Colin L Stewart

Summary

Affiliation: National Cancer Institute
Country: USA

Publications

  1. pmc Mouse models of the laminopathies
    Colin L Stewart
    Laboratory of Cancer and Developmental Biology, National Cancer Institute, Frederick, Maryland 21702, USA
    Exp Cell Res 313:2144-56. 2007
  2. pmc Profiling gene expression in growth-arrested mouse embryos in diapause
    Eiichi Hondo
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Division of Basic Science, National Cancer Institute at Frederick, Frederick, MD 21702, USA
    Genome Biol 6:202. 2005
  3. pmc Functional coupling between the extracellular matrix and nuclear lamina by Wnt signaling in progeria
    Lidia Hernandez
    Cancer and Developmental Biology Laboratory, NCI, Frederick, MD 21702, USA
    Dev Cell 19:413-25. 2010
  4. ncbi request reprint Lsh controls silencing of the imprinted Cdkn1c gene
    Tao Fan
    Laboratory of Molecular Immunoregulation, Basic Research Program, SAIC Frederick, National Cancer Institute, Frederick, MD 21702 1201, USA
    Development 132:635-44. 2005
  5. pmc The LEM domain proteins emerin and LAP2alpha are dispensable for human immunodeficiency virus type 1 and murine leukemia virus infections
    Alok Mulky
    HIV Drug Resistance Program, National Cancer Institute at Frederick, Frederick, MD 21702 1201, USA
    J Virol 82:5860-8. 2008
  6. ncbi request reprint Generation of a conditional Ppap2b/Lpp3 null allele
    Diana Escalante-Alcalde
    Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, USA
    Genesis 45:465-9. 2007
  7. ncbi request reprint Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice
    Leslie C Mounkes
    National Cancer Institute, Cancer and Developmental Biology Laboratory, Frederick, PO Box B, Building 539, Room 121A, MD 21702, USA
    Hum Mol Genet 14:2167-80. 2005
  8. ncbi request reprint The imprinted gene Magel2 regulates normal circadian output
    Serguei V Kozlov
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, Maryland 21702, USA
    Nat Genet 39:1266-72. 2007
  9. ncbi request reprint Cochlin, a secreted von Willebrand factor type a domain-containing factor, is regulated by leukemia inhibitory factor in the uterus at the time of embryo implantation
    Clara I Rodriguez
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Division of Basic Science, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA
    Endocrinology 145:1410-8. 2004
  10. pmc Paternal and maternal genomes confer opposite effects on proliferation, cell-cycle length, senescence, and tumor formation
    Lidia Hernandez
    Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA
    Proc Natl Acad Sci U S A 100:13344-9. 2003

Collaborators

Detail Information

Publications57

  1. pmc Mouse models of the laminopathies
    Colin L Stewart
    Laboratory of Cancer and Developmental Biology, National Cancer Institute, Frederick, Maryland 21702, USA
    Exp Cell Res 313:2144-56. 2007
    ..These mouse lines are providing insights into the functions of the lamina and how changes to the lamina affect the mechanical integrity of the nucleus as well as signaling pathways that, when disrupted, may contribute to the disease...
  2. pmc Profiling gene expression in growth-arrested mouse embryos in diapause
    Eiichi Hondo
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Division of Basic Science, National Cancer Institute at Frederick, Frederick, MD 21702, USA
    Genome Biol 6:202. 2005
    ..A recent report has identified changes in embryonic gene expression that are associated with, and may halt, embryonic cell proliferation...
  3. pmc Functional coupling between the extracellular matrix and nuclear lamina by Wnt signaling in progeria
    Lidia Hernandez
    Cancer and Developmental Biology Laboratory, NCI, Frederick, MD 21702, USA
    Dev Cell 19:413-25. 2010
    ..These results establish a functional link between the nuclear envelope/lamina and the cell surface/ECM and may provide insights into the role of Wnt signaling and the ECM in aging...
