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Jian Wang

Researcher at Guangzhou Medical University

Publications -  1831
Citations -  76717

Jian Wang is an academic researcher from Guangzhou Medical University. The author has contributed to research in topics: Medicine & Chemistry. The author has an hindex of 94, co-authored 1018 publications receiving 57783 citations. Previous affiliations of Jian Wang include Northwestern University & Johns Hopkins University School of Medicine.

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Genome-wide determination of on-target and off-target characteristics for RNA-guided DNA methylation by dCas9 methyltransferases.

TL;DR: It is proved that dCas9 methyltransferases cause efficient RNA-guided methylation of specific endogenous CpGs and can mediate transient inhibition of gene expression, which might be caused by d Cas9-mediated de novo DNA methylation as well as interference with transcription.
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Mutational spectrum of p53 gene in arsenic-related skin cancers from the blackfoot disease endemic area of Taiwan.

TL;DR: The findings showed that p53 gene mutation rate in arsenic-related skin cancers from the blackfoot disease endemic area of Taiwan is high and that the mutation types are different from those in UV-induced skin cancers.
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Mendelian randomization analyses support causal relationships between blood metabolites and the gut microbiome

TL;DR: Wang et al. as discussed by the authors performed bidirectional Mendelian randomization analyses on 3,432 Chinese individuals with whole-genome, whole-metagenome, anthropometric and blood metabolic trait data.
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Perturbation of MicroRNA‐370/Lin‐28 homolog A/nuclear factor kappa B regulatory circuit contributes to the development of hepatocellular carcinoma

TL;DR: It is reported that miR‐370 was repressed in human hepatocellular carcinoma (HCC) tissues and hepatoma cell lines, and the involvement of a novel regulatory circuit consisting of miR-370, LIN28A, RelA/p65 and IL‐6 in HCC progression is demonstrated.
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Distinct role of heme oxygenase-1 in early- and late-stage intracerebral hemorrhage in 12-month-old mice.

TL;DR: It is concluded that HO-1 activation mediates early brain damage after ICH but promotes neurologic function recovery in the later stage of ICH.