Lamin-B1 is a protein that in humans is encoded by the LMNB1 gene.[5][6][7]
LMNB1 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Aliases | LMNB1, ADLD, LMN, LMN2, LMNB, lamin B1, MCPH26 | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 150340 MGI: 96795 HomoloGene: 55912 GeneCards: LMNB1 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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Wikidata | |||||||||||||||||||||||||||||||||||||||||||||||||||
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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.[7] Lamin B, along with heterochromatin, is anchored to the inner surface of the nuclear membrane by the lamin B receptor.
LMNB1 has been shown to interact with Thymopoietin.[8][9] When double-strand breaks are induced in DNA by ionizing radiation, lamin B1 promotes repair of the breaks, as well as cell survival, by maintaining the level of the RAD51 protein that is employed in homologous recombinational repair.[10]
Mutations affecting the LMNB1 gene cause autosomal dominant adult-onset demyelinating leukodystrophy.