1. Age-Associated Loss of Lamin-B Leads to Systemic Inflammation and Gut Hyperplasia

    Cell 159(4):829 (2014)

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoe...
  2. Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.

    Cell 159(4):829 (2014) PMID 25417159 PMCID PMC4243052

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoes immunose...
  3. Age-Associated Loss of Lamin-B Leads to Systemic Inflammation and Gut Hyperplasia

    Cell 159(4):829 (2014)

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoe...
  4. Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.

    Cell 159(4):829 (2014) PMID 25417159 PMCID PMC4243052

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoes immunose...
  5. Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.

    Cell 159(4):829 (2014) PMID 25417159 PMCID PMC4243052

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoes immunose...
  6. Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.

    Cell 159(4):829 (2014) PMID 25417159 PMCID PMC4243052

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoes immunose...
  7. Age-Associated Loss of Lamin-B Leads to Systemic Inflammation and Gut Hyperplasia

    Cell 159(4):829 (2014)

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoe...
  8. Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.

    Cell 159(4):829 (2014) PMID 25417159 PMCID PMC4243052

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoes immunose...
  9. Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.

    Cell 159(4):829 (2014) PMID 25417159 PMCID PMC4243052

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoes immunose...
  10. Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia.

    Cell 159(4):829 (2014) PMID 25417159 PMCID PMC4243052

    Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unclear. We report that the Drosophila fat body, a major immune organ, undergoes immunose...
  11. A computational model for the formation of lamin-B mitotic spindle envelope and matrix.

    Interface Focus 4(3):20130063 (2014) PMID 24904732 PMCID PMC3996581

    Recent reports show that, after nuclear envelope breakdown, lamin-B, a component of the nuclear lamina in interphase, localizes around the mitotic spindle as a membranous network. How this process occurs, however, and how it influences mitotic spindle morphogenesis is unclear. Here, we develop a...
  12. Concentration-dependent lamin assembly and its roles in the localization of other nuclear proteins.

    Molecular Biology of the Cell 25(8):1287 (2014) PMID 24523288 PMCID PMC3982994

    The nuclear lamina (NL) consists of lamin polymers and proteins that bind to the polymers. Disruption of NL proteins such as lamin and emerin leads to developmental defects and human diseases. However, the expression of multiple lamins, including lamin-A/C, lamin-B1, and lamin-B2, in mammals has...
  13. Concentration-dependent lamin assembly and its roles in the localization of other nuclear proteins.

    Molecular Biology of the Cell 25(8):1287 (2014) PMID 24523288 PMCID PMC3982994

    The nuclear lamina (NL) consists of lamin polymers and proteins that bind to the polymers. Disruption of NL proteins such as lamin and emerin leads to developmental defects and human diseases. However, the expression of multiple lamins, including lamin-A/C, lamin-B1, and lamin-B2, in mammals has...
  14. Borg5 is required for angiogenesis by regulating persistent directional migration of the cardiac microvascular endothelial cells.

    Molecular Biology of the Cell 25(6):841 (2014) PMID 24451259 PMCID PMC3952853

    The microvasculature is important for vertebrate organ development and homeostasis. However, the molecular mechanism of microvascular angiogenesis remains incompletely understood. Through studying Borg5 (Binder of the Rho GTPase 5), which belongs to a family of poorly understood effector protein...
  15. A microtubule-associated zinc finger protein, BuGZ, regulates mitotic chromosome alignment by ensuring Bub3 stability and kinetochore targeting.

    Developmental Cell 28(3):268 (2014) PMID 24462186 PMCID PMC3927447

    Equal chromosome segregation requires proper assembly of many proteins, including Bub3, onto kinetochores to promote kinetochore-microtubule interactions. By screening for mitotic regulators in the spindle envelope and matrix (Spemix), we identify a conserved Bub3 interacting and GLE-2-binding s...
  16. A microtubule-associated zinc finger protein, BuGZ, regulates mitotic chromosome alignment by ensuring Bub3 stability and kinetochore targeting.

    Developmental Cell 28(3):268 (2014) PMID 24462186 PMCID PMC3927447

    Equal chromosome segregation requires proper assembly of many proteins, including Bub3, onto kinetochores to promote kinetochore-microtubule interactions. By screening for mitotic regulators in the spindle envelope and matrix (Spemix), we identify a conserved Bub3 interacting and GLE-2-binding s...
  17. A microtubule-associated zinc finger protein, BuGZ, regulates mitotic chromosome alignment by ensuring Bub3 stability and kinetochore targeting.

    Developmental Cell 28(3):268 (2014) PMID 24462186 PMCID PMC3927447

    Equal chromosome segregation requires proper assembly of many proteins, including Bub3, onto kinetochores to promote kinetochore-microtubule interactions. By screening for mitotic regulators in the spindle envelope and matrix (Spemix), we identify a conserved Bub3 interacting and GLE-2-binding s...
  18. A microtubule-associated zinc finger protein, BuGZ, regulates mitotic chromosome alignment by ensuring Bub3 stability and kinetochore targeting.

    Developmental Cell 28(3):268 (2014) PMID 24462186 PMCID PMC3927447

    Equal chromosome segregation requires proper assembly of many proteins, including Bub3, onto kinetochores to promote kinetochore-microtubule interactions. By screening for mitotic regulators in the spindle envelope and matrix (Spemix), we identify a conserved Bub3 interacting and GLE-2-binding s...
  19. A microtubule-associated zinc finger protein, BuGZ, regulates mitotic chromosome alignment by ensuring Bub3 stability and kinetochore targeting.

    Developmental Cell 28(3):268 (2014) PMID 24462186 PMCID PMC3927447

    Equal chromosome segregation requires proper assembly of many proteins, including Bub3, onto kinetochores to promote kinetochore-microtubule interactions. By screening for mitotic regulators in the spindle envelope and matrix (Spemix), we identify a conserved Bub3 interacting and GLE-2-binding s...
  20. A microtubule-associated zinc finger protein, BuGZ, regulates mitotic chromosome alignment by ensuring Bub3 stability and kinetochore targeting.

    Developmental Cell 28(3):268 (2014) PMID 24462186 PMCID PMC3927447

    Equal chromosome segregation requires proper assembly of many proteins, including Bub3, onto kinetochores to promote kinetochore-microtubule interactions. By screening for mitotic regulators in the spindle envelope and matrix (Spemix), we identify a conserved Bub3 interacting and GLE-2-binding s...