The Gene for a Novel Human Lamin Maps at a Highly Transcribed Locus of Chromosome 19 which Replicates at the Onset of S-Phase

Biamonti, Giuseppe; Giacca, Mauro; Perini, Giovanni; Contreas, Giovanna; Zentilin, Lorena; Weighardt, Florian; Guerra, Maribel; Valle, Giuliano Della; Saccone, Salvatore; Riva, Silvano; Falaschi, Arturo

doi:10.1128/mcb.12.8.3499-3506.1992

Cited by 13 publications

(8 citation statements)

References 32 publications

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“…1 A ). LA and LC are derived from the LMNA gene by alternative splicing ( Lin and Worman, 1993 ), whereas LB1 and LB2 are encoded by LMNB1 and LMNB2 , respectively ( Biamonti et al, 1992 ; Höger et al, 1990 ; Lin and Worman, 1995 ; Maeno et al, 1995 ). In recent years, the detailed structure of the NL has been revealed by three-dimensional structured illumination microscopy (3D-SIM) combined with computer vision analysis and cryo-electron tomography (cryo-ET; Shimi et al, 2015 ; Turgay et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Nucleoplasmic lamin C rapidly accumulates at sites of nuclear envelope rupture with BAF and cGAS

Kono

Adam

Sato

et al. 2022

Journal of Cell Biology

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In mammalian cell nuclei, the nuclear lamina (NL) underlies the nuclear envelope (NE) to maintain nuclear structure. The nuclear lamins, the major structural components of the NL, are involved in the protection against NE rupture induced by mechanical stress. However, the specific role of the lamins in repair of NE ruptures has not been fully determined. Our analyses using immunofluorescence and live-cell imaging revealed that the nucleoplasmic pool of lamin C rapidly accumulated at sites of NE rupture induced by laser microirradiation in mouse embryonic fibroblasts. The accumulation of lamin C at the rupture sites required both the immunoglobulin-like fold domain that binds to barrier-to-autointegration factor (BAF) and a nuclear localization signal. The accumulation of nuclear BAF and cytoplasmic cyclic GMP-AMP synthase (cGAS) at the rupture sites was in part dependent on lamin A/C. These results suggest that nucleoplasmic lamin C, BAF, and cGAS concertedly accumulate at sites of NE rupture for rapid repair.

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Section: Introductionmentioning

confidence: 99%

Nucleoplasmic lamin C rapidly accumulates at sites of nuclear envelope rupture with BAF and cGAS

Kono

Adam

Sato

et al. 2022

Journal of Cell Biology

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“…The somatic cell A-type lamins, lamin A, lamin C, and lamin Adelta10, are alternative splice isoforms encoded by the LMNA gene ( , ). Two different genes encode the somatic cell B-type lamins, lamin B1 and lamin B2 ( , ). While B-type lamins are expressed in most cell types, A-type lamin expression is developmentally regulated ().…”

mentioning

confidence: 99%

“…The somatic cell A-type lamins, lamin A, lamin C, and lamin Adelta10, are alternative splice isoforms encoded by the LMNA gene (26,27). Two different genes encode the somatic cell B-type lamins, lamin B1 and lamin B2 (28,29) B-type lamins are expressed in most cell types, A-type lamin expression is developmentally regulated (30). Because the lamina is a discontinuous structure (31), the inner nuclear membrane proteins may also be able to directly associate with the chromatin at certain points.…”

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confidence: 99%

Dependence of Diffusional Mobility of Integral Inner Nuclear Membrane Proteins on A-Type Lamins

et al. 2006

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Integral proteins of the nuclear envelope inner membrane have been proposed to reach their sites by diffusion after their co-translational insertion in the rough endoplasmic reticulum. They are then retained in the inner nuclear membrane by binding to nuclear structures. One such structure is the nuclear lamina, an intermediate filament meshwork composed of A-type and B-type lamin proteins. Emerin, MAN1, and LBR are three integral inner nuclear membrane proteins. We expressed these proteins fused to green fluorescent protein in embryonic fibroblasts from wild-type mice and Lmna -/- mice, which lack A-type lamins. We then studied the diffusional mobilities of emerin, MAN1, and LBR using fluorescence recovery after photobleaching. We show that emerin and MAN1, but not LBR, are more mobile in the inner nuclear membrane of cells from Lmna -/- mice than in cells from wild-type mice. In cells from Lmna -/- mice expressing exogenous lamin A, the protein mobilities were similar to those in cells from wild-type mice. This supports a model where emerin and MAN1 are at least partly retained in the inner nuclear membrane by binding to A-type lamins, while LBR depends on other binding partners for its retention.

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“…We also analyzed whether these genes were significantly associated with the patients’ prognosis. Among several targets, the human LMNB2 gene, which locates in chromosome 19p13.3 [ 40 ] and encodes a 68-kDa protein, was a potential target for KLF16 in lung cancer development. The main function of LMNB2 is to maintain the nuclear skeleton integrity, which is involved in cell proliferation and aging, gene expression, and DNA damage repair by affecting the distribution of the chromosomes [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

Kruppel like factor 16 promotes lung adenocarcinoma progression by upregulating lamin B2

Jiao

Gao

Ren³

et al. 2022

Bioengineered

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Lung cancer is one of the most common causes of cancer-related death. In the past decade, the treatment and diagnosis of lung cancer have progressed significantly in early efforts to promote the survival of lung cancer patients. Kruppel like factor 16 (KLF16) is a zinc finger transcription factor that regulates a diverse array of developmental events and cellular processes. KLF16 is involved in the progression of various cancer types. However, the role of KLF16 in the development of lung cancer remains unknown. In this study, KLF16 was overexpressed in lung cancer samples. KLF16 downregulation inhibited lung cancer cell proliferation and migration. Conversely, KLF16 overexpression promoted lung cancer cell growth and invasion. Mechanistically, the expression level LMNB2 was suppressed by KLF16 knockdown and was promoted by KLF16 overexpression. The overall survival of patients with high LMNB2 levels was poor. Luciferase assays showed that KLF16 promoted the transcription activity of LMNB2 gene. Concomitantly, the expression level of LMNB2 was also higher in lung adenocarcinoma (LUAD) than in normal tissues, and its knockdown or overexpression can reverse the effect of KLF16 overexpression or knockdown on lung cancer cell proliferation, migration, and even tumorigenesis, indicating that LMNB2 also functions as an oncogene. In conclusion, KLF16 can be used as a potential therapeutic and preventive biomarker in lung cancer treatment and prognosis by actively regulating the expression of LMNB2.

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The Gene for a Novel Human Lamin Maps at a Highly Transcribed Locus of Chromosome 19 which Replicates at the Onset of S-Phase

Cited by 13 publications

References 32 publications

Nucleoplasmic lamin C rapidly accumulates at sites of nuclear envelope rupture with BAF and cGAS

Nucleoplasmic lamin C rapidly accumulates at sites of nuclear envelope rupture with BAF and cGAS

Dependence of Diffusional Mobility of Integral Inner Nuclear Membrane Proteins on A-Type Lamins

Kruppel like factor 16 promotes lung adenocarcinoma progression by upregulating lamin B2

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