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Human Lamin B1 Protein expressed in Human - 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 (show KIF11 Proteins) to restrain spindle pole separation during spindle assembly.
Data show that lamins A and B are differently processed in staurosporine and beta-Amyloid peptide (show APP Proteins) fragments Abeta42-treated cells.
The tail domain of lamin B1 is more strongly modulated by divalent cations than lamin A (show LMNA Proteins).
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 Proteins) 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.
Data indicate that lamin B1 promotes DNA double-strand breaks (DSBs) repair and cell survival.
maintenance of lamin B1 levels is required for DNA replication and repair through regulation of the expression of key factors involved in these essential nuclear functions
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 Proteins) and lamin-B2 (show LMNB2 Proteins) in mouse embryonic stem cells and Lamin-B1 is required for organization of lamin-A/C (show LMNA Proteins) and lamin-B2 (show LMNB2 Proteins) in differentiated cells
farnesylation of lamin B1--but not lamin B2 (show LMNB2 Proteins)--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 Proteins) 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 Proteins) in keratinocytes has no effect on cell proliferation or the development of skin and hair.
lamin B1 mutant mice provide evidence for a broad and nonredundant function of lamin B1 in mammalian development.
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).