1. Cell-autonomous activation of Hedgehog signaling inhibits brown adipose tissue development.

    PNAS 112(16):5069 (2015) PMID 25848030 PMCID PMC4413261

    Although recent studies have shown that brown adipose tissue (BAT) arises from progenitor cells that also give rise to skeletal muscle, the developmental signals that control the formation of BAT remain largely unknown. Here, we show that brown preadipocytes possess primary cilia and can respond...
  2. On the meaning of the word 'epimutation': a comment.

    Trends in Genetics 31(1):1 (2015) PMID 25480537

  3. Phase-change properties of GeSbTe thin films deposited by plasma-enchanced atomic layer depositon.

    Nanoscale Research Letters 10:89 (2015) PMID 25852385 PMCID PMC4385138

    Phase-change access memory (PCM) appears to be the strongest candidate for next-generation high-density nonvolatile memory. The fabrication of ultrahigh-density PCM depends heavily on the thin-film growth technique for the phase-changing chalcogenide material. In this study, Ge2Sb2Te5 (GST) and ...
  4. On the meaning of the word 'epimutation': a comment.

    Trends in Genetics 31(1):1 (2015) PMID 25480537

  5. Comment on “On the meaning of the word ‘epimutation”’

    Trends in Genetics (2014)

  6. CDC42 inhibition suppresses progression of incipient intestinal tumors.

    Cancer Research 74(19):5480 (2014) PMID 25113996 PMCID PMC4184946

    Mutations in the APC or β-catenin genes are well-established initiators of colorectal cancer, yet modifiers that facilitate the survival and progression of nascent tumor cells are not well defined. Using genetic and pharmacologic approaches in mouse colorectal cancer and human colorectal cancer ...
  7. CDC42 inhibition suppresses progression of incipient intestinal tumors.

    Cancer Research 74(19):5480 (2014) PMID 25113996 PMCID PMC4184946

    Mutations in the APC or β-catenin genes are well-established initiators of colorectal cancer, yet modifiers that facilitate the survival and progression of nascent tumor cells are not well defined. Using genetic and pharmacologic approaches in mouse colorectal cancer and human colorectal cancer ...
  8. CDC42 inhibition suppresses progression of incipient intestinal tumors.

    Cancer Research 74(19):5480 (2014) PMID 25113996 PMCID PMC4184946

    Mutations in the APC or β-catenin genes are well-established initiators of colorectal cancer, yet modifiers that facilitate the survival and progression of nascent tumor cells are not well defined. Using genetic and pharmacologic approaches in mouse colorectal cancer and human colorectal cancer ...
  9. CDC42 inhibition suppresses progression of incipient intestinal tumors.

    Cancer Research 74(19):5480 (2014) PMID 25113996 PMCID PMC4184946

    Mutations in the APC or β-catenin genes are well-established initiators of colorectal cancer, yet modifiers that facilitate the survival and progression of nascent tumor cells are not well defined. Using genetic and pharmacologic approaches in mouse colorectal cancer and human colorectal cancer ...
  10. Targeted p16(Ink4a) epimutation causes tumorigenesis and reduces survival in mice.

    Journal of Clinical Investigation 124(9):3708 (2014) PMID 25061879 PMCID PMC4151219

    Cancer has long been viewed as a genetic disease; however, epigenetic silencing as the result of aberrant promoter DNA methylation is frequently associated with cancer development, suggesting an epigenetic component to the disease. Nonetheless, it has remained unclear whether an epimutation (an ...
  11. Targeted p16(Ink4a) epimutation causes tumorigenesis and reduces survival in mice.

    Journal of Clinical Investigation 124(9):3708 (2014) PMID 25061879 PMCID PMC4151219

    Cancer has long been viewed as a genetic disease; however, epigenetic silencing as the result of aberrant promoter DNA methylation is frequently associated with cancer development, suggesting an epigenetic component to the disease. Nonetheless, it has remained unclear whether an epimutation (an ...
  12. Targeted p16(Ink4a) epimutation causes tumorigenesis and reduces survival in mice.

    Journal of Clinical Investigation 124(9):3708 (2014) PMID 25061879 PMCID PMC4151219

    Cancer has long been viewed as a genetic disease; however, epigenetic silencing as the result of aberrant promoter DNA methylation is frequently associated with cancer development, suggesting an epigenetic component to the disease. Nonetheless, it has remained unclear whether an epimutation (an ...
  13. Targeted p16(Ink4a) epimutation causes tumorigenesis and reduces survival in mice.

    Journal of Clinical Investigation 124(9):3708 (2014) PMID 25061879 PMCID PMC4151219

    Cancer has long been viewed as a genetic disease; however, epigenetic silencing as the result of aberrant promoter DNA methylation is frequently associated with cancer development, suggesting an epigenetic component to the disease. Nonetheless, it has remained unclear whether an epimutation (an ...
  14. Targeted p16(Ink4a) epimutation causes tumorigenesis and reduces survival in mice.

    Journal of Clinical Investigation 124(9):3708 (2014) PMID 25061879 PMCID PMC4151219

    Cancer has long been viewed as a genetic disease; however, epigenetic silencing as the result of aberrant promoter DNA methylation is frequently associated with cancer development, suggesting an epigenetic component to the disease. Nonetheless, it has remained unclear whether an epimutation (an ...
  15. Comparison and quantitative verification of mapping algorithms for whole-genome bisulfite sequencing.

    Nucleic Acids Research 42(6):e43 (2014) PMID 24391148 PMCID PMC3973287

    Coupling bisulfite conversion with next-generation sequencing (Bisulfite-seq) enables genome-wide measurement of DNA methylation, but poses unique challenges for mapping. However, despite a proliferation of Bisulfite-seq mapping tools, no systematic comparison of their genomic coverage and quant...
  16. Comparison and quantitative verification of mapping algorithms for whole-genome bisulfite sequencing.

    Nucleic Acids Research 42(6):e43 (2014) PMID 24391148 PMCID PMC3973287

    Coupling bisulfite conversion with next-generation sequencing (Bisulfite-seq) enables genome-wide measurement of DNA methylation, but poses unique challenges for mapping. However, despite a proliferation of Bisulfite-seq mapping tools, no systematic comparison of their genomic coverage and quant...
  17. Major epigenetic development distinguishing neuronal and non-neuronal cells occurs postnatally in the murine hypothalamus.

    Human Molecular Genetics 23(6):1579 (2014) PMID 24186871 PMCID PMC3929094

    Prenatal and early postnatal environment can persistently alter one's risk of obesity. Environmental effects on hypothalamic developmental epigenetics constitute a likely mechanism underlying such 'developmental programming' of energy balance regulation. To advance our understanding of these pro...
  18. Major epigenetic development distinguishing neuronal and non-neuronal cells occurs postnatally in the murine hypothalamus.

    Human Molecular Genetics 23(6):1579 (2014) PMID 24186871 PMCID PMC3929094

    Prenatal and early postnatal environment can persistently alter one's risk of obesity. Environmental effects on hypothalamic developmental epigenetics constitute a likely mechanism underlying such 'developmental programming' of energy balance regulation. To advance our understanding of these pro...
  19. On the meaning of the word ‘epimutation’: a comment

    Trends in Genetics 31(1) (2014) PMID 25480537

  20. On the meaning of the word ‘epimutation’: a comment

    Trends in Genetics (2014)