Q
Qingjun Tian
Researcher at Johns Hopkins University
Publications - 3
Citations - 144
Qingjun Tian is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Working memory & Hippocampus. The author has an hindex of 3, co-authored 3 publications receiving 120 citations. Previous affiliations of Qingjun Tian include National Institutes of Health.
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Journal ArticleDOI
Working Memory Deficits, Increased Anxiety-Like Traits, and Seizure Susceptibility in BDNF Overexpressing Mice.
Francesco Papaleo,Jill L. Silverman,Jordan Aney,Qingjun Tian,Charlotte L. Barkan,Kathryn K. Chadman,Jacqueline N. Crawley +6 more
TL;DR: It is reported that genetic overexpression of the BDNF mature isoform (BDNF-tg) in female mice impaired working memory functions while sparing components of fear conditioning, indicating detrimental effects of life-long increased BDNF in mice.
Journal ArticleDOI
KCNH2-3.1 expression impairs cognition and alters neuronal function in a model of molecular pathology associated with schizophrenia.
Gregory V. Carr,Jingshan Chen,Feng Yang,Ming Ren,Peixiong Yuan,Qingjun Tian,Audrey Bebensee,Grace Y Zhang,Jing Du,Paul Glineburg,Randy Xun,Omoye Akhile,Daniel Akuma,James Pickel,James C. Barrow,Francesco Papaleo,Daniel R. Weinberger +16 more
TL;DR: Insight is provided into the mechanism of association of KCNH2-3.1 with variation in human cognition and neuronal physiology and may explain its role in schizophrenia.
Journal ArticleDOI
KCNH2-3.1 mediates aberrant complement activation and impaired hippocampal-medial prefrontal circuitry associated with working memory deficits
Ming Ren,Zhonghua Hu,Zhonghua Hu,Qiang Chen,Andrew E. Jaffe,Yingbo Li,Yingbo Li,Vijay Sadashivaiah,Shujuan Zhu,Shujuan Zhu,Nina Rajpurohit,Joo Heon Shin,Wei Xia,Yankai Jia,Jingxian Wu,Jingxian Wu,Sunny Lang Qin,Xinjian Li,Jian Zhu,Qingjun Tian,Daniel Paredes,Fengyu Zhang,Kuan Hong Wang,Venkata S. Mattay,Joseph H. Callicott,Karen F. Berman,Daniel R. Weinberger,Feng Yang,Feng Yang +28 more
TL;DR: The data uncover a previously unrecognized role of the truncated KCNH2-3.1 potassium channel in mediating complement activation, which may explain its association with altered hippocampal–prefrontal connectivity and synaptic function.