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Ming-Jer Tsai

Researcher at Baylor College of Medicine

Publications -  434
Citations -  42119

Ming-Jer Tsai is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Transcription factor & Nuclear receptor. The author has an hindex of 99, co-authored 428 publications receiving 40109 citations. Previous affiliations of Ming-Jer Tsai include Academia Sinica & National Tsing Hua University.

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Molecular mechanisms of action of steroid/thyroid receptor superfamily members

TL;DR: The role of Ligand in RECEPTOR TRANSFORMATION and ACTIVATION is studied, as well as the role of serotonin, which plays a role in both transformation and inhibition.
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Sequence and Characterization of a Coactivator for the Steroid Hormone Receptor Superfamily

TL;DR: Results indicate that SRC-1 encodes a coactivator that is required for full transcriptional activity of the steroid receptor superfamily.
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Steroid receptor coactivator-1 is a histone acetyltransferase

TL;DR: It is shown that SRC-1 possesses intrinsic histone acetyltransferase activity and that it also interacts with another HAT, p300/CBP-associated factor (PCAF), which could be a mechanism by which the activation functions of steroid receptors and associated coactivators enhance formation of a stable preinitiation complex, thereby increasing transcription of specific genes from transcriptionally repressed chromatin templates.
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Diabetes, defective pancreatic morphogenesis, and abnormal enteroendocrine differentiation in BETA2/NeuroD-deficient mice

TL;DR: BETA2 is critical for the normal development of several specialized cell types arising from the gut endoderm, and the absence of these two pancreatic secretagogs may explain the abnormal cellular polarity and inability to secrete zymogen granules in pancreatic acinar exocrine cells.
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A steroid receptor coactivator, SRA, functions as an RNA and is present in an SRC-1 complex.

TL;DR: Functional and mechanistic evidence is provided that SRA acts as an RNA transcript; transfected SRA, unlike other steroid receptor coregulators, functions in the presence of cycloheximide, and SRA mutants containing multiple translational stop signals retain their ability to activate steroid receptor-dependent gene expression.