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The molecular basis of the human serum paraoxonase activity polymorphism

Richard Humbert
David A. Adler
Clement E. Furlong
Research01 Jan 1993
Nature Genetics

Volume: 3, P: 73-76
Correction: Corrigendum: Mutations in 15-hydroxyprostaglandin dehydrogenase cause primary hypertrophic osteoarthropathy

Sandeep Uppal
Christine P Diggle
David T Bonthron
Amendments and Corrections01 Jul 2008
Nature Genetics

Volume: 40, P: 927
Correction: Corrigendum: Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome

Miguel A. Lanaspa
Takuji Ishimoto
Richard J. Johnson
Amendments and Corrections04 Dec 2013
Nature Communications

Volume: 4, P: 1
Mutations in MEGF10, a regulator of satellite cell myogenesis, cause early onset myopathy, areflexia, respiratory distress and dysphagia (EMARDD)

Markus Schuelke, Colin Johnson and colleagues report the identification of mutations in MEGF10 that cause infantile myopathy with diaphragmatic weakness, areflexia, respiratory distress and dysphagia.

Clare V Logan
Barbara Lucke
Colin A Johnson
Research20 Nov 2011
Nature Genetics

Volume: 43, P: 1189-1192
Mutations in 15-hydroxyprostaglandin dehydrogenase cause primary hypertrophic osteoarthropathy

Sandeep Uppal
Christine P Diggle
David T Bonthron
Research25 May 2008
Nature Genetics

Volume: 40, P: 789-793
A novel RyR1-selective inhibitor prevents and rescues sudden death in mouse models of malignant hyperthermia and heat stroke

Mutations in ryanodine receptor 1 (RyR1), a Ca2+ release channel in skeletal muscle, cause malignant hyperthermia (MH) and are involved in heat stroke. Here, the authors show that an oxolinic acid-derivative RyR1 inhibitor effectively prevents and treats MH and heat stroke in various MH mouse models.

Toshiko Yamazawa
Takuya Kobayashi
Takashi Murayama
ResearchOpen Access13 Jul 2021
Nature Communications

Volume: 12, P: 1-14
Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome

Consumption of high amounts of glucose leads to the development of insulin resistance and metabolic syndrome. Here, Lanaspa et al.show that the hepatic conversion of glucose into fructose is a key step in the development of glucose-induced metabolic syndrome and fatty liver in mice.

Miguel A. Lanaspa
Takuji Ishimoto
Richard J. Johnson
Research10 Sept 2013
Nature Communications

Volume: 4, P: 1-9
Phase variation has a role in Burkholderia ambifaria niche adaptation

Ludovic Vial
Marie-Christine Groleau
Eric Déziel
Research27 Aug 2009
The ISME Journal

Volume: 4, P: 49-60
Aging mice have increased chromosome instability that is exacerbated by elevated Mdm2 expression

T Lushnikova
A Bouska
C M Eischen
Research23 May 2011
Oncogene

Volume: 30, P: 4622-4631

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The molecular basis of the human serum paraoxonase activity polymorphism

Correction: Corrigendum: Mutations in 15-hydroxyprostaglandin dehydrogenase cause primary hypertrophic osteoarthropathy

Correction: Corrigendum: Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome

Mutations in MEGF10, a regulator of satellite cell myogenesis, cause early onset myopathy, areflexia, respiratory distress and dysphagia (EMARDD)

Mutations in 15-hydroxyprostaglandin dehydrogenase cause primary hypertrophic osteoarthropathy

A novel RyR1-selective inhibitor prevents and rescues sudden death in mouse models of malignant hyperthermia and heat stroke

Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome

Phase variation has a role in Burkholderia ambifaria niche adaptation

Aging mice have increased chromosome instability that is exacerbated by elevated Mdm2 expression

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