  4. ncbi request reprint Lsh controls silencing of the imprinted Cdkn1c gene
    Tao Fan
    Laboratory of Molecular Immunoregulation, Basic Research Program, SAIC Frederick, National Cancer Institute, Frederick, MD 21702 1201, USA
    Development 132:635-44. 2005
    ..Furthermore, it suggests that Lsh is not required for maintenance of imprinting marks in general, but is only crucial for imprinting at distinct genomic sites...
  5. pmc The LEM domain proteins emerin and LAP2alpha are dispensable for human immunodeficiency virus type 1 and murine leukemia virus infections
    Alok Mulky
    HIV Drug Resistance Program, National Cancer Institute at Frederick, Frederick, MD 21702 1201, USA
    J Virol 82:5860-8. 2008
    ..Notably, both viruses efficiently infected human cells expressing high levels of dominant-negative emerin. We thus conclude that emerin and LAP2alpha are not required for the early replication of HIV-1 and MLV in mouse or human cells...
  6. ncbi request reprint Generation of a conditional Ppap2b/Lpp3 null allele
    Diana Escalante-Alcalde
    Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, USA
    Genesis 45:465-9. 2007
    ..A generalized Cre-mediated recombination of this allele yielded a phenotype fundamentally identical to our previously reported Ppap2b null allele...
  7. ncbi request reprint Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice
    Leslie C Mounkes
    National Cancer Institute, Cancer and Developmental Biology Laboratory, Frederick, PO Box B, Building 539, Room 121A, MD 21702, USA
    Hum Mol Genet 14:2167-80. 2005
    ....
  8. ncbi request reprint The imprinted gene Magel2 regulates normal circadian output
    Serguei V Kozlov
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, Maryland 21702, USA
    Nat Genet 39:1266-72. 2007
    ....
  9. ncbi request reprint Cochlin, a secreted von Willebrand factor type a domain-containing factor, is regulated by leukemia inhibitory factor in the uterus at the time of embryo implantation
    Clara I Rodriguez
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Division of Basic Science, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA
    Endocrinology 145:1410-8. 2004
    ..Although loss of Coch expression is not essential to reproduction in mice, it may serve as a useful marker for assessing the state of uterine receptivity in response to LIF at the onset of implantation...
  10. pmc Paternal and maternal genomes confer opposite effects on proliferation, cell-cycle length, senescence, and tumor formation
    Lidia Hernandez
    Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA
    Proc Natl Acad Sci U S A 100:13344-9. 2003
    ..They also suggest that the derivation of stem cells from parthenogenetic embryos, for the purposes of therapeutic cloning, may be ineffective...
  11. pmc Lamin A/C-mediated neuromuscular junction defects in Emery-Dreifuss muscular dystrophy
    Alexandre Mejat
    National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Cell Biol 184:31-44. 2009
    ..These results suggest that lamin A/C-mediated NMJ defects contribute to the AD-EDMD disease phenotype and provide insights into the cellular and molecular mechanisms for the muscle-specific phenotype of AD-EDMD...
  12. ncbi request reprint A progeroid syndrome in mice is caused by defects in A-type lamins
    Leslie C Mounkes
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, Maryland 21702, USA
    Nature 423:298-301. 2003
    ..Here we present a mouse model for progeria that may elucidate mechanisms of ageing and development in certain tissue types, especially those developing from the mesenchymal cell lineage...
  13. ncbi request reprint The nuclear envelope protein MAN1 regulates TGFbeta signaling and vasculogenesis in the embryonic yolk sac
    Tatiana V Cohen
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick MD 21702, USA
    Development 134:1385-95. 2007
    ....
  14. pmc The lamin B receptor under transcriptional control of C/EBPepsilon is required for morphological but not functional maturation of neutrophils
    Tatiana V Cohen
    Cancer and Developmental Biology Laboratory, CCR, Frederick, MD 21702, USA
    Hum Mol Genet 17:2921-33. 2008
    ..Our findings indicate that the Lbr(GT/GT) mice are a model for Pelger-Huët anomaly and that Lbr, under transcriptional regulation of C/EBPepsilon, is necessary for morphological but not necessarily functional granulocyte maturation...
