ライフサイエンスコーパス: lamin

1 tions in the human LMNA gene encoding A-type lamins.

2 reased nuclear envelope proteins and nuclear lamins.

3 described previously for mice lacking A-type lamins.

4 eus and nuclear blebbing, without perturbing lamins.

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

6 main structural proteins of the nucleus, the lamins.

7 uptures facilitated by the downmodulation of lamins.

8 cular weight human heart proteoforms such as lamin A (72 kDa) and trifunctional enzyme subunit alpha

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

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

11 Our findings establish a direct link between lamin A and PcG epigenetic silencing and indicate that l

12 Increased levels of lamin A are known to increase the rigidity of nuclei, in

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

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

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

16 zed mechanosensitive markers, but found that lamin A expression, as well as YAP and MRTF-A nuclear tr

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

18 rogeria syndrome, in which a mutation in the lamin A gene yields an altered form of the protein, name

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

20 We show that lamin A has the greatest effect on chromatin viscoelasti

21 G) of proteins are epigenetic repressors and lamin A interactors, primarily involved in the maintenan

22 Lamin A is a component of the inner nuclear membrane tha

23 Lamin A is a nuclear intermediate filament protein criti

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

25 muscular dystrophy (EDMD), we show here that lamin A loss deregulated PcG positioning in muscle satel

26 roblasts expressing a cardiomyopathy-causing lamin A mutant.

27 The lamin A mutation further promotes spatial clustering of

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

29 existence of degenerative diseases linked to lamin A mutations suggests that perinuclear binding of c

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

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

32 wofold overexpression of the nuclear protein lamin A or we introduce into the cells stiff polystyrene

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

34 on of specific LMNA mutant-driven changes to lamin A phosphorylation and protein structure was perfor

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

36 pression mechanism where coiled coils in the lamin A rod can slide onto each other to contract rod le

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

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

39 We also identified that Lamin A, a cell nuclear lamina member, is a unique marke

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

41 substitution mutation in the gene coding for lamin A, causing the production of a toxic isoform calle

42 Lamin A, lamin C, and progerin, products of the Lmna gen

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

44 eus, including nuclear morphology, levels of lamin A,C, and histone deacetylation, as these tensile s

45 r mechanisms involved in the pathogenesis of lamin A-dependent dystrophies are still largely unknown.

46 d PcG epigenetic silencing and indicate that lamin A-dependent muscular dystrophy can be ascribed to

47 ed precursor of the nuclear scaffold protein lamin A.

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

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

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

51 Lamin A/C (LMNA) gene mutations are a known cause of fam

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

53 Lamin A/C (LMNA) is one of the most frequently mutated g

54 178 patients (37%): 54 (11%) Titin; 19 (4%) Lamin A/C (LMNA); 24 (5%) structural cytoskeleton-Z disk

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

56 Mutations in LMNA encoding lamin A/C and EMD encoding emerin cause cardiomyopathy a

57 erozygous deletion of this gene lacking both lamin A/C and emerin are born at the expected Mendelian

58 Mice without lamin A/C and emerin are born at the expected Mendelian

59 d a shorter lifespan than those only lacking lamin A/C and emerin.

60 slower heart rates in the mice lacking both lamin A/C and emerin.

61 nd recruitment of PKC-delta to phosphorylate lamin A/C and facilitate porcine circoviral nuclear egre

62 to LRRK2 knockdown, cause disorganization of lamin A/C and leakage of nuclear proteins.

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

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

65 ane, hence abolishing the phosphorylation of lamin A/C and the rearrangement of nuclear lamina.

66 utations mostly abolish the interaction with lamin A/C and, similar to LRRK2 knockdown, cause disorga

67 We identify increased levels of lamin A/C as a robust molecular phenotype in the heart o

68 aa 41 to 60) of p17 and p17 colocalized with lamin A/C at the nuclear envelope.

69 New pS22-Lamin A/C binding was accompanied by increased histone a

70 l changes observed in cells of patients with Lamin A/C cardiomyopathies.

