• NEWS

Publication 2019 Jan: UBQLN4 Represses Homologous Recombination and Is Overexpressed in Aggressive Tumors. https://www.ncbi.nlm.nih
.gov/pubmed/30612738

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Publication 2018 Oct: The Cdkn1aSUPER Mouse as a Tool to Study p53-Mediated Tumor Suppression. https://www.ncbi.nlm.
nih.gov/pubmed/30355482

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Publication 2018 June:
Evaluation of small
intestinal damage in
a rat model of 6 Minutes
cardiac arrest.
https://www.ncbi.nlm.nih
.gov/pubmