Bin Yan

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint The PIM-2 kinase phosphorylates BAD on serine 112 and reverses BAD-induced cell death
    Bin Yan
    Center for Molecular Biology and Gene Therapy, The Department of Microbiology, Loma Linda University School of Medicine, Loma Linda, California 92354, USA
    J Biol Chem 278:45358-67. 2003
  2. pmc Genome-wide identification of novel expression signatures reveal distinct patterns and prevalence of binding motifs for p53, nuclear factor-kappaB and other signal transcription factors in head and neck squamous cell carcinoma
    Bin Yan
    Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Center Drive, Bethesda, Maryland 20892, USA
    Genome Biol 8:R78. 2007
  3. pmc Systems biology-defined NF-kappaB regulons, interacting signal pathways and networks are implicated in the malignant phenotype of head and neck cancer cell lines differing in p53 status
    Bin Yan
    Head and Neck Surgery Branch, NIDCD, National Institutes of Health, Bethesda, MD 20892, USA
    Genome Biol 9:R53. 2008
  4. doi request reprint A signal network involving coactivated NF-kappaB and STAT3 and altered p53 modulates BAX/BCL-XL expression and promotes cell survival of head and neck squamous cell carcinomas
    Tin Lap Lee
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892 1419, USA
    Int J Cancer 122:1987-98. 2008
  5. pmc TNF-α promotes c-REL/ΔNp63α interaction and TAp73 dissociation from key genes that mediate growth arrest and apoptosis in head and neck cancer
    Hai Lu
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, USA
    Cancer Res 71:6867-77. 2011
  6. doi request reprint Proteomic signatures of epidermal growth factor receptor and survival signal pathways correspond to gefitinib sensitivity in head and neck cancer
    Francisco G Pernas
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Clin Cancer Res 15:2361-72. 2009
  7. ncbi request reprint A novel nuclear factor-kappaB gene signature is differentially expressed in head and neck squamous cell carcinomas in association with TP53 status
    Tin Lap Lee
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland 20892 1419, USA
    Clin Cancer Res 13:5680-91. 2007
  8. pmc ΔNp63 versatilely regulates a Broad NF-κB gene program and promotes squamous epithelial proliferation, migration, and inflammation
    Xinping Yang
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland 20892, USA
    Cancer Res 71:3688-700. 2011
  9. ncbi request reprint Deficient TP53 expression, function, and cisplatin sensitivity are restored by quinacrine in head and neck cancer
    Jay Friedman
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA
    Clin Cancer Res 13:6568-78. 2007
  10. pmc Attenuated transforming growth factor beta signaling promotes nuclear factor-kappaB activation in head and neck cancer
    Jonah Cohen
    Howard Hughes Medical Institute NIH Research Scholars Program, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, USA
    Cancer Res 69:3415-24. 2009