71 otype in the heart of SMA mice and show that lamin A/C dysregulation is also apparent in SMA patient

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

73 In addition, altered lamin A/C expression is found in various cancers.

74 Furthermore, the lamin A/C expression was increased and redistributed to

75 Lamin A/C expression was regulated in vitro by knockdown

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

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

78 Mutations in the lamin A/C gene (LMNA) are identified in patients with va

79 Mutations in the lamin A/C gene (LMNA) cause an autosomal dominant inheri

80 Mutations in the lamin A/C gene (LMNA) cause cardiomyopathy and also disr

81 Mutations in the lamin A/C gene cause several diseases belonging to the c

82 pathogenic mechanism in heart failure due to lamin A/C haploinsufficiency.

83 dually, lamin B1 highlights acute leukemias, lamin A/C helps distinguish normal from neoplastic matur

84 We catalogued all known lamin A/C human mutations and their associated phenotype

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

86 further decouples the roles of chromatin and lamin A/C in compression, showing they separately resist

87 identify a novel interplay between SIRT7 and Lamin A/C in L1 repression.

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

89 Remarkably, mutation of lamin A/C in muscles or motoneurons had no effect on NMJ

90 These results reveal a role of lamin A/C in NMJ maintenance and suggest that nuclear dy

91 These results reveal a role of lamin A/C in NMJ maintenance and suggest that nuclear dy

92 Here, we provide evidence that loss of lamin A/C in skeletal muscles, but not osteoblast (OB)-l

93 pS22-Lamin A/C interacted with a subset of putative active en

94 The nuclear lamina protein lamin A/C is a key component of the nuclear envelope.

95 Knockdown of hnRNP A1 or lamin A/C led to inhibition of nucleocytoplasmic shuttli

96 The increased lamin A/C levels in the hearts of SMA mice therefore pro

97 Therapeutic strategies directed at lamin A/C may therefore offer a new approach to target c

98 latory rather than LAD tethering function of Lamin A/C may underlie the pathogenesis of disorders cau

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

100 rovides novel insights into how hnRNP A1 and lamin A/C modulate nucleocytoplasmic shuttling of the AR

101 atal defects are primarily driven by loss of lamin A/C or lamina-associated polypeptide 1 rather than

102 Reports indicate that lamin A/C plays a role in DNA double strand break repair

103 These results suggest that Lamin A/C regulates gene expression by enhancer binding.

104 Here we report that hnRNP A1 and lamin A/C serve as carrier and mediator proteins to modu

105 LMNA encodes nuclear Lamin A/C that tethers lamina-associated domains (LADs)

106 suggest a critical role for skeletal muscle lamin A/C to prevent cellular senescence, IL-6 expressio

107 clear membrane, which further phosphorylates lamin A/C to promote the rearrangement of nuclear lamina

108 channel expression and increased binding of Lamin A/C to the promoter of SCN5A, the channel's gene.

109 We report that Ser22-phosphorylated (pS22) Lamin A/C was localized to the nuclear interior in human

110 this work, the interaction site of p17 with lamin A/C was mapped within the amino terminus (aa 41 to

111 Mutations in the LMNA (lamin A/C) gene have been associated with neuromuscular

112 Mutations in the LMNA gene, encoding LMNA (lamin A/C), are responsible for laminopathies.

113 The A-type lamins (lamin A/C), encoded by the LMNA gene, are important stru

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

115 STATEMENT This study provides evidence that lamin A/C, a scaffolding component of the nuclear envelo

116 In particular, lamin A/C, an intermediate filament protein critical for

117 ivity to 4 antigens, vimentin, beta-tubulin, lamin A/C, and apolipoprotein L2, was significantly diff

118 autophagy, which promotes the degradation of lamin A/C, B1, and B2 in iDCs only.

119 d lamin-depleted MCF-10A cells revealed that lamin A/C, but not lamin B2, protects the nuclear membra

120 in LMNA, which encodes the nuclear proteins Lamin A/C, can cause cardiomyopathy and conduction disor

121 Mutation in the LMNA gene, encoding lamin A/C, causes a diverse group of diseases called lam

122 tors LEMD2 or emerin, and to a lesser extent lamin A/C, increased the duration of nucleus ruptures, c

123 nd in the nucleus it directly interacts with lamin A/C, independent of its kinase activity.

