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Thomas Günther

Researcher at Heinrich Pette Institute

Publications -  82
Citations -  5828

Thomas Günther is an academic researcher from Heinrich Pette Institute. The author has contributed to research in topics: Gene & Viral replication. The author has an hindex of 30, co-authored 69 publications receiving 5056 citations. Previous affiliations of Thomas Günther include Max Planck Society & Baylor College of Medicine.

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LSD1 demethylates repressive histone marks to promote androgen-receptor-dependent transcription.

TL;DR: It is shown that lysine-specific demethylase 1 co-localizes with the androgen receptor in normal human prostate and prostate tumour and pargyline is identified as an inhibitor of LSD1, providing a mechanism by which demethylases control specific gene expression.
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Cooperative demethylation by JMJD2C and LSD1 promotes androgen receptor-dependent gene expression.

TL;DR: The Jumonji C (JMJC) domain-containing protein JMJD2C is identified as the first histone tridemethylase regulating androgen receptor function and suggests that specific gene regulation requires the assembly and coordinate action of demethylases with distinct substrate specificities.
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Genetic ablation of parathyroid glands reveals another source of parathyroid hormone.

TL;DR: Gcm2 deletion uncovers an auxiliary mechanism for the regulation of calcium homeostasis in the absence of parathyroid glands, and it is proposed that this backup mechanism may be a general feature of endocrine regulation.
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The expression of the mouse zic1, zic2, and zic3 gene suggests an essential role for zic genes in body pattern formation

TL;DR: Zic genes are the vertebrate homologues of Drosophila odd-paired, which may play an essential role in parasegmental subdivision and in visceral mesoderm development and analysis of gene expression patterns in different mouse mutants indicated that Zic genes may act upstream of many known developmental regulatory genes.
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Phosphorylation of histone H3T6 by PKCβ I controls demethylation at histone H3K4

TL;DR: In this paper, the authors show that phosphorylation of histone H3 at threonine 6 (H3T6) by protein kinase C beta I (PKCbeta(I), also known as PRKCbeta) is the key event that prevents LSD1 from demethylating H3K4 during AR-dependent gene activation.