  15. ncbi request reprint Mutations in the mouse Lmna gene causing progeria, muscular dystrophy and cardiomyopathy
    Serguei Kozlov
    Cancer and Developmental Biology Laboratory, CCR, NCI at Frederick, P O Box B, Frederick, Maryland 21702, USA
    Novartis Found Symp 264:246-58; discussion 258-63. 2005
    ....
  16. ncbi request reprint Structural organization and functions of the nucleus in development, aging, and disease
    Leslie Mounkes
    Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA
    Curr Top Dev Biol 61:191-228. 2004
  17. ncbi request reprint Aging and nuclear organization: lamins and progeria
    Leslie C Mounkes
    Cancer and Developmental Biology Laboratory, National Cancer Institute at Frederick, National Institutes of Health, PO Box B, Frederick, Maryland 21702, USA
    Curr Opin Cell Biol 16:322-7. 2004
    ..Aspects of the diseases associated with disrupted nuclear envelope/lamin functions may be explained by decreased cellular proliferation, loss of tissue repair capability and a decline in the ability to maintain a differentiated state...
  18. ncbi request reprint Intraspecific mating with CzechII/Ei mice rescue lethality associated with loss of function mutations of the imprinted genes, Igf2r and Cdkn1c
    John P Hagan
    Cancer and Developmental Biology Laboratory, Center for Cancer Research, NCI FCRDC, National Institutes of Health, P O Box B, Frederick, MD 21702, USA
    Genomics 84:836-43. 2004
    ..These polymorphisms may prove useful in determining the effects of different mutant backgrounds on genomic imprinting...
  19. ncbi request reprint The lipid phosphatase LPP3 regulates extra-embryonic vasculogenesis and axis patterning
    Diana Escalante-Alcalde
    Cancer and Developmental Biology Laboratory, Division of Basic Science, National Cancer Institute, Frederick, MD 21702, USA
    Development 130:4623-37. 2003
    ..The exact biochemical roles of LPP3 phosphatase activity and its undefined effect on beta-catenin-mediated TCF transcription remain to be determined...
  20. ncbi request reprint A novel cell-based system for the rapid quantitative evaluation of (anti)-inflammatory potential of test substances
    Serguei V Kozlov
    Cancer and Developmental Biology Laboratory, National Cancer Institute, P O Box B, Building 539, Frederick, MD 21702, USA
    J Immunol Methods 281:51-63. 2003
    ..In addition, the dual selection capability of the model provides a powerful tool to discover novel molecular components of the NF-kappaB signal transduction pathway...
  21. ncbi request reprint Endogenous leukemia inhibitory factor attenuates endotoxin response
    Marietta A Weber
    Cancer and Developmental Biology Laboratory, NCI FCRDC, Frederick, MD, USA
    Lab Invest 85:276-84. 2005
    ....
  22. ncbi request reprint Disruption of the ubiquitin ligase HERC4 causes defects in spermatozoon maturation and impaired fertility
    Clara I Rodriguez
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Division of Basic Science, National Cancer Institute at Frederick, Frederick, MD 21702, USA
    Dev Biol 312:501-8. 2007
    ..Our results show that Herc4 ligase is required for proper maturation and removal of the cytoplasmic droplet for the spermatozoon to become fully functional...
  23. pmc Structure of the lamin A/C R482W mutant responsible for dominant familial partial lipodystrophy (FPLD)
    Eugenia Magracheva
    Basic Research Program SAIC Frederick, NCI Frederick, Frederick, MD 21702, USA
    Acta Crystallogr Sect F Struct Biol Cryst Commun 65:665-70. 2009
    ..5 A resolution. A completely novel aggregation state of the C-terminal globular domain and the position of the mutated amino-acid residue suggest means by which the mutation may affect lamin A/C-protein and protein-DNA interactions...
