Positions

Selected Publications

Academic Article

Year Title Altmetric
2017 Identification of the amino acids inserted during suppression of CFTR nonsense mutations and determination of their functional consequences 2017
2014 Therapeutics based on stop codon readthrough 2014
2013 Attenuation of Nonsense-Mediated mRNA Decay Enhances In Vivo Nonsense Suppression 2013
2012 The designer aminoglycoside NB84 significantly reduces glycosaminoglycan accumulation associated with MPS I-H in the Idua-W392X mouse 2012
1994 Preliminary Crystallographic Studies of Four Crystal forms of Serum Albumin 1994
1994 Three-Dimensional structure of schistosoma japonicum glutathione s -transferase fused with a six-amino acid conserved neutralizing epitope of gp41 from hiv 1994
Aminoglycoside suppression of a premature stop mutation in a Cftr-/- mouse carrying a human CFTR-G542X transgene
Aminoglycosides as potential pharmacogenetic agents in the treatment of Hailey-Hailey disease [2]
Characterization of an MPS I-H knock-in mouse that carries a nonsense mutation analogous to the human IDUA-W402X mutation
Clinical doses of amikacin provide more effective suppression of the human CFTR-G542X stop mutation than gentamicin in a transgenic CF mouse model
Clinically relevant aminoglycosides can suppress disease-associated premature stop mutations in the IDUA and P53 cDNAS in a mammalian translation system
Corrigendum to "Characterization of an MPS I-H knock-in mouse that carries a nonsense mutation analogous to the human IDUA-W402X mutation" [Mol. Genet. Metab. 99 (2010) 62-71] (DOI:10.1016/j.ymgme.2009.08.002)
Diffusion-controlled crystallization apparatus for microgravity (DCAM): flight and ground-based applications
Discovery of clinically approved agents that promote suppression of cystic fibrosis transmembrane conductance regulator nonsense mutations
Distinct eRF3 Requirements Suggest Alternate eRF1 Conformations Mediate Peptide Release during Eukaryotic Translation Termination
Enhancement of alveolar epithelial sodium channel activity with decreased cystic fibrosis transmembrane conductance regulator expression in mouse lung
Eukaryotic release factor 1 phosphorylation by CK2 protein kinase is dynamic but has little effect on the efficiency of translation termination in Saccharomyces cerevisiae
Fusion proteins as alternate crystallization paths to difficult structure problems
Gentamicin-mediated suppression of Hurler syndrome stop mutations restores a low level of α-L-iduronidase activity and reduces lysosomal glycosaminoglycan accumulation
Leaky termination at premature stop codons antagonizes nonsense-mediated mRNA decay in S. cerevisiae
Long-term nonsense suppression therapy moderates MPS I-H disease progression
Lower dimer impurity incorporation may result in higher perfection of HEWL crystals grown in microgravity, a case study.
PCAM: a multi-user facility-based protein crystallization apparatus for microgravity
Pharmacological suppression of premature stop mutations that cause genetic diseases
Poly-L-aspartic acid enhances and prolongs gentamicin-mediated suppression of the CFTR-G542X mutation in a cystic fibrosis Mouse model
Suppression of nonsense mutations as a therapeutic approach to treat genetic diseases
Suppression of premature termination codons as a therapeutic approach
Tpa1p is part of an mRNP complex that influences translation termination, mRNA deadenylation, and mRNA turnover in Saccharomyces cerevisiae

Chapter

Year Title Altmetric
2010 Recoding Therapies for Genetic Diseases 2010
2005 Therapies of Nonsense-Associated Diseases.  121-136. 2005

Research Overview

  • translation
    translation termination
    mRNA stability
    mRNA turnover
    rare or orphan diseases
    mucopolysaccharidosis I-Hurler (MPS I-H)
    lysosomal storage disease
    cystic fibrosis
  • Education And Training

  • Bachelor of Science or Mathematics in Chemistry, University of Alabama at Birmingham 1990
  • UAB Microbiology, Postdoctoral Fellowship 2003
  • Full Name

  • Kim Keeling