Collaborators

Detail Information

Publications22

  1. ncbi request reprint The PIM-2 kinase phosphorylates BAD on serine 112 and reverses BAD-induced cell death
    Bin Yan
    Center for Molecular Biology and Gene Therapy, The Department of Microbiology, Loma Linda University School of Medicine, Loma Linda, California 92354, USA
    J Biol Chem 278:45358-67. 2003
    ..Our results indicate that pim-2 functions similarly to pim-1 as a pro-survival kinase and suggest that BAD is a legitimate PIM-2 substrate...
  2. pmc Genome-wide identification of novel expression signatures reveal distinct patterns and prevalence of binding motifs for p53, nuclear factor-kappaB and other signal transcription factors in head and neck squamous cell carcinoma
    Bin Yan
    Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Center Drive, Bethesda, Maryland 20892, USA
    Genome Biol 8:R78. 2007
    ..However, the molecular expression signatures and transcriptional regulatory controls that underlie the heterogeneity in HNSCCs are not well defined...
  3. pmc Systems biology-defined NF-kappaB regulons, interacting signal pathways and networks are implicated in the malignant phenotype of head and neck cancer cell lines differing in p53 status
    Bin Yan
    Head and Neck Surgery Branch, NIDCD, National Institutes of Health, Bethesda, MD 20892, USA
    Genome Biol 9:R53. 2008
    ..However, how NF-kappaB acts as a key regulatory node to modulate global gene expression, and contributes to the malignant heterogeneity of head and neck cancer, is not well understood...
  4. doi request reprint A signal network involving coactivated NF-kappaB and STAT3 and altered p53 modulates BAX/BCL-XL expression and promotes cell survival of head and neck squamous cell carcinomas
    Tin Lap Lee
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892 1419, USA
    Int J Cancer 122:1987-98. 2008
    ..Inhibition of signal activation of both NF-kappaB and STAT3 together with reexpression of p53 could be the most effective strategy to restore BAX/BCL-XL regulation and for cytotoxic therapy of HNSCC...
  5. pmc TNF-α promotes c-REL/ΔNp63α interaction and TAp73 dissociation from key genes that mediate growth arrest and apoptosis in head and neck cancer
    Hai Lu
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, USA
    Cancer Res 71:6867-77. 2011
    ....
  6. doi request reprint Proteomic signatures of epidermal growth factor receptor and survival signal pathways correspond to gefitinib sensitivity in head and neck cancer
    Francisco G Pernas
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Clin Cancer Res 15:2361-72. 2009
    ..To investigate the underlying molecular mechanism, the proteomic signatures and responses of EGFR and downstream signals have been studied in a panel of HNSCC cell lines and tumor specimens pre- and post-gefitinib treatment...
  7. ncbi request reprint A novel nuclear factor-kappaB gene signature is differentially expressed in head and neck squamous cell carcinomas in association with TP53 status
    Tin Lap Lee
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland 20892 1419, USA
    Clin Cancer Res 13:5680-91. 2007
    ....
  8. pmc ΔNp63 versatilely regulates a Broad NF-κB gene program and promotes squamous epithelial proliferation, migration, and inflammation
    Xinping Yang
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland 20892, USA
    Cancer Res 71:3688-700. 2011
    ..Our study reveals ΔNp63 as a master transcription factor that, in coordination with NF-κB/Rels, orchestrates a broad gene program promoting epidermal hyperplasia, inflammation, and the malignant phenotype of HNSCC...
  9. ncbi request reprint Deficient TP53 expression, function, and cisplatin sensitivity are restored by quinacrine in head and neck cancer
    Jay Friedman
    Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA
    Clin Cancer Res 13:6568-78. 2007
    ....
  10. pmc Attenuated transforming growth factor beta signaling promotes nuclear factor-kappaB activation in head and neck cancer
    Jonah Cohen
    Howard Hughes Medical Institute NIH Research Scholars Program, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, USA
    Cancer Res 69:3415-24. 2009
    ..Together, these findings elucidate a regulatory framework in which attenuated TGFbeta signaling promotes NF-kappaB activation and squamous epithelial malignancy in the setting of altered TP53 status...
  11. ncbi request reprint A novel conditionally replicative adenovirus vector targeting telomerase-positive tumor cells
    Qian Huang
    Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Clin Cancer Res 10:1439-45. 2004
    ..To develop a novel conditionally replicative adenovirus vector that targets telomerase-positive cancer cells...
