protei

159 Lamin B receptor (LBR), an integral inner nuclear membra

160 We found that Lamin B receptor expression was required to attach centr

161 Wang et al question whether Lamin B receptor is required for Xist-mediated silencing

162 e show that Xist directly interacts with the Lamin B receptor, an integral component of the nuclear l

163 he mechanosensitive proteins YAP, Lamin A/C, Lamin B, MRTF-A, and MRTF-B were analyzed on these gradi

164 The two factors compete for lamin-B in response to matrix elasticity, knockdown, myo

165 sue or matrix stiffness anti-correlates with lamin-B receptor (LBR), which contributes to lipid/stero

166 , we identified 182 proteins associated with lamin B1 (a constitutive component of lamina) in mouse h

167 A duplication of the human lamin B1 (LMNB1) gene has been linked to adult-onset aut

168 somal rearrangements with duplication of the lamin B1 (LMNB1) gene underlie autosomal dominant adult-

169 Ablation of endogenous Lamin B1 (Lmnb1) in the mouse strongly impairs embryonic

170 over neurons, while overexpression of human Lamin B1 (LMNB1) increases the proportion of neurons.

171 e mouse, experimental ablation of endogenous lamin B1 (Lmnb1) severely impairs embryonic corticogenes

172 ), chemokine (C-X-C motif) ligand 1 (CXCL1), lamin B1 (LMNB1), and thioredoxin interacting protein (T

173 xample, we validated the association between lamin B1 and core histone macroH2A1, a histone associate

174 Lamin B1 and lamin B2 are essential building blocks of t

175 We also show that lamin B1 and lamin B2 are extremely long-lived proteins

176 Deficiencies in lamin B1 and lamin B2 impair neurodevelopment, but disti

177 results indicate that finely tuned levels of Lamin B1 are required for NSC differentiation into neuro

178 ouse and human loss-of-function mutations in lamin B1 are susceptibility factors for neural tube defe

179 Here, we identify lamin B1 as a key regulator of gene expression required

180 Duplication of the LMNB1 gene encoding lamin B1 causes adult-onset autosomal-dominant leukodyst

181 elial stem cells in adult mice, we show that lamin B1 deficient neurons exhibit attenuated response t

182 Lamin B1 degradation is achieved by nucleus-to-cytoplasm

183 3-lamin B1 interaction does not downregulate lamin B1 during starvation, but mediates its degradation

184 d to the nuclear envelope and interacts with lamin B1 during T-cell adhesion through alpha4beta1 inte

185 We demonstrate that reducing nuclear lamin B1 expression by short hairpin RNA-mediated silenc

186 highlight a previously unrecognized role of lamin B1 in dendrite development of mouse cortical neuro

187 Here we show that embryonic depletion of lamin B1 in retinal progenitors and postmitotic neurons

188 This LC3-lamin B1 interaction does not downregulate lamin B1 duri

189 Inhibiting autophagy or the LC3-lamin B1 interaction prevents activated RAS-induced lami

190 We further demonstrate that lamin B1 interacts directly with the promoters of some g

191 However, down-regulation of lamin B1 led to redistribution of macroH2A1.

192 We have studied a mouse model where Lamin B1 level are increased in oligodendrocytes, the ce

193 g and homologous repair is misregulated when lamin B1 levels are reduced.

194 the results suggest that the maintenance of lamin B1 levels is required for DNA replication and repa

195 Here, we report that Lamin B1 levels modulate the differentiation of murine n

196 he embryonic retina has no obvious effect on lamin B1 localization or nuclear integrity in embryonic

197 1 interaction prevents activated RAS-induced lamin B1 loss and attenuates oncogene-induced senescence

198 which results in reduced nuclear blebbing in lamin B1 null nuclei.

199 the observed mainly cerebral localization of lamin B1 overexpression and myelin degeneration.

200 this, we used a transgenic mouse model where Lamin B1 overexpression is targeted to oligodendrocytes.

201 Lamin B1 overexpression was confirmed in further ADLD-1-

202 LMNB1 despite linkage to the LMNB1 locus and lamin B1 overexpression.

203 e results support that the broadly expressed lamin B1 regulates expression of a subset of genes invol

204 nucleus-to-cytoplasm transport that delivers lamin B1 to the lysosome.

