N
Nicholas J. Hudson
Researcher at University of Queensland
Publications - 77
Citations - 1999
Nicholas J. Hudson is an academic researcher from University of Queensland. The author has contributed to research in topics: Skeletal muscle & Gene. The author has an hindex of 23, co-authored 74 publications receiving 1762 citations. Previous affiliations of Nicholas J. Hudson include Autonomous University of Barcelona & Commonwealth Scientific and Industrial Research Organisation.
Papers
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A differential wiring analysis of expression data correctly identifies the gene containing the causal mutation
TL;DR: A new algorithm is proposed that correctly identifies the gene containing the causal mutation from microarray data alone and yields the correct answer, “myostatin”, the myostatin mutation that releases the brakes on Piedmontese muscle growth by translating a dysfunctional protein.
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Gene expression studies of developing bovine longissimus muscle from two different beef cattle breeds
Sigrid A. Lehnert,Sigrid A. Lehnert,Antonio Reverter,Antonio Reverter,Keren Byrne,Keren Byrne,Yonghong Wang,Yonghong Wang,Greg Nattrass,Greg Nattrass,Nicholas J. Hudson,Nicholas J. Hudson,Paul L. Greenwood,Paul L. Greenwood +13 more
TL;DR: The developing longissimus muscle of fetuses carrying the Piedmontese mutation shows an emphasis on glycolytic muscle biochemistry and a large-scale up-regulation of the translational machinery at birth, as well as gene expression differences that may underpin the phenotype differences between the two breeds.
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Regulatory impact factors
Antonio Reverter,Nicholas J. Hudson,Shivashankar H. Nagaraj,Miguel Pérez-Enciso,Brian P. Dalrymple +4 more
TL;DR: In this article, a regulatory impact factor (RIF) metric is proposed to identify critical transcription factors (TF) from gene expression data, and a set of experiments spanning a wide range of scenarios including breast cancer survival, fat, gonads and sex differentiation.
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Beyond differential expression: the quest for causal mutations and effector molecules
TL;DR: With a well designed experiment, it is now possible to use gene expression to identify causal mutations and the other major effector molecules with whom they cooperate, irrespective of whether they themselves are DE, according to a universally powerful way of quantifying differential connectivity.
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Maintaining muscle mass during extended disuse: aestivating frogs as a model species.
TL;DR: The role of reactive oxygen species and antioxidants during muscle disuse is emphasised, and the metabolic depression that occurs during dormancy would appear to have a protective role, reducing or preventing muscle atrophy despite periods of inactivity lasting 6-9 months.