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

125 Cap to the nuclear membrane to phosphorylate lamin A/C, resulting in a rearrangement of nuclear lamin

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

127 /C-binding sites were lost, whereas new pS22-Lamin A/C-binding sites emerged in normally quiescent lo

128 ogeria-patient fibroblasts, a subset of pS22-Lamin A/C-binding sites were lost, whereas new pS22-Lami

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

130 atment with the conditioned medium (CM) from lamin A/C-deficient muscle cells.

131 tosidase (SA-beta-gal), p16Ink4a, and p53 in lamin A/C-deficient muscles and C2C12 muscle cells, and

132 6, whose expression is markedly increased in lamin A/C-deficient muscles.

133 ovide evidence for reduced BER efficiency in lamin A/C-depleted cells (Lmna null MEFs and lamin A/C-k

134 lamin A/C-depleted cells (Lmna null MEFs and lamin A/C-knockdown U2OS).

135 Knockout (KO) of IL-6 in muscle lamin A/C-KO mice diminishes the deficits in trabecular

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

137 ovide mechanistic insights into hnRNP A1 and lamin A/C-modulated nucleocytoplasmic shuttling of the A

138 ocus restored muscle stem cell properties in lamin A/C-null dystrophic mice.

139 Surprisingly, in contrast to lamin A/C-null mice, SUN2-null mice fail to show coincid

140 C-CMs) with a haploinsufficient mutation for lamin A/C.

141 ve shorter lifespans than those lacking only lamin A/C.

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

143 ncodes the nuclear lamina-associated protein lamin A/C.

144 ith mutations in LMNA, which encodes nuclear lamin A/C.

145 Here we show that reduction of lamin A/progerin by a single-dose systemic administratio

146 Lamins A and C are intermediate filaments that provide s

147 Deficiencies in lamin-A and repair factors exacerbate these effects, but

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

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

150 low phosphorylation and slow degradation of lamin-A by matrix-metalloprotease-2 (MMP2), and inhibiti

151 both actomyosin assembly and nucleoskeletal lamin-A increase.

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

153 Lamin-A is thus stress stabilized to mechano-protect the

154 elopmental Cell, Cho et al. (2019) find that lamin-A levels in the nuclear envelope are regulated in

155 lloprotease-2 (MMP2), and inhibition of this lamin-A turnover and also actomyosin contractility are s

156 ticity cause rapid and reversible changes in lamin-A, DNA damage, and cell cycle.

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

158 essing HCV proteins showed downregulation of lamin-A,C and upregulation of beta-actin, corroborating

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

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

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

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

163 repair factors exacerbate these effects, but lamin-A-associated defects are rescued by repair factor

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

165 lpha and the mechanosensitive nuclear marker lamin-A.

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

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

168 sociated with nuclear membrane but devoid of lamin and nuclear pore complexes in Drosophila melanogas

169 te the pathological defects caused by mutant lamins and identify potential therapeutic targets.

170 h the inner nuclear membrane and consists of lamins and lamina-associated proteins.

171 is known about the molecular architecture of lamins and mechanisms of their assembly.

172 We suggest that A-type lamins and SUN2 play antagonistic roles in the modulatio

173 embrane proteins that associate with nuclear lamins and/or chromatin.

174 These aberrations of histone methylation, lamins, and HP1alpha, which regulate heterochromatin str

175 show that acentrics pass through membrane-, lamin-, and nuclear pore-based channels in the nuclear e

176 Lamins are intermediate filaments that line the inner nu

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

178 We provide a quantitative understanding of lamin-associated chromatin organization in a crowded mac

179 Comparison to Lamin-associated domains (LADs) revealed that NPC bindin

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

181 L1s are enriched at lamin-associated domains, heterochromatic regions of the

182 promotes the assembly or maintenance of the lamin-associated LINC complex and this activity is also

183 al polymer model reproduces the formation of lamin-associated-domains and provides an in silico tool

184 y reproduce observed length distributions of lamin-associated-domains.

