scispace - formally typeset
G

Gangqing Hu

Researcher at West Virginia University

Publications -  85
Citations -  5266

Gangqing Hu is an academic researcher from West Virginia University. The author has contributed to research in topics: Medicine & Chromatin. The author has an hindex of 31, co-authored 67 publications receiving 4292 citations. Previous affiliations of Gangqing Hu include National Institutes of Health & Peking University.

Papers
More filters
Journal ArticleDOI

c-Myc Is a Universal Amplifier of Expressed Genes in Lymphocytes and Embryonic Stem Cells

TL;DR: To observe Myc target expression and function in a system where Myc is temporally and physiologically regulated, the transcriptomes and the genome-wide distributions of Myc, RNA polymerase II, and chromatin modifications were compared during lymphocyte activation and in ES cells as well.
Journal ArticleDOI

Expression and regulation of intergenic long noncoding RNAs during T cell development and differentiation

TL;DR: It is found that the lincRNA LincR-Ccr2-5′AS, together with GATA-3, was an essential component of a regulatory circuit in gene expression specific to the TH2 subset of helper T cells and was important for the migration of TH2 cells.
Journal ArticleDOI

The Transcription Factor GATA3 Is Critical for the Development of All IL-7Rα-Expressing Innate Lymphoid Cells

TL;DR: It is reported that GATA3 was indispensable for the development of all IL-7Rα(+) ILC subsets and T cells but was not required for theDevelopment of classical natural killer cells.
Journal ArticleDOI

H2A.Z Facilitates Access of Active and Repressive Complexes to Chromatin in Embryonic Stem Cell Self-renewal and Differentiation

TL;DR: It is proposed that H2A.Z mediates both self-renewal and differentiation of embryonic stem cells by acting as a general facilitator that generates access for a variety of complexes, both activating and repressive.
Journal ArticleDOI

The transcription factor T-bet is induced by multiple pathways and prevents an endogenous Th2 cell program during Th1 cell responses.

TL;DR: It is determined that interleukin-12 and interferon-γ were redundant in inducing T-bet in mice infected with Toxoplasma gondii and that T-Bet did not contribute to its own expression when induced by IL- 12 and IFN-γ, and a critical role of T- Bet in suppressing an endogenous Th2 cell-associated program is revealed.