8 Papers
1 Citations
Qi Yang is an academic researcher from Sunnybrook Health Sciences Centre. The author has contributed to research in topics: Biology & Medicine. The author has an hindex of 3, co-authored 3 publications. Previous affiliations of Qi Yang include University of Toronto.
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Papers
A Circular RNA Binds To and Activates AKT Phosphorylation and Nuclear Localization Reducing Apoptosis and Enhancing Cardiac Repair.
Yan Zeng,William W. Du,William W. Du,Yingya Wu,Yingya Wu,Zhenguo Yang,Zhenguo Yang,Faryal Mehwish Awan,Faryal Mehwish Awan,Xiangmin Li,Xiangmin Li,Weining Yang,Chao Zhang,Chao Zhang,Qi Yang,Qi Yang,Albert Yee,Albert Yee,Yu Chen,Fenghua Yang,Huan Sun,Ren Huang,Albert Yee,Ren-Ke Li,Zhong-Kai Wu,Peter H. Backx,Peter H. Backx,Burton B. Yang,Burton B. Yang +28 more
TL;DR: It is concluded that circ-Amotl1 physically binds to both PDK1 and AKT1, facilitating the cardio-protective nuclear translocation of pAKT.
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A circular RNA promotes tumorigenesis by inducing c-myc nuclear translocation.
Qi Yang,William W. Du,William W. Du,Nan Wu,Nan Wu,Weining Yang,Faryal Mehwish Awan,Faryal Mehwish Awan,Ling Fang,Ling Fang,Ling Fang,Jian Ma,Jian Ma,Xiangmin Li,Xiangmin Li,Yan Zeng,Yan Zeng,Zhenguo Yang,Zhenguo Yang,Jun Dong,Jun Dong,Azam Khorshidi,Azam Khorshidi,Burton B. Yang,Burton B. Yang +24 more
TL;DR: A novel function of circRNAs in tumorigenesis is revealed, and this subclass of noncoding RNAs may represent a potential target in cancer therapy.
[MiR-30e-5p overexpression promotes proliferation and migration of colorectal cancer cells by activating the CXCL12 axis via downregulating PTEN].
TL;DR: Overexpression of miR-30e-5p promotes the malignant behaviors of colorectal cancer cells by downregulating PTEN to activate the CXCL12 axis.
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[Interference of CTPS gene promotes toosendanin-induced apoptosis of human gastric cancer MKN-45 cells].
TL;DR: Investigation of the effect of interference of CTPS gene on toosendanin-induced apoptosis of gastric cancer MKN-45 cells suggested that CTPS was highly expressed in human Gastric cancer tissues, and gastric cancers patients with high CTPSGene expression had a shorter overall survival.
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Gain and loss of function variants in EZH1 disrupt neurogenesis timing and cause overlapping neurodevelopmental disorders
C. Gracia-Diaz,Yi Zhou,Qi Yang,C.-H. Lee,P. Espana-Bonilla,S. Zhang,Natalia Padilla,Raquel Fueyo,G. Otrimski,D. Li,Shaoline Sheppard,Paul R. Mark,Margaret Harr,Hakon Hakonarson,Lance H. Rodan,Angus W. Jackson,Prabhakaran Vasudevan,Charles C. Powel,Shekeeb S Mohammed,Sateesh Maddirevula,H. Alzaidan,Eissa Faqeih,Stephanie Efthymiou,Valentina Turchetti,Fahmia Rahman,Sundus Naila Maqbool,Vincenzo Salpietro,Samar H. Ibrahim,Gabriella Di Rosa,Henry Houlden,Conchi Estarás,Anna C.E. Hurst,A. Thompson,Anna Chassevent,Constance Smith-Hicks,X. De La Cruz,Anja Holtz,Erin Torti,M. J. Hajianpour,Claudine Rieubland,Daniela A. Braun,Siddharth Banka,G. England Consortium +42 more
TL;DR: This work identifies EZH1 LOF and GOF variants as the genetic basis of previously undefined NDDs and uncovers an essential role of EZh1 in regulating the timing of neurogenesis, which is consistent with a pathogenic effect.
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