185 identifies a role of the TRIM43-pericentrin-lamin axis in intrinsic immunity, which may be targeted

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

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

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

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

190 Reduction of lamin-B and other caspase-substrate, such as filamin, in

191 iates nuclear rupture with dilution of stiff lamin-B filaments, loss of repair factors, and entry fro

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

193 4-dehydrocholesterol reductase (DHCR14), and lamin-B receptor (LBR), share evolutionary ties with a h

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

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

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

197 Thus, lamin B1 acts as a tumor suppressor in lung cancer, link

198 Importantly, loss of a single lamin B1 allele induced spontaneous lung tumor formation

199 hat the isolated micronuclei lack functional lamin B1 and become prone to envelope rupture, which lea

200 q) to validate the interaction of ncRNA with lamin B1 and EXOSC2.

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

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

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

204 le in mediating the malignant phenotype upon lamin B1 disruption.

205 Individually, lamin B1 highlights acute leukemias, lamin A/C helps dis

206 However, the level of lamin B1 in ANSPCs declines during aging.

207 Furthermore, the reduction of lamin B1 in ANSPCs recapitulates age-related anxiety-lik

208 Our results indicate that higher levels of lamin B1 in ANSPCs safeguard against premature different

209 Precocious loss of lamin B1 in ANSPCs transiently promotes neurogenesis but

210 nsed nuclei and lower steady-state levels of lamin B1 in proband lymphoblasts.

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

212 We found that lamin B1 levels were reduced in lung cancer patients.

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

214 Deficiencies in either lamin B1 or lamin B2 cause both defective migration of c

215 The presence of functional lamin B1 partly correlates with micronuclei size, sugges

216 Lamin B1 plays an important role in the nuclear envelope

217 Mechanistically, we show that lamin B1 recruits the polycomb repressive complex 2 (PRC

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

219 Lamin B1 silencing in lung epithelial cells promoted epi

220 Our results indicate that the decline in lamin B1 underlies stem cell aging and impacts the homeo

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

222 Here we report that loss of lamin B1, a determinant of nuclear architecture, plays a

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

224 nteracting with the nuclear envelope protein Lamin B1, and heterochromatin-associated proteins, KAP1

225 1 expression, micronuclei formation, reduced Lamin B1, and increased expression of the immune regulat

226 type 1 receptor, endothelin type A receptor, lamin B1, BPI fold-containing family B member 1, peroxis

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

228 how that the age-dependent downregulation of lamin B1, one of the nuclear lamins in adult neural stem

229 n of double-strand breaks (DSBs) by inducing lamin B1-dependent replication fork collapse and inhibit

230 patterns of trans-chromosomal contact beads, Lamin-B1 enriched topologically associating domains (TAD

231 re, we show that the nuclear lamina filament Lamin B2 (Lmnb2), whose expression decreases in mice aft

232 Deficiencies in either lamin B1 or lamin B2 cause both defective migration of cortical neur

233 (2020) show that Lamin B2, a nuclear lamina filament supporting cardiomyo

234 F-10A cells revealed that lamin A/C, but not lamin B2, protects the nuclear membranes against rupture

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

236 ically linked to the LINC complex and A-type lamins, but a full understanding of disease etiology in

237 ng LMNA mutations were modeled in Drosophila Lamin C (LamC) and expressed in indirect flight muscle (

238 We demonstrate that aged lamin C only-expressing mice (Lmna (LCS/LCS) ) become ob

239 r the first time that the sole expression of lamin C protects from glucose intolerance through a beta

240 iabetes, we investigated the contribution of lamin C to beta-cell function in physiopathological cond

241 Lamin C, albeit promoting obesity, increases life span,

242 Lamin A, lamin C, and progerin, products of the Lmna gene, have a

243 Mutations in A-type nuclear lamins cause dilated cardiomyopathy, which is postulated

244 indings highlight the crucial role played by lamin-chromatin and lamin-cytoskeletal alterations in de

245 segment distribution and the strength of the lamin-chromatin attractive interaction.

