J
Jiaming Wang
Researcher at University of California, San Francisco
Publications - 36
Citations - 3208
Jiaming Wang is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Spontaneously hypertensive rat & Induced pluripotent stem cell. The author has an hindex of 21, co-authored 36 publications receiving 3000 citations.
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Journal ArticleDOI
Identification of Telmisartan as a Unique Angiotensin II Receptor Antagonist With Selective PPARγ–Modulating Activity
Stephen C. Benson,Harrihar A. Pershadsingh,Christopher I. Ho,Amar G. Chittiboyina,Prashant V. Desai,Michal Pravenec,N. Qi,Jiaming Wang,Mitchell A. Avery,Theodore W. Kurtz +9 more
TL;DR: In this paper, the authors showed that telmisartan, a structurally unique angiotensin II receptor antagonist used for the treatment of hypertension, can function as a partial agonist of peroxisome proliferator-activated receptor-gamma (PPARgamma) and reduce glucose, insulin, and triglyceride levels in rats fed a high-fat, high-carbohydrate diet.
Journal ArticleDOI
Seamless gene correction of β-thalassemia mutations in patient-specific iPSCs using CRISPR/Cas9 and piggyBac
TL;DR: This study provides an effective approach to correct HBB mutations without leaving any genetic footprint in patient-derived iPSCs, thereby demonstrating a critical step toward the future application of stem cell-based gene therapy to monogenic diseases.
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Seamless modification of wild-type induced pluripotent stem cells to the natural CCR5Δ32 mutation confers resistance to HIV infection
Lin Ye,Jiaming Wang,Ashley I. Beyer,Fernando Teque,Thomas J. Cradick,Zhongxia Qi,Judy C. Chang,Gang Bao,Marcus O. Muench,Jingwei Yu,Jay A. Levy,Yuet Wai Kan +11 more
TL;DR: For the first time in induced pluripotent stem cells (iPSCs) the efficient and seamless derivation of a homozygous CCR5Δ32 mutation is reported, exactly mimicking the natural mutation, which may provide an approach toward a functional cure of HIV-1 infection.
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Genome editing using CRISPR-Cas9 to create the HPFH genotype in HSPCs: An approach for treating sickle cell disease and β-thalassemia
TL;DR: It is proposed that this strategy of using nonhomologous end joining (NHEJ) to modify the genome may provide an efficient approach toward the development of a safe autologous transplantation for patients with homozygous β-thalassemia and SCD.
Journal ArticleDOI
Linkage of 11 beta-hydroxylase mutations with altered steroid biosynthesis and blood pressure in the Dahl rat.
Cicila Gt,Cicila Gt,Cicila Gt,John P. Rapp,Jiaming Wang,St Lezin E,Ng Sc,Ng Sc,Theodore W. Kurtz +8 more
TL;DR: The robust salt-resistance of the Dahl R rat may be due in part to reduced synthesis of the mineralocorticoid 18-OH-DOC stemming from mutations in the 11β-hydroxylase gene.