205 sues and in a postmortem brain sample, where lamin B1 was increased in the frontal lobe.

206 min A) or a MAPLE3 photoconvertible tag (for lamin B1) and membrane phospholipid incorporation using

207 Lamin B1, a key component of the nuclear lamina, plays a

208 Lamin B1, a key component of the nuclear lamina, plays a

209 ly interacts with the nuclear lamina protein lamin B1, and binds to lamin-associated domains on chrom

210 confidence, including the nucleoporin ELYS, lamin B1, and four proteins (emerin, MAN1, LAP1, and LBR

211 egrity in embryonic retinas, suggesting that lamin B1, but not lamin B2, is strictly required for nuc

212 orial patterns of chromatin association with lamin B1, core histone modification, and core and linker

213 if1 coats late-replicating domains and, with Lamin B1, identifies most of the late-replicating genome

214 eral nuclear envelope-associated components (Lamin B1, Lamin A/C, Sun1, Nesprin-3, Plectin) compared

215 eta actin, desmoplakin, fibrillarin, nuclear lamin B1, nonmuscle myosin heavy chain IIB, paxillin, Se

216 l for the expression of either lamins A/C or lamin B1, the remaining lamin meshworks are altered comp

217 the cytoskeleton (ezrin, moesin, plastin 1, lamin B1, vimentin, and beta-actin) or in protein biosyn

218 ial determinant of replication timing of non-Lamin B1-bound late domains.

219 To address this, we mapped LADs using Lamin B1-DamID during Jurkat T-cell activation, finding

220 by increased levels of the nuclear protein, Lamin B1.

221 clear matrix compartment, defined in part by lamin B1.

222 estingly, each type of lamin that we tested (lamins B1, B2, B3, and A) similarly affected nuclear siz

223 Lamin B1 and lamin B2 are essential building blocks of the nuclear la

224 We also show that lamin B1 and lamin B2 are extremely long-lived proteins in rod and co

225 Deficiencies in lamin B1 and lamin B2 impair neurodevelopment, but distinct functions

226 In stark contrast, a deficiency of lamin B2 in the embryonic retina has no obvious effect o

227 However, the absence of lamin B2 prevents proper lamination of adult retinal neu

228 In vitro assembly analysis of mutant lamin B2 protein revealed a distinct defect in the assem

229 erved region of the alpha-helical rod of the lamin B2 protein.

230 c retinas, suggesting that lamin B1, but not lamin B2, is strictly required for nucleokinesis during

231 hworks in wild-type nuclei or nuclei lacking lamin B2.

232 fibrous arrays typically formed by wild-type lamin B2.

233 report that PKC-mediated phosphorylation of lamin B3 (LB3) contributes to this mechanism of nuclear

234 The lamin-based complexes and their specific functions also

235 Lamins bind to a growing number of nuclear protein compl

236 The alternatively spliced products of LMNA, lamin C and prelamin A (the precursor to lamin A), are p

237 Neurons in the brain produce lamin C but almost no lamin A, a consequence of the remo

238 tisense oligonucleotide (ASO) that increased lamin C production at the expense of prelamin A when tra

239 d by shifting the output of LMNA more toward lamin C.

240 Mutations in lamins cause defective organogenesis in mouse models and

241 crease in the frequency of acentric-bearing, lamin-coated micronuclei.

242 ticity and viscosity primarily depend on the lamin composition, may utilize mechanically induced, sel

243 one or in combination, suggesting that total lamin concentration, and not lamin type, is more critica

244 For example, lamin deletion in various cell types can lead to an unev

245 These results suggest that a lamin derivative has been co-opted to enhance tissue sta

246 her than arthropod lineage and that nuclear, lamin-derived proteins instead acquired new cytoplasmic

247 A number of prior studies suggest that lamins dictate nuclear morphology, but the contributions

248 at nuclear Wash interacts with B-type Lamin (Lamin Dm0), and, like Lamin, Wash associates with consti

249 A cellular consequence of lamin dysfunction in laminopathies is relaxation of hete

250 We show that lamin dysfunction is conserved in human tauopathy, as su

251 Thus, lamins exhibit a structure that is remarkably different

252 d carcinogenesis where both nuclear size and lamin expression levels change.