246 heteropolymer segments, coupled with strong lamin-chromatin interactions, can qualitatively reproduc

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

248 f nuclear lamins, switching from a stem-cell lamin configuration to a differentiated lamin configurat

249 cell lamin configuration to a differentiated lamin configuration.

250 e crucial role played by lamin-chromatin and lamin-cytoskeletal alterations in determining nuclear sh

251 We hypothesize that inhibition of autophagic lamin degradation in mDCs represents a very powerful cel

252 levels of KIF1B and KIF2A in mDCs inhibited lamin degradation, likely by hampering autophagosome-lys

253 uxes of nuclear probes between wild-type and lamin-depleted MCF-10A cells revealed that lamin A/C, bu

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

255 pectrometry to determine interactions within lamin dimers and between dimers in higher-order polymers

256 on acute targeting of Hey or perturbation of lamin expression in ECs in young adults.

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

258 Our results suggest that lamin filaments arrange to form an emergent meshwork who

259 r, structural-mechanical characterization of lamin filaments assembled in situ remains elusive.

260 ly measure the mechanical response of single lamin filaments in three-dimensional meshwork.

261 Endogenous lamin filaments portray non-Hookean behavior - they defo

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

263 (NE) proteins including nesprins, SUN2, and lamins form Linkers of the Nucleoskeleton and Cytoskelet

264 phorylation, are postulated as regulators of lamin function.

265 caused by a null mutation in the single worm lamin homolog.

266 wnregulation of lamin B1, one of the nuclear lamins in adult neural stem/progenitor cells (ANSPCs), u

267 Chromatin regions associated with lamins in animals are characterized mostly by constituti

268 icted migration that disrupts and segregates lamins in situ.

269 findings indicate that the timely removal of lamin is essential for the merging of parental chromosom

270 -a meshwork of intermediate filaments termed lamins-is primarily responsible for the mechanical stabi

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

272 The A-type lamins (lamin A/C), encoded by the LMNA gene, are import

273 Here, we present the connection between the lamin-like protein, CROWDED NUCLEI1 (CRWN1), and the chr

274 kthrough findings providing new insight into lamin-linked mechanisms of mechanotransduction and chrom

275 ic Polo-like kinase PLK-1 phosphorylates the lamin LMN-1 to promote timely lamina disassembly and sub

276 Ce-lamin (lmn-1) knockdown softened the nucleus, whereas ne

277 Further, lamin-mediated interaction can enhance the formation of

278 integrative unified disease model, in which lamin-mediated pathways in mechanotransduction and chrom

279 f PAD4 showed that chromatin decondensation, lamin meshwork and NE rupture and extracellular DNA rele

280 lear envelope (NE) permeabilization, nuclear lamin meshwork and then NE rupture to release DNA into t

281 Graph theory analysis shows that the lamin meshwork is not a random arrangement of filaments

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

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

284 orsinA activity prevents nuclear collapse in lamin mutants by disrupting the function of the LINC com

285 ression of Hey in ECs, suggesting that a Hey-lamin network safeguards nuclear organization and differ

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

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

288 henotype- and mutant-specific alterations in lamin phosphorylation, and that some changes in phosphor

289 al stretch and flexibility properties of the lamin polymer and other intermediate filament networks.

290 In contrast, lamin protein levels remain stable in HSV-1-infected mDC

291 occur independently of predicted changes in lamin protein structure.

292 the interaction of the chromatin fibers with lamin proteins along the nuclear membrane.

293 Lamin proteins are known to be a major factor that influ

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

295 Plants lack lamin proteins but contain a class of coiled-coil protei

296 leads to alterations in the coupling of the lamin shell with cytoskeletal or chromatin tethers as we

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

298 ty, Hey determines the expression of nuclear lamins, switching from a stem-cell lamin configuration t

299 he geometrical organization of the chromatin-lamin tether affects nuclear morphology and shape fluctu

300 In cells with perturbed chromatin or lamins, this increase in heterochromatin suppresses nucl