  12. doi request reprint Characterizing regulation of metabolism in Geobacter sulfurreducens through genome-wide expression data and sequence analysis
    Radhakrishnan Mahadevan
    Department of Chemical Engineering and Applied Chemistry, Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Canada
    OMICS 12:33-59. 2008
    ..sulfurreducens and simulated Fe(II)-limited growth. The resulting prediction was consistent with data, suggesting that regulatory constraints are important for simulating growth phenotypes in nonoptimal environments...
  13. ncbi request reprint Computational prediction of conserved operons and phylogenetic footprinting of transcription regulatory elements in the metal-reducing bacterial family Geobacteraceae
    Bin Yan
    Department of Preventive Medicine, Center of Genomics and Bioinformatics, University of Tennesee Health Science Center, 66 N Pauline St, Ste 633, Memphis, TN 38163, USA
    J Theor Biol 230:133-44. 2004
    ..These predictions will aid in further elucidation of regulatory networks of gene interactions in Geobacteraceae...
  14. doi request reprint Site-directed mutagenesis of substrate binding sites of azoreductase from Rhodobacter sphaeroides
    Guangfei Liu
    School of Environmental and Biological Science and Technology, Dalian University of Technology, 116024, Dalian, P R China
    Biotechnol Lett 30:869-75. 2008
    ..K109 might only be involved in the binding of the 2'-phosphate group of NADPH and have no effect on the binding of NADH. Y74W and H75N mutations decreased the binding of methyl red/nitrofurazone and had no affect on the binding of NADPH...
  15. ncbi request reprint Improved temporal clustering analysis method for detecting multiple response peaks in fMRI
    Na Lu
    Key Laboratory of Nuclear Analysis Techniques, Institute of High Energy Physics, 19 Yuquan Road, Beijing 100 049, China
    J Magn Reson Imaging 23:285-90. 2006
    ..To develop an improved temporal clustering analysis (TCA) method for detecting multiple active peaks by running the method once...
  16. pmc A unique role of the DNA fragmentation factor in maintaining genomic stability
    Bin Yan
    Departments of Radiation Oncology and Pathology, Duke University Medical Center, Durham, NC 27710, USA
    Proc Natl Acad Sci U S A 103:1504-9. 2006
    ....
  17. pmc Regulation of HIF-1alpha stability through S-nitrosylation
    Fang Li
    Department of Radiation Oncology, University of Colorado Health Sciences Center, Aurora, CO 80045, USA
    Mol Cell 26:63-74. 2007
    ..This interaction between NO and HIF-1 sheds new light on their involvement in tumor response to treatment as well as mammalian inflammation process in general...
  18. ncbi request reprint Small interfering RNA-mediated caveolin-1 knockout on plasminogen activator inhibitor-1 expression in insulin-stimulated human vascular endothelial cells
    Huiling Yang
    Institute of Clinic Medicine, The First Affiliated Hospital of Nanhua University, Hengyang, China
    Acta Biochim Biophys Sin (Shanghai) 39:224-33. 2007
    ....
  19. ncbi request reprint Construction and functional analysis of a lentiviral expression vector containing a scavenger receptor (SR-PSOX) that binds uniquely phosphatidylserine and oxidized lipoprotein
    Zhihua Quan
    Institute of Cardiovascular Disease, Nanhua University, Hengyang, China
    Acta Biochim Biophys Sin (Shanghai) 39:208-16. 2007
    ..Our data suggested that the overexpression of recombinant human SR-PSOX protein can promote foam cell formation and upregulate the expression of the inflammatory factor TNF-alpha...
  20. ncbi request reprint Genome-wide similarity search for transcription factors and their binding sites in a metal-reducing prokaryote Geobacter sulfurreducens
    Bin Yan
    Department of Preventive Medicine, University of Tennessee Health Science Center, 66 N Pauline St, Ste 633, Memphis, TN 38163, USA
    Biosystems 90:421-41. 2007
    ..The closest homolog of E. coli RpoE in G. sulfurreducens may be more similar to FecI than to RpoE. These findings represent the first step in the understanding of the regulatory relationships in G. sulfurreducens on the genome scale...
  21. ncbi request reprint Tumor necrosis factor-alpha is a potent endogenous mutagen that promotes cellular transformation
    Bin Yan
    Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina, USA
    Cancer Res 66:11565-70. 2006
    ....
  22. ncbi request reprint Computational prediction of RpoS and RpoD regulatory sites in Geobacter sulfurreducens using sequence and gene expression information
    Bin Yan
    Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN, 38163, USA
    Gene 384:73-95. 2006
    ....