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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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Identification of Telmisartan as a Unique Angiotensin II Receptor Antagonist With Selective PPARγ–Modulating Activity

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.
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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

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.
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Linkage of 11 beta-hydroxylase mutations with altered steroid biosynthesis and blood pressure in the Dahl rat.

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.