  24. ncbi request reprint Control of uterine receptivity and embryo implantation by steroid hormone regulation of LIF production and LIF receptor activity: towards a molecular understanding of "the window of implantation"
    Jr Gang Cheng
    Cancer and Developmental Biology Laboratory, National Cancer Institute, Division of Basic Science, National Cancer Institute Frederick Cancer Research and Development Center, Frederick, MD 21702, USA
    Rev Endocr Metab Disord 3:119-26. 2002
  25. ncbi request reprint Loss of cyclooxygenase-2 retards decidual growth but does not inhibit embryo implantation or development to term
    Jr Gang Cheng
    Cancer and Developmental Biology Laboratory, National Cancer Institute at Frederick, Frederick, Maryland 21702, USA
    Biol Reprod 68:401-4. 2003
    ..These results support previous findings that COX2 has a role in mediating the initial uterine decidual response but is not essential to sustaining decidual growth and embryo development throughout the remainder of pregnancy...
  26. ncbi request reprint The laminopathies: nuclear structure meets disease
    Leslie Mounkes
    Cancer and Developmental Biology Laboratory, National Cancer Institute at Frederick, PO Box B, Frederick, Maryland 21702, USA
    Curr Opin Genet Dev 13:223-30. 2003
    ....
  27. pmc Abnormal nuclear shape and impaired mechanotransduction in emerin-deficient cells
    Jan Lammerding
    Cardiovascular Division, Brigham and Women s Hospital, Boston, MA 02115, USA
    J Cell Biol 170:781-91. 2005
    ....
  28. ncbi request reprint Cell nuclei spin in the absence of lamin b1
    Julie Y Ji
    Cardiovascular Division, Brigham and Women s Hospital, Cambridge, Massachusetts 02139, USA
    J Biol Chem 282:20015-26. 2007
    ..These findings demonstrate that lamin B1 serves a fundamental role within the nuclear envelope: anchoring the nucleus to the cytoskeleton...
  29. doi request reprint Myonuclear degeneration in LMNA null mice
    Michel Mittelbronn
    Institute of Neuropathology, University Hospital of Zurich, Switzerland
    Brain Pathol 18:338-43. 2008
    ..These results favor the notion that myonuclei lacking a functional lamina are susceptible to mechanical stress in vivo. These alterations may contribute to the development of early joint contractures, a feature of ADEDMD...
  30. ncbi request reprint Effect of pathogenic mis-sense mutations in lamin A on its interaction with emerin in vivo
    Ian Holt
    Biochemistry Group, North East Wales Institute, Wrexham LL11 2AW, UK
    J Cell Sci 116:3027-35. 2003
    ..Subtle effects on the function of the lamina-emerin complex in EDMD/CMD1A patients might be responsible for the skeletal and/or cardiac muscle phenotype...
  31. pmc Lamin A/C deficiency causes defective nuclear mechanics and mechanotransduction
    Jan Lammerding
    Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA
    J Clin Invest 113:370-8. 2004
    ..These findings suggest that the tissue-specific effects of lamin A/C mutations observed in the laminopathies may arise from varying degrees of impaired nuclear mechanics and transcriptional activation...
  32. pmc Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice
    Loren G Fong
    Department of Medicine, University of California, Los Angeles, CA 90095, USA
    Proc Natl Acad Sci U S A 101:18111-6. 2004
    ..These data suggest that prelamin A is toxic and that reducing its levels by as little as 50% provides striking protection from disease...
  33. pmc Lamin A/C haploinsufficiency causes dilated cardiomyopathy and apoptosis-triggered cardiac conduction system disease
    Cordula M Wolf
    Department of Cardiology, Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
    J Mol Cell Cardiol 44:293-303. 2008
    ....
  34. ncbi request reprint Lamin a truncation in Hutchinson-Gilford progeria
    Annachiara De Sandre-Giovannoli
    INSERM U491 Génétique Médicale et Développement, Faculte de Medecine Timone, Marseille, France
    Science 300:2055. 2003
  35. pmc Nuclear lamin A/C deficiency induces defects in cell mechanics, polarization, and migration
    Jerry S H Lee
    Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, Maryland, USA
    Biophys J 93:2542-52. 2007
    ..These results also suggest that cell polarization during cell migration requires tight mechanical coupling between MTOC and nucleus, which is mediated by lamin A/C...
