S. H. Kang

Publications (2)2.34 Total impact

• Article: Complete genome sequence of a newly isolated lytic bacteriophage, EFAP‐1 of Enterococcus faecalis, and antibacterial activity of its endolysin EFAL‐1

  J.S. Son, S.Y. Jun, E.B. Kim, J.E. Park, H.R. Paik, S.J. Yoon, S.H. Kang, Y.-J. Choi
  [show abstract] [hide abstract]
  ABSTRACT: Aims:  In this work, we aimed to identify an effective treatment of infections caused by Enterococcus spp. strains resistant to conventional antibiotics.Methods and Results:  We report the isolation and characterization of a new lytic bacteriophage, designated bacteriophage EFAP-1, that is capable of lysing Enterococcus faecalis bacteria that exhibit resistance to multiple antibiotics. EFAP-1 has low sequence similarity to all known bacteriophages. Transmission electron microscopy confirmed that EFAP-1 belongs to the Siphoviridae family. A putative lytic protein of EFAP-1, endolysin EFAL-1, is encoded in ORF 2 and was expressed in Escherichia coli. Recombinant EFAL-1 had broad-spectrum lytic activity against several Gram-positive pathogens, including Ent. faecalis and Enterococcus faecium.Conclusions:  The complete genome sequence of the newly isolated enterococcal lytic phage was analysed, and it was demonstrated that its recombinant endolysin had broad lytic activity against various Gram-positive pathogens.Significance and Impact of the Study:  Bacteriophage EFAP-1 and its lytic protein, EFAL-1, can be utilized as potent antimicrobial agents against Enterococcus spp. strains resistant to conventional antibiotics in hospital infections and also as environmental disinfectants to control disease-causing Enterococcus spp. in dairy farms.
  Journal of Applied Microbiology 04/2010; 108(5):1769 - 1779. · 2.34 Impact Factor
• Article: Phenotypic spectrum and genotype-phenotype correlations of NRXN1 exon deletions

  C. P. Schaaf, P. M. Boone, S. Sampath, C. Williams, P. I. Bader, J. M. Mueller, O. A. Shchelochkov, C. W. Brown, H. P. Crawford, J. A. Phalen, [......], L. Parsley, S. W. Grayson, A. Scheuerle, C. D. Luzzi, S. K. Thomas, P. A. Eng, S. H. Kang, A. Patel, P. Stankiewicz, S. W. Cheung
  [show abstract] [hide abstract]
  ABSTRACT: Copy number variants (CNVs) and intragenic rearrangements of the NRXN1 (neurexin 1) gene are associated with a wide spectrum of developmental and neuropsychiatric disorders, including intellectual disability, speech delay, autism spectrum disorders (ASDs), hypotonia and schizophrenia. We performed a detailed clinical and molecular characterization of 24 patients who underwent clinical microarray analysis and had intragenic deletions of NRXN1. Seventeen of these deletions involved exons of NRXN1, whereas seven deleted intronic sequences only. The patients with exonic deletions manifested developmental delay/intellectual disability (93%), infantile hypotonia (59%) and ASDs (56%). Congenital malformations and dysmorphic features appeared infrequently and inconsistently among this population of patients with NRXN1 deletions. The more C-terminal deletions, including those affecting the beta isoform of neurexin 1, manifested increased head size and a high frequency of seizure disorder (88%) when compared with N-terminal deletions of NRXN1.European Journal of Human Genetics advance online publication, 23 May 2012; doi:10.1038/ejhg.2012.95.
  Eur J Hum Genet.