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Human Lamin A/C Protein expressed in Wheat germ - ABIN1309507
Chen, Lin, Chow, Lee: Proteomic identification of Hsp70 as a new Plk1 substrate in arsenic trioxide-induced mitotically arrested cells. in Proteomics 2011
Show all 2 Pubmed References
The loss of lamin-B (show LMNB1 Proteins) leads to systemic inflammation and aging.
nuclear Wash interacts with B-type Lamin (Lamin Dm0), and, like Lamin, Wash associates with constitutive heterochromatin
of single phosphorylation sites of Drosophila melanogaster lamin Dm and lamin C
Rab5 associated in vivo with nuclear Lamin and mushroom body defect (Mud), the Drosophila counterpart of nuclear mitotic apparatus protein (NuMA).
Kugelkern and lamin Dm0 affect nuclear shape without requiring filament formation or the presence of a classical nuclear lamina.
Lamin mutation is associated with neuromuscular defects and premature aging.
prometaphase spindle can be made robust to natural fluctuations in motor ratios by a disassembling lamin-B (show LMNB1 Proteins) envelope.
Molecular interactions with lamin Dm0 may link JIL-1 kinase to nuclear morphology and integrity of nurse cells during oogenesis.
The lamin Dm0 allele Ari3 acts as an enhancer of position effect variegation of the wm4 allele in Drosophila.
Both lamin Dm0 and C. elegans Ce-lamin bind directly to histone H2A in vitro and this binding requires the nuclear localization signal
results have important implications for understanding the tissue-specific regulation and functions of the lamin A gene
The induction of embryonic senescence and laminopathies in zebrafish harboring disturbed expressions of the lamin A gene, is described.
our findings indicate that altered mTOR (show FRAP1 Proteins) signaling in Lmna(-/-) mice leads to a lipodystrophic phenotype that can be rescued with rapamycin, highlighting the effect of loss of adipose tissue in Lmna(-/-) mice and the consequences of altered mTOR (show FRAP1 Proteins) signaling
results suggest that lamin A plays important roles in maintaining the osteoblast differentiation and function
these findings show that cardiac ERK1/2 activity is modulated in part by TGF-b/Smad (show SMAD1 Proteins) signaling, leading to altered activation of CTGF/CCN2 (show CTGF Proteins) to mediate fibrosis and alter cardiac function. This identifies a novel mechanism in the development of LMNA cardiomyopathy.
Activation of WNT/b-catenin activity improved cardiac contractility and ameliorated intraventricular conduction defects in LmnaH222P/H222P mice, which was associated with increased expression of myocardial connexin 43. These results indicate that decreased WNT/b-catenin contributes to the pathophysiology of LMNA cardiomyopathy and that drugs activating b-catenin may be beneficial in affected individuals
SUMO1 (show SUMO1 Proteins) conjugation of RB and Lamin A/C is modulated by the SUMO protease SENP1 (show SENP1 Proteins) and that sumoylation of both proteins is required for their interaction.
Lmna-deficient cells show a compromised strain avoidance response, which is completely abolished when topographical cues and uniaxial strain are applied along the same direction.
While the distribution patterns of both lamins closely paralleled the respective stages of mitosis, Nup160 (show NUP160 Proteins) localization in metaphase oocytes corresponded to that in mitotic prometaphase rather than metaphase.
changes in nuclear size and shape, which are mediated by nuclear envelope structural proteins lamin A/C and/or emerin (show EMD Proteins), also impact gene regulation and lineage differentiation in early embryos.
administration of the exon 11 ASO reduced lamin A expression in wild-type mice and progerin expression in an HGPS mouse model.
stabilization of perinuclear actin strengthens the transient interactions of lamin A with chromatin
Standard Sanger sequencing of LMNA exon 11 DNA from blood-derived WBCs and cultured skin fibroblasts sequenced at passages 1, 3 and 8 detected differing progerin-producing mutations in the same nucleotide of the exon 11 intronic splice donor site (see online supplementary figure.
the CNOT1-LMNA-Hedgehog (show SHH Proteins) signaling pathway axis exerts an oncogenic role in osteosarcoma progression, which could be a potential target for gene therapy.
Pathogenic variants in the LMNA gene responsible for nearly 10%-15%% of Familial Dilated Cardiomyopathy cases.
low lamin A but not lamin C expression in pleural metastatic cells could represent a major actor in the development of metastasis, associated with epithelial to mesenchymal transition and could account for a pejorative factor correlated with a poor Performance status.
LmnA binds AIMP3 (show EEF1E1 Proteins) via its extreme C-terminus. Together these findings provide a structural insight for understanding the interaction between AIMP3 (show EEF1E1 Proteins) and LmnA in AIMP3 (show EEF1E1 Proteins) degradation.
The R482W mutation results in a loss of function of differentiation-dependent lamin A binding to the MIR335 locus and epigenetic regulation of adipogenesis.
Pathogenic variants of the LMNA gene were determined in nine families with familial partial lipodystrophy
The interaction of progerin with lamin A/C contributes to the development of the senescence phenotype of Hutchinson-Gilford progeria syndrome and aged cells.
we expressed a LEMD2 transgene alone or in combination with lamin C in these cells and observed no restoration of peripheral heterochromatin in either case. We conclude that in contrary to the B-tether, the A-tether has a more intricate composition and consists of multiple components that presumably vary, at differing degrees of redundancy, between cell types and differentiation stages
These abnormalities are associated with increased transforming growth factor-b (show ATP5S Proteins) signaling and defects in matrix metalloproteinase 9 (show MMP9 Proteins) activity. Our data demonstrate that lamin A/C gene mutations responsible for FPLD2 and related lipodystrophies are associated with transforming growth factor-beta activation
Both anti-lamin A/C and anti-lamin B (show LMNB1 Proteins) staining were clearly present in all embryonic stages.
A study mapping the location of procine lamin type A to chromosome 4q is presented.
These results indicate that thyroid hormone (show PTH Proteins)-regulated expression of nuclear lamin A and LIII closely correlates with dedifferentiation of the epithelial cells in the X. laevis intestine.
LIII filaments appear identical to the endogenous lamina, whereas lamin B2 (show LMNB2 Proteins) assembles into filaments that are organized less precisely; Lamin A induces sheets of thicker filaments on the endogenous lamina and increases the rigidity of the nuclear envelope
The nuclear lamina consists of a two-dimensional matrix of proteins located next to the inner nuclear membrane. The lamin family of proteins make up the matrix and are highly conserved in evolution. During mitosis, the lamina matrix is reversibly disassembled as the lamin proteins are phosphorylated. Lamin proteins are thought to be involved in nuclear stability, chromatin structure and gene expression. Vertebrate lamins consist of two types, A and B. Alternative splicing results in multiple transcript variants. Mutations in this gene lead to several diseases: Emery-Dreifuss muscular dystrophy, familial partial lipodystrophy, limb girdle muscular dystrophy, dilated cardiomyopathy, Charcot-Marie-Tooth disease, and Hutchinson-Gilford progeria syndrome.
, intermediate filament-like lamina
, lamin A
, lamin B
, lamin D
, lamin D[]
, lamin D[[m]]0
, lamin D[[o]]
, lamin Dm0
, lamin Dm[]
, lamin Dmo
, nuclear lamin
, lamin B3
, lamin A/C
, lamin LIII
, lamin C
, 70 kDa lamin
, lamin A/C-like 1
, renal carcinoma antigen NY-REN-32
, lamin C2