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Lamin B counteracts the kinesin Eg5 (show KIF11 ELISA Kits) to restrain spindle pole separation during spindle assembly.
We show that epithelial cells failing to undergo proliferation arrest during TGF-beta (show TGFB1 ELISA Kits)-induced EMT (show ITK ELISA Kits) sustain mitotic abnormalities due to failed cytokinesis, resulting in aneuploidy. This genomic instability is associated with the suppression of multiple nuclear envelope proteins implicated in mitotic regulation and is phenocopied by modulating the expression of LaminB1.
The primary response of cells to various stresses leading to senescence consists of the down-regulation of LBR (show LBR ELISA Kits) and LB1 (show CKAP2 ELISA Kits) to attain reversal of the chromatin architecture.
Data show that lamins A and B are differently processed in staurosporine and beta-Amyloid peptide (show APP ELISA Kits) fragments Abeta42-treated cells.
The tail domain of lamin B1 is more strongly modulated by divalent cations than lamin A (show LMNA ELISA Kits).
An upstream mutation alters LMNB1 gene expression in autosomal dominant adult-onset demyelinating leukodystrophy.
Deregulation of LMNB1 expression induces modified splicing of several genes, likely driven by raver-2 overexpression, and suggest that an alteration of mRNA processing could be a pathogenic mechanism in adult-onset autosomal dominant leukodystrophy.
Lamin B1 levels are increased in oligodendrocytes, the cell type that produces myelin in the central nervous system.
Nuclear envelope remodelling during human spermiogenesis involves somatic B-type lamins and a spermatid-specific B3 lamin (show LMNA ELISA Kits) isoform.
LMNB1-related autosomal-dominant leukodystrophy is a slowly progressive neurological disease with survival lasting more than two decades after clinical onset.
Lamin B1 overexpression increases nuclear rigidity in autosomal dominant leukodystrophy fibroblasts.
While the distribution patterns of both lamins closely paralleled the respective stages of mitosis, Nup160 (show NUP160 ELISA Kits) localization in metaphase oocytes corresponded to that in mitotic prometaphase rather than metaphase.
Here we report that in primary mouse cortical neurons, LMNB1 overexpression reduces axonal outgrowth, whereas deficiency of endogenous Lmnb1 results in aberrant dendritic development.
Analysis of lamin B1 expression in different regions of the brain in wild-type animals showed that the level of Lmnb1 transcript decreased significantly in an age-dependent manner.
Lamin-B1 is required for organization of lamin-A/C (show LMNA ELISA Kits) and lamin-B2 (show LMNB2 ELISA Kits) in mouse embryonic stem cells and Lamin-B1 is required for organization of lamin-A/C (show LMNA ELISA Kits) and lamin-B2 (show LMNB2 ELISA Kits) in differentiated cells
farnesylation of lamin B1--but not lamin B2 (show LMNB2 ELISA Kits)--is crucial for brain development and for retaining chromatin within the bounds of the nuclear lamina during neuronal migration.
lamin B1 overexpression mediates oligodendrocyte cell-autonomous neuropathology in adult-onset autosomal-dominant leukodystrophy.
We conclude that lamin B1 is a modifier gene of major effect for Neural tube defects resulting from loss of Grhl3 (show GRHL3 ELISA Kits) function
Lamin B1 is lost from primary human and murine cell strains when they are induced to senesce.
Lamin B1 is essential for brain development and is required for the integrity of the nuclear lamina.
Absence of both Lmnb1 and Lmnb2 (show LMNB2 ELISA Kits) in keratinocytes has no effect on cell proliferation or the development of skin and hair.
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. This gene encodes one of the two B type proteins, B1. Alternative splicing results in transcript variants and a duplication of this gene is associated with autosomal dominant adult-onset leukodystrophy (ADLD).