B
Ba-Bie Teng
Researcher at University of Texas Health Science Center at Houston
Publications - 62
Citations - 9858
Ba-Bie Teng is an academic researcher from University of Texas Health Science Center at Houston. The author has contributed to research in topics: Apolipoprotein B & RNA editing. The author has an hindex of 34, co-authored 62 publications receiving 9237 citations. Previous affiliations of Ba-Bie Teng include Texas Medical Center & University of Chicago.
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Journal ArticleDOI
Induction of apoptosis in BPH stromal cells by adenoviral-mediated overexpression of caspase-7.
Marco Marcelli,T.C. Shao,Xiaoying Li,Heather Yin,Michela Marani,Larry Denner,Ba-Bie Teng,Glenn R. Cunningham +7 more
TL;DR: It is hypothesized that expression/activity of critical components of the apoptotic pathway can be used to induce apoptosis of a human prostate cell line derived from benign prostatic hyperplasia (BPH) tissue and it is postulated that overexpression and activation of a type II caspase should cause apoptosis.
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Epac1 (Exchange Protein Directly Activated by cAMP 1) Upregulates LOX-1 (Oxidized Low-Density Lipoprotein Receptor 1) to Promote Foam Cell Formation and Atherosclerosis Development.
William G. Robichaux,Fang C Mei,Wenli Yang,Hui Wang,Hua Sun,Zhen Zhou,Dianna M. Milewicz,Ba-Bie Teng,Xiaodong Cheng +8 more
TL;DR: This study demonstrates a fundamental role of cAMP/Epac1 signaling in vascular remodeling by promoting ox-LDL uptake and foam cell formation during atherosclerotic lesion development and represents a promising, unexplored therapeutic target for atherosclerosis.
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Fortilin reduces apoptosis in macrophages and promotes atherosclerosis.
TL;DR: Testing the hypothesis that fortilin in and of itself facilitates atherosclerosis by protecting macrophages against apoptosis found that anti-fortilin therapy may represent a promising next generation antiatherosclerotic therapeutic strategy.
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Maximum immunobioactivity of murine small intestinal intraepithelial lymphocytes resides in a subpopulation of CD43+ T cells.
TL;DR: DNA microarray analyses showed that S7+ IELs expressed higher levels of genes associated with activated T cells, whereas S7− Iels expressed genes used in the regulation of NK cells, and these findings define two functionally distinct populations of IELS based on CD43 expression independent of TCR class.
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Paradoxical Upregulation of Tumor Suppressor Protein p53 in Serum-Stimulated Vascular Smooth Muscle Cells A Novel Negative-Feedback Regulatory Mechanism
TL;DR: Through the mediation of p21WAF1/CIP1 and Bax, the induced p53 protein negatively regulates the growth of dividing VSMCs, thereby minimizing the inappropriate accumulation ofVSMCs.