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Xiaoju Hu

Researcher at Rutgers University

Publications -  16
Citations -  453

Xiaoju Hu is an academic researcher from Rutgers University. The author has contributed to research in topics: Gene & Medicine. The author has an hindex of 9, co-authored 12 publications receiving 300 citations. Previous affiliations of Xiaoju Hu include Chinese Academy of Sciences.

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Systematic identification and characterization of long intergenic non-coding RNAs in fetal porcine skeletal muscle development

TL;DR: It is found that the porcine lincRNAs were preferentially located near genes mediating transcriptional regulation rather than those with developmental functions, which indicates that the functions of these genes in the skeletal muscle developmental process are under investigation.
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Non-Genetic Intra-Tumor Heterogeneity Is a Major Predictor of Phenotypic Heterogeneity and Ongoing Evolutionary Dynamics in Lung Tumors

TL;DR: Analysis of ITH in lung squamous cell carcinoma at the levels of genome, transcriptome, and tumor-immune interactions and histopathological characteristics by multi-region bulk and single-cell sequencing suggests that non-genetic heterogeneity is a major determinant of heterogeneity in histopathology characteristics and impacts evolutionary dynamics in lung cancer.
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The Genome Landscape of Tibetan Sheep Reveals Adaptive Introgression from Argali and the History of Early Human Settlements on the Qinghai-Tibetan Plateau.

TL;DR: The genomic variation in Tibetan sheep is investigated using whole-genome sequences, single nucleotide polymorphism arrays, mitochondrial DNA, and Y-chromosomal variants in 986 samples throughout their distribution range to contribute to a depth understanding of early pastoralism and the local adaptation of Tibetan sheep as well as the late-Holocene human occupation of the QTP.
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Mutational signature SBS8 predominantly arises due to late replication errors in cancer

TL;DR: Analyzing somatic mutation data from multiple cancer types in their epigenomic contexts, it is shown that SBS8 preferentially occurs in gene-poor, lamina-proximal, late replicating heterochromatin domains and likely arises from late replication errors during cancer progression.