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Human Lamin B1 Protein expressed in HEK-293 Cells - ABIN2724477
Baghirova, Hughes, Poirier, Kondo, Schulz: Nuclear matrix metalloproteinase-2 in the cardiomyocyte and the ischemic-reperfused heart. in Journal of molecular and cellular cardiology 2016
Lamin B counteracts the kinesin Eg5 (zeige KIF11 Proteine) to restrain spindle pole separation during spindle assembly.
down-regulation of Lamin B1 and up-regulation of Nephroblastoma overexpressed (NOV (zeige NOV Proteine)) are at least partially responsible for the inhibitory effect of Huaier on the proliferative and invasive capacity of SKHEP-1 cells
The aim of the present study was to elucidate the influence of LMNB1 upregulation on colon cancer cell line after treatment with 5-FU. The results indicate, that overexpression of LMNB1 induced dose-dependent cell death mainly by mitotic catastrophe pathway.
In this report we show that increased self-association propensity of mutant LA modulates the LA-LB1 (zeige CKAP2 Proteine) interaction and precludes the formation of an otherwise uniform laminar network. Our results might highlight the role of homotypic and heterotypic interactions of LA in the pathogenesis of DCM and hence laminopathies in the broader sense.
These results suggest that the nuclear lamins and progerin have marginal roles in the activation of the antioxidant Nrf2 (zeige GABPA Proteine) response to arsenic and cadmium.
We show that epithelial cells failing to undergo proliferation arrest during TGF-beta (zeige TGFB1 Proteine)-induced EMT (zeige ITK Proteine) 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 (zeige LBR Proteine) and LB1 (zeige CKAP2 Proteine) to attain reversal of the chromatin architecture.
Data show that lamins A and B are differently processed in staurosporine and beta-Amyloid peptide (zeige APP Proteine) fragments Abeta42-treated cells.
The tail domain of lamin B1 is more strongly modulated by divalent cations than lamin A (zeige LMNA Proteine).
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.
The parts of chromatin interact with nuclear lamina proteins like Lamin B1 and, therefore, can be identified in a given cell type by chromatin profiling of these proteins.
While the distribution patterns of both lamins closely paralleled the respective stages of mitosis, Nup160 (zeige NUP160 Proteine) 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 (zeige LMNA Proteine) and lamin-B2 (zeige LMNB2 Proteine) in mouse embryonic stem cells and Lamin-B1 is required for organization of lamin-A/C (zeige LMNA Proteine) and lamin-B2 (zeige LMNB2 Proteine) in differentiated cells
farnesylation of lamin B1--but not lamin B2 (zeige LMNB2 Proteine)--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 (zeige GRHL3 Proteine) 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.
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).