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
Apolipoprotein B messenger RNA editing is developmentally regulated in pig small intestine: Nucleotide comparison of apolipoprotein B editing regions in five species
TL;DR: It is speculated that the regulation of apo B mRNA editing may be developmentally modulated in pig small intestine.
Journal Article
Proposed nomenclature for the catalytic subunit of the mammalian apolipoprotein B mRNA editing enzyme: APOBEC-1.
Nicholas O. Davidson,Thomas L. Innerarity,James F. Scott,Harold C. Smith,Donna M. Driscoll,Ba-Bie Teng,L. Chan +6 more
Journal ArticleDOI
Hepatic gene expression profiling reveals perturbed calcium signaling in a mouse model lacking both LDL receptor and Apobec1 genes
TL;DR: This study demonstrated the global differential gene expression profiles, which are influenced by feeding a high fat diet to LDb mice, and discovered that many genes involved in calcium signaling and bone formation were up regulated.
Journal ArticleDOI
Adipose tissue glyceride synthesis in patients with hyperapobetalipoproteinemia.
TL;DR: The data indicate that fatty acid incorporation into adipose tissue glycerides was twice as rapid in controls as in patients with hyperapobetalipoproteinemia, which may explain the delayed chylomicron triglyceride clearance previously observed in the disorder.
Journal ArticleDOI
Effective Lowering of Plasma, LDL, and Esterified Cholesterol in LDL Receptor–Knockout Mice by Adenovirus-Mediated Gene Delivery of ApoB mRNA Editing Enzyme (Apobec1)
Ba-Bie Teng,Brian Y. Ishida,Trudy M. Forte,Scott Blumenthal,Li Zhen Song,Antonio M. Gotto,Lawrence Chan +6 more
TL;DR: In the absence of a functioning LDL receptor, hepatic overexpression of Apobec1 is highly efficient in lowering plasma apoB-100 levels, leading to the almost complete elimination of LDL particles and a reduction in LDL cholesterol and cholesteryl ester content.