Martin Etzrodt

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The mechanisms underlying haematopoietic lineage decisions remain disputed. Lineage-affiliated transcription factors with the capacity for lineage reprogramming, positive auto-regulation and mutual inhibition have been described as being expressed in uncommitted cell populations. This led to the assumption that lineage choice is cell-intrinsically initiated(More)
703 gaps in auto-tracking results or to analyze images manually when (semi-) automatic methods fail. They also provide no or only limited support to track cells over multiple overlapping fields of view. CellProfiler17 can handle large amounts of multi-dimensional image data, but lacks interfaces for manual curation and further analysis of results. We(More)
Understanding the molecular control of cell fates is central to stem cell research. Such insight requires quantification of molecular and cellular behavior at the single-cell level. Recent advances now permit high-throughput molecular readouts from single cells as well as continuous, noninvasive observation of cell behavior over time. Here, we review(More)
Hematopoiesis is the cumulative consequence of finely tuned signaling pathways activated through extrinsic factors, such as local niche signals and systemic hematopoietic cytokines. Whether extrinsic factors actively instruct the lineage choice of hematopoietic stem and progenitor cells or are only selectively allowing survival and proliferation of already(More)
Open microfluidic cell culturing devices offer new possibilities to simplify loading, culturing, and harvesting of individual cells or microtissues due to the fact that liquids and cells/microtissues are directly accessible. We present a complete workflow for microfluidic handling and culturing of individual cells and microtissue spheroids, which is based(More)
Cells receive a multitude of signals from the environment, but how they process simultaneous signaling inputs is not well understood. Response to infection, for example, involves parallel activation of multiple Toll-like receptors (TLRs) that converge on the nuclear factor κB (NF-κB) pathway. Although we increasingly understand inflammatory responses for(More)
Presenilin 1 (PSEN1) mutations are the main cause of monogenic Alzheimer's disease. We studied the functional effects of the mutation K239N, which shows incomplete penetrance at the age of 65 years and compared it with the more aggressive mutation E120G. We engineered stable cell lines expressing human PSEN1 wild type or with K239N or E120G mutations. Both(More)
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