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Alexander Nolze

Researcher at Martin Luther University of Halle-Wittenberg

Publications -  9
Citations -  95

Alexander Nolze is an academic researcher from Martin Luther University of Halle-Wittenberg. The author has contributed to research in topics: Vascular smooth muscle & Endothelial dysfunction. The author has an hindex of 4, co-authored 8 publications receiving 61 citations.

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FMRP regulates actin filament organization via the armadillo protein p0071

TL;DR: It is shown that FMRP regulates actin organization and neurite outgrowth via the armadillo protein p0071, and impaired actin cytoskeletal functions mediated by an excess of p00 71 are key aspects underlying the fragile X syndrome.
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Identification of a novel lncRNA induced by the nephrotoxin ochratoxin A and expressed in human renal tumor tissue.

TL;DR: WISP1-AS1 is a novel lncRNA with modulatory transcriptional function and the potential to alter the cellular phenotype in situations of stress or oncogenic transformation, however, its precise mode of action and impact on cellular functions require further investigations.
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Activated mineralocorticoid receptor regulates micro-RNA-29b in vascular smooth muscle cells

TL;DR: The findings provide novel insights into the molecular mechanism of aldosterone‐mediated vascular pathogenesis by identifying miR‐29b as a pathophysiologic relevant target of activated MR in VSMCs and by highlighting the importance of miR processing for miR regulation.
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Weighted Correlation Network Analysis Reveals CDK2 as a Regulator of a Ubiquitous Environmental Toxin-Induced Cell-Cycle Arrest.

TL;DR: Differential expression analyses revealed that OTA led to the regulation of gene expression in kidney human cell lines, including for genes enriched in cell cycle-related pathways, and OTA-induced gap 1 and 2 (G1 and G2) cell-cycle arrests were observed.
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Knockout of vascular smooth muscle EGF receptor in a mouse model prevents obesity-induced vascular dysfunction and renal damage in vivo

TL;DR: It is proposed that a potentiated EGFR/ErbB2–ROCK–MRTF–SRF signalling axis and mitochondrial dysfunction underlie the role of EGFR and may be a therapeutic target in cases of type 2 diabetes-induced renovascular disease.