F
Fang Fang
Researcher at Guangzhou Institutes of Biomedicine and Health
Publications - 16
Citations - 950
Fang Fang is an academic researcher from Guangzhou Institutes of Biomedicine and Health. The author has contributed to research in topics: Osteoblast & Peroxisome proliferator-activated receptor. The author has an hindex of 11, co-authored 15 publications receiving 720 citations. Previous affiliations of Fang Fang include University of Michigan.
Papers
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Journal ArticleDOI
Suppression of autophagy by FIP200 deletion leads to osteopenia in mice through the inhibition of osteoblast terminal differentiation
Fei Liu,Fang Fang,Hebao Yuan,Dongye Yang,Yongqiang Chen,Linford Williams,Steven A. Goldstein,Paul H. Krebsbach,Jun-Lin Guan +8 more
TL;DR: FIP200 is identified as an important regulator of bone development and a novel role of autophagy is revealed in osteoblast function through its positive role in supporting osteooblast nodule formation and differentiation.
Journal ArticleDOI
Molecular genetics of osteosarcoma.
TL;DR: Much work remains in order to complete the understanding of the somatic mutation basis of osteosarcoma, to develop reliable animal models of human disease, and to apply this information to guide new therapeutic approaches for reducing morbidity and mortality of this rare disease.
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Vitamin E tocotrienols improve insulin sensitivity through activating peroxisome proliferator-activated receptors
TL;DR: Data is presented that tocotrienols within palm oil functioned as PPAR modulators and improved whole body glucose utilization and insulin sensitivity of diabetic Db/Db mice by selectively regulating PPAR target genes, suggesting that PPARs represent a set of molecular targets of tocotrianols.
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Functionalization of PCL-3D electrospun nanofibrous scaffolds for improved BMP2-induced bone formation
Jacob M. Miszuk,Tao Xu,Qingqing Yao,Fang Fang,Josh D. Childs,Zhongkui Hong,Jianning Tao,Hao Fong,Hongli Sun +8 more
TL;DR: In vivo studies showed synergistically enhanced osteogenic differentiation capabilities of C2C12 cells with phenamil was able to generate significantly increased new bone in an ectopic mouse model, suggesting PCL/HA-3D scaffolds act as a favorable synthetic extracellular matrix for bone regeneration.
Journal ArticleDOI
Autophagy deficiency by hepatic FIP200 deletion uncouples steatosis from liver injury in NAFLD.
Di Ma,Matthew M. Molusky,Jianrui Song,Chun-Rui Hu,Fang Fang,Crystal Rui,Anna V. Mathew,Subramaniam Pennathur,Fei Liu,Ji-Xin Cheng,Jun-Lin Guan,Jiandie D. Lin +11 more
TL;DR: It is demonstrated that hepatocyte-specific autophagy deficiency per se does not exacerbate hepatic steatosis and may play a protective role in the liver after exposure to gut-derived endotoxins and its blockade may accelerate nonalcoholic steatohepatitis progression.