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Study found TMPO is significantly upregulated in glioblastoma tissues.TMPO knockdown promoted cell apoptosis by upregulation of the cleavage of caspase-3 and PARP protein levels.
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Results suggest that TMPObeta and -gamma isoforms could provide a potential reliable diagnostic marker for breast cancer.
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The findings unveil a unique mechanism where the nuclear periphery proteins lamin-A/C, LAP2alpha and BAF1 are assembled into a protein complex during mitosis in order to regulate assembly and positioning of the mitotic spindle.
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The authors find that LAP2alpha (lamina-associated polypeptide-alpha) interacts with lamin A, while its interaction with progerin is significantly reduced.
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LAP2alpha can regulate extracellular matrix components independently of lamins A/C, which may help explain the proliferation-promoting function of LAP2alpha in cells expressing progerin.
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Results highlight the interactions at the nuclear envelope where mutations in the EMD and TMPO gene in combination with mutations in SUN1 have an impact on several components of the network.
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Data indicate that cells lacking either high mobility group protein N5 (HMGN5) and lamina-associated polypeptide 2alpha (LAP2alpha) showed that loss of either protein affects the genome-wide distribution of the remaining partner.
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this study provides evidence for elevated LAP2alpha expression in cervical cancer and suggests that E2F and p53 activities associate with the positive and negative regulation of LAP2alpha expression, respectively
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data suggest that hypophosphorylated Rb is anchored in the nucleus by the interaction of pocket C with LAP2alpha-lamin A/C complexes
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Results indicate that in vitro, the interaction between HA95 and LAP2beta is influenced by a PKA-mediated phosphorylation of HA95 rather than by CDK1- or PKC-mediated phosphorylation of LAP2beta
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LAP2alpha and BAF transiently localize to telomeres and specific regions on chromatin during nuclear assembly
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A predicted Arg690Cys substitution within the LAP2 gene is implicated in the pathogenesis of genetic forms of dilated cardiomyopathy.
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The effects of LAP2alpha on cell cycle progression and differentiation may be highly relevant for the cell- and tissue-specific phenotypes observed in laminopathic diseases.
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In agreement with its regulation by E2F, LAP2alpha over expression in primary tumors was found to be correlated with tumor proliferation rate
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LAP2alpha forms higher order structures containing multiple LAP2alpha molecules in vivo and that complex formation is mediated by the C terminus.
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Results suggest that LAP2alpha and lamin A/C are involved in controlling retinoblastoma protein localization and phosphorylation, and a lack or mislocalization of either protein leads to cell cycle arrest in fibroblasts.
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Lamina associated protein 2Beta (LAP2beta) is expressed in acute hematopoietic malignant cells, but not in chronic hematopoietic malignant cells.
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Co-expression of LAP2beta and LAP2zeta results in inhibition of LAP2beta-induced gene silencing while overexpression of LAP2zeta alone leads to a small increase in transcriptional activity of various transcription factors.