253 tin through the hole and its relation to the lamin expression levels in the nuclear envelope.

254 how that the biomechanical effects of mutant lamin extend beyond nuclear mechanics to include interfe

255 Data analysis of individual lamin filaments resolves a globular-decorated fibre appe

256 Genetic manipulation of lamin function significantly modifies neurodegeneration

257 in the nuclear lamina and that A- and B-type lamins have distinct roles in maintaining the organizati

258 n vitro cell culture studies have shown that lamins help maintain nuclear shape and facilitate cell m

259 Deletion of B-type lamins in mESCs caused a reduced interaction between reg

260 icted migration that disrupts and segregates lamins in situ.

261 th a repressive chromatin state, the role of lamins in tethering chromatin to NL and how such tether

262 we report that MLIP (muscle enriched A-type lamin-interacting protein), a unique protein of unknown

263 symmetric NPC distribution in the absence of lamins is caused by dynein forces acting on NPCs via the

264 These studies demonstrate that individual lamin isoforms assemble into complex networks within the

265 ces are linked to differential expression of Lamin isoforms, with primary mouse erythroblasts express

266 find that nuclear Wash interacts with B-type Lamin (Lamin Dm0), and, like Lamin, Wash associates with

267 chromatin landscapes, referred to as histone lamin landscapes (HiLands)-red (R), -orange (O), -yellow

268 Furthermore, we show that altering lamin levels in vivo, both in Xenopus embryos and mammal

269 These LamC mutations were modeled after A-lamin (LMNA) mutations causing progeroid syndromes (PSs)

270 n a detailed view of the organization of the lamin meshwork within the lamina.

271 ysical links on the nuclear envelope and the lamin meshwork.

272 either lamins A/C or lamin B1, the remaining lamin meshworks are altered compared with the lamin mesh

273 dings define the architecture of the nuclear lamin meshworks at molecular resolution, providing insig

274 amin meshworks are altered compared with the lamin meshworks in wild-type nuclei or nuclei lacking la

275 Here we demonstrate that acquired lamin misregulation though aberrant cytoskeletal-nucleos

276 ll confinement and with depletion of nuclear lamins, NE proteins that structurally support the nucleu

277 there seems to be a connection between this lamin nuclear mutation and cell adhesion behavior since

278 horylation of the retinoblastoma protein and lamins, nuclear envelope breakdown, and duplication of c

279 The filamentous meshwork formed by the lamin nucleoskeleton provides a scaffold for the anchori

280 eurodegeneration in vivo, demonstrating that lamin pathology plays a causal role in tau-mediated neur

281 er, these data demonstrate that PKC-mediated lamin phosphorylation is a conserved mechanism of nuclea

282 Nuclear lamins play important roles in the organization and stru

283 Chromatin and nuclear envelope A-type lamin proteins are known to be key nuclear mechanical co

284 Lamin proteins form a meshwork beneath the nuclear envel

285 gy of PMEs to include dysfunction in nuclear lamin proteins.

286 Therefore lamins regulate microtubule-based motor forces in vivo t

287 How lamins regulate these functions is unknown.

288 nuclear envelope, whereas deletion of B-type lamins results in spindle orientation defects in mitotic

289 us; however, the specific mechanisms linking lamin structure to nuclear functions are poorly defined.

290 GST pull-down indicated that nesprin-1/lamin/SUN interactions were disrupted.

291 Interestingly, each type of lamin that we tested (lamins B1, B2, B3, and A) similarl

292 a lamina component functionally analogous to lamins, the major lamina proteins of metazoa.

293 Lamins, the major structural components of the nuclear l

294 Insight into the importance of lamins to cellular viability can be gleaned from laminop

295 ting that total lamin concentration, and not lamin type, is more critical to determining nuclear size

296 prior to nuclear migration, when nuclei and lamins undergo extreme morphological changes to squeeze

297 cts with B-type Lamin (Lamin Dm0), and, like Lamin, Wash associates with constitutive heterochromatin

298 lls deleted of different combinations or all lamins, we show that lamins are required to prevent the

299 It is composed mainly of lamins, which are intermediate filament proteins that as

300 size are sensitive to the levels of nuclear lamins, with low and high concentrations increasing and