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M Keeling

Showing results (71-80 of 121) with videos related to

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Disease Models & Mechanisms|August 2, 2020
A regulated NMD mouse model supports NMD inhibition as a viable therapeutic option to treat genetic diseasesJosh Echols, Amna Siddiqui, Yanying Dai, et al.
Journal of Molecular Medicine (Berlin, Germany)|July 20, 2022
Ataluren suppresses a premature termination codon in an MPS I-H mouseDan Wang, Xiaojiao Xue, Gwen Gunn, et al.
Annals of Surgery|May 1, 1983
Intraoperative autotransfusion. Experience in 725 consecutive casesM M Keeling, L A Gray, M A Brink, et al.
Nature Communications|March 21, 2024
Extended stop codon context predicts nonsense codon readthrough efficiency in human cellsKotchaphorn Mangkalaphiban, Lianwu Fu, Ming Du, et al.
Archives of Disease in Childhood|December 13, 2003
Brain haemorrhage in five infants with coagulopathyE B A Vorstman, P Anslow, D M Keeling, et al.
European Journal of Immunology|October 30, 1999
T cells are the main cell type expressing B7-1 and B7-2 in the central nervous system during acute, relapsing and chronic experimental autoimmune encephalomyelitisA H Cross, J A Lyons, M San, et al.
Journal of Neuroimmunology|May 16, 2000
A catalyst of peroxynitrite decomposition inhibits murine experimental autoimmune encephalomyelitisA H Cross, M San, M K Stern, et al.
Journal of Molecular Medicine (Berlin, Germany)|March 17, 2006
Clinical doses of amikacin provide more effective suppression of the human CFTR-G542X stop mutation than gentamicin in a transgenic CF mouse modelMing Du, Kim M Keeling, Liming Fan, et al.
American Journal of Physiology. Lung Cellular and Molecular Physiology|July 12, 2011
Enhancement of alveolar epithelial sodium channel activity with decreased cystic fibrosis transmembrane conductance regulator expression in mouse lungAhmed Lazrak, Asta Jurkuvenaite, Lan Chen, et al.
Human Molecular Genetics|February 13, 2001
Gentamicin-mediated suppression of Hurler syndrome stop mutations restores a low level of alpha-L-iduronidase activity and reduces lysosomal glycosaminoglycan accumulationK M Keeling, D A Brooks, J J Hopwood, et al.
Pageof 13

Showing results (71-80 of 121) with videos related to

Sort By:
Pageof 13
Disease Models & Mechanisms|August 2, 2020
A regulated NMD mouse model supports NMD inhibition as a viable therapeutic option to treat genetic diseasesJosh Echols, Amna Siddiqui, Yanying Dai, et al.
Journal of Molecular Medicine (Berlin, Germany)|July 20, 2022
Ataluren suppresses a premature termination codon in an MPS I-H mouseDan Wang, Xiaojiao Xue, Gwen Gunn, et al.
Annals of Surgery|May 1, 1983
Intraoperative autotransfusion. Experience in 725 consecutive casesM M Keeling, L A Gray, M A Brink, et al.
Nature Communications|March 21, 2024
Extended stop codon context predicts nonsense codon readthrough efficiency in human cellsKotchaphorn Mangkalaphiban, Lianwu Fu, Ming Du, et al.
Archives of Disease in Childhood|December 13, 2003
Brain haemorrhage in five infants with coagulopathyE B A Vorstman, P Anslow, D M Keeling, et al.
European Journal of Immunology|October 30, 1999
T cells are the main cell type expressing B7-1 and B7-2 in the central nervous system during acute, relapsing and chronic experimental autoimmune encephalomyelitisA H Cross, J A Lyons, M San, et al.
Journal of Neuroimmunology|May 16, 2000
A catalyst of peroxynitrite decomposition inhibits murine experimental autoimmune encephalomyelitisA H Cross, M San, M K Stern, et al.
Journal of Molecular Medicine (Berlin, Germany)|March 17, 2006
Clinical doses of amikacin provide more effective suppression of the human CFTR-G542X stop mutation than gentamicin in a transgenic CF mouse modelMing Du, Kim M Keeling, Liming Fan, et al.
American Journal of Physiology. Lung Cellular and Molecular Physiology|July 12, 2011
Enhancement of alveolar epithelial sodium channel activity with decreased cystic fibrosis transmembrane conductance regulator expression in mouse lungAhmed Lazrak, Asta Jurkuvenaite, Lan Chen, et al.
Human Molecular Genetics|February 13, 2001
Gentamicin-mediated suppression of Hurler syndrome stop mutations restores a low level of alpha-L-iduronidase activity and reduces lysosomal glycosaminoglycan accumulationK M Keeling, D A Brooks, J J Hopwood, et al.
Pageof 13