  36. ncbi request reprint Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi syndrome
    Jocelyn M Bischof
    Department of Medical Genetics, University of Alberta, 8 16 Medical Sciences Building, Edmonton, AB, Canada T6G 2H7
    Hum Mol Genet 16:2713-9. 2007
    ..Magel2-null mice provide an important opportunity to examine the physiological basis for PWS neonatal failure to thrive and post-weaning weight gain and for the relationships among circadian rhythm, feeding behavior, and metabolism...
  37. ncbi request reprint Characterization of adiposity and metabolism in Lmna-deficient mice
    Dedra A Cutler
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1770, USA
    Biochem Biophys Res Commun 291:522-7. 2002
    ..In conclusion, Lmna+/- and -/- mice do not mimic Dunnigan's FPLD, and differential expression of lamins A and C does not appear to contribute to sex- or tissue-specific LMNA phenotypes...
  38. pmc Leukemia inhibitory factor regulates microvessel density by modulating oxygen-dependent VEGF expression in mice
    Yoshiaki Kubota
    Department of Cell Differentiation, Sakaguchi Laboratory, School of Medicine, Keio University, Tokyo, Japan
    J Clin Invest 118:2393-403. 2008
    ....
  39. ncbi request reprint Blurring the boundary: the nuclear envelope extends its reach
    Colin L Stewart
    Institute of Medical Biology, 61 Biopolis Drive, Proteos, Singapore 138668, Singapore
    Science 318:1408-12. 2007
    ..It is becoming apparent that the nuclear envelope defines not only nuclear organization but also that of the cytoskeleton and, in this way, integrates both nuclear and cytoplasmic architecture...
  40. pmc Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin
    Yuexia Wang
    Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Hum Mol Genet 17:2357-69. 2008
    ....
  41. pmc Homozygous defects in LMNA, encoding lamin A/C nuclear-envelope proteins, cause autosomal recessive axonal neuropathy in human (Charcot-Marie-Tooth disorder type 2) and mouse
    Annachiara De Sandre-Giovannoli
    INSERM U491, Génétique Médicale et Développement, Faculte de Medecine de la Timone, Marseille, France
    Am J Hum Genet 70:726-36. 2002
    ....
  42. ncbi request reprint Grb10 and active Raf-1 kinase promote Bad-dependent cell survival
    Sem Kebache
    Biotechnology Research Institute, National Research Council, Montreal PQ, Canada
    J Biol Chem 282:21873-83. 2007
    ..Because total Raf-1, ERK, and Akt kinase activities are not impaired in the absence of Grb10, we propose that this adapter protein creates a subpopulation of Raf-1 with specific anti-apoptotic activity...
  43. ncbi request reprint Lamins A and C but not lamin B1 regulate nuclear mechanics
    Jan Lammerding
    Cardiovascular Division, Department of Medicine, and Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02139, USA
    J Biol Chem 281:25768-80. 2006
    ..Our study indicates that lamins A and C are important contributors to the mechanical stiffness of nuclei, whereas lamin B1 contributes to nuclear integrity but not stiffness...
  44. ncbi request reprint Disruption of spermatogenesis in mice lacking A-type lamins
    Manfred Alsheimer
    Department of Cell and Developmental Biology, Biocenter, University of Wurzburg, Am Hubland, 97074 Wurzburg, Germany
    J Cell Sci 117:1173-8. 2004
    ..In contrast, oogenesis remains largely unaffected in Lmna(-/-) mice. These results reveal A-type lamins as important determinants of male fertility...
  45. pmc Formation of nuclear splicing factor compartments is independent of lamins A/C
    Jaromira Vecerova
    Department of Cell Biology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Institute of Cellular Biology and Pathology, 1st Faculty of Medicine, Charles University, Prague, Czech Republic
    Mol Biol Cell 15:4904-10. 2004
    ....
  46. ncbi request reprint Targeted disruption of the 2B4 gene in mice reveals an in vivo role of 2B4 (CD244) in the rejection of B16 melanoma cells
    Swapnil V Vaidya
    Department of Molecular Biology and Immunology and Institute for Cancer Research, University of North Texas Health Science Center, Fort Worth, TX 76107, USA
    J Immunol 174:800-7. 2005
    ..In vitro and in vivo experiments reveal a complex role of NK cells in gender specificity...
  47. pmc Defects in nuclear structure and function promote dilated cardiomyopathy in lamin A/C-deficient mice
    Vesna Nikolova
    Molecular Cardiology Program, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia
    J Clin Invest 113:357-69. 2004
    ..Despite severe DCM, defects in nuclear function prevent Lmna(-/-) cardiomyocytes from developing compensatory hypertrophy and accelerate disease progression...
  48. ncbi request reprint To knockout in 129 or in C57BL/6: that is the question
    Eunju Seong
    Mental Health Research Institute and Neuroscience Program, University of Michigan, Ann Arbor, MI 48109, USA
    Trends Genet 20:59-62. 2004
    ..We compared C57BL/6- with 129-derived ES cells directly and reviewed the literature. We found that, although some steps are less efficient, the advantages of C57BL/6 mice more than compensate for these drawbacks...
  49. pmc Actin-myosin-based contraction is responsible for apoptotic nuclear disintegration
    Daniel R Croft
    Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Cell Biol 168:245-55. 2005
    ....
  50. pmc Juxtaparanodal clustering of Shaker-like K+ channels in myelinated axons depends on Caspr2 and TAG-1
    Sebastian Poliak
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    J Cell Biol 162:1149-60. 2003
    ....
  51. ncbi request reprint Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation
    Ignacio Varela
    Departamento de Bioquimica y Biologia Molecular, Facultad de Medicina, Instituto Universitario de Oncologia, Universidad de Oviedo, 33006 Oviedo, Spain
    Nature 437:564-8. 2005
    ....
  52. ncbi request reprint Loss of emerin at the nuclear envelope disrupts the Rb1/E2F and MyoD pathways during muscle regeneration
    Gisela Melcon
    Research Center for Genetic Medicine, Children s National Medical Center, Washington DC, USA
    Hum Mol Genet 15:637-51. 2006
    ..We suggest that the dominant LMNA mutations seen in many clinically disparate laminopathies may similarly alter Rb function, with regard to either the timing of exit from the cell cycle or terminal differentiation programs or both...
  53. ncbi request reprint Nuclear lamin A inhibits adipocyte differentiation: implications for Dunnigan-type familial partial lipodystrophy
    Revekka L Boguslavsky
    Department of Medicine and Anatomy, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA
    Hum Mol Genet 15:653-63. 2006
    ..They also had increased basal phosphorylation of AKT1, a mediator of insulin signaling. We conclude that A-type lamins act as inhibitors of adipocyte differentiation, possibly by affecting PPARgamma2 and insulin signaling...
  54. pmc Dependence of diffusional mobility of integral inner nuclear membrane proteins on A-type lamins
    Cecilia Ostlund
    Department of Medicine, College of Physicians and Surgeons, Columbia University, Room 10 509, 630 West 168th Street, New York, New York 10032, USA
    Biochemistry 45:1374-82. 2006
    ..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...
  55. pmc Prelamin A and lamin A appear to be dispensable in the nuclear lamina
    Loren G Fong
    Department of Medicine Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA
    J Clin Invest 116:743-52. 2006
    ..These studies suggest a new therapeutic strategy for treating progeria and other lamin A diseases...
  56. ncbi request reprint The laminopathies: the functional architecture of the nucleus and its contribution to disease
    Brian Burke
    Department of Anatomy and Cell Biology, University of Florida, Gainesville, Florida 32610
    Annu Rev Genomics Hum Genet 7:369-405. 2006
    ....
  57. pmc A-type lamins regulate retinoblastoma protein function by promoting subnuclear localization and preventing proteasomal degradation
    Brett R Johnson
    Massachusetts General Hospital Cancer Center, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 101:9677-82. 2004
    ..They further raise the possibility that altered pRB function may be a contributing factor in dystrophic syndromes arising from LMNA mutation...