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Yifang Hu
Researcher at Walter and Eliza Hall Institute of Medical Research
Publications - 35
Citations - 25473
Yifang Hu is an academic researcher from Walter and Eliza Hall Institute of Medical Research. The author has contributed to research in topics: Haematopoiesis & Cellular differentiation. The author has an hindex of 23, co-authored 34 publications receiving 16561 citations. Previous affiliations of Yifang Hu include University of Melbourne.
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Journal ArticleDOI
Genotype to phenotype: Diet-by-mitochondrial DNA haplotype interactions drive metabolic flexibility and organismal fitness.
Wen C. Aw,Samuel G. Towarnicki,Richard G. Melvin,Neil A. Youngson,Michael R. Garvin,Yifang Hu,Shaun Nielsen,Torsten Thomas,Russell Pickford,Sonia Bustamante,Antón Vila-Sanjurjo,Gordon K. Smyth,Gordon K. Smyth,J. William O. Ballard +13 more
TL;DR: It is proposed that individuals with specific mtDNA variations may differentially metabolise carbohydrates, which has implications for a variety of diseases including cardiovascular disease, obesity, and perhaps Parkinson’s Disease.
Journal ArticleDOI
Increased autophagy in EphrinB2-deficient osteocytes is associated with elevated secondary mineralization and brittle bone
Christina Vrahnas,Christina Vrahnas,Christina Vrahnas,Martha Blank,Martha Blank,Toby A. Dite,Toby A. Dite,Toby A. Dite,Liliana Tatarczuch,Niloufar Ansari,Niloufar Ansari,Blessing Crimeen-Irwin,Huynh Nguyen,Mark R. Forwood,Yifang Hu,Mika Ikegame,Keith R. Bambery,Cyril Petibois,Eleanor J. Mackie,Mark J. Tobin,Gordon K. Smyth,Gordon K. Smyth,Jonathan S. Oakhill,Jonathan S. Oakhill,Jonathan S. Oakhill,T. John Martin,T. John Martin,Natalie A. Sims,Natalie A. Sims +28 more
TL;DR: It is concluded that secondary mineralization involves EphrinB2-RhoA-limited autophagy in osteocytes, and disruption leads to a bone fragility independent of bone mass, as reported in mice with osteocyte-targeted EphrineB2 deletion.
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Murine Oncostatin M Acts via Leukemia Inhibitory Factor Receptor to Phosphorylate Signal Transducer and Activator of Transcription 3 (STAT3) but Not STAT1, an Effect That Protects Bone Mass.
Emma C. Walker,Rachelle W. Johnson,Yifang Hu,Holly J. Brennan,Ingrid J Poulton,Jian-Guo Zhang,Brendan J. Jenkins,Brendan J. Jenkins,Gordon K. Smyth,Nicos A. Nicola,Natalie A. Sims,Natalie A. Sims +11 more
TL;DR: In a mouse model of spontaneous osteopenia caused by hyperactivation of STAT1/3 signaling downstream of gp130, STAT1 deletion rescued the osteopenic phenotype, indicating a beneficial effect of promoting STAT3 signaling over STAT1 downstream ofgp130 in this low bone mass condition, and this may have therapeutic value.
Journal ArticleDOI
Lung Basal Stem Cells Rapidly Repair DNA Damage Using the Error-Prone Nonhomologous End-Joining Pathway
Clare E. Weeden,Clare E. Weeden,Yunshun Chen,Yunshun Chen,Stephen B. Ma,Stephen B. Ma,Yifang Hu,Georg Ramm,Kate D. Sutherland,Kate D. Sutherland,Gordon K. Smyth,Gordon K. Smyth,Marie Liesse Asselin-Labat,Marie Liesse Asselin-Labat +13 more
TL;DR: The results favour a model in which heavy smoking promotes proliferation of BSCs, and their predilection for error-prone NHEJ could lead to the high mutagenic burden that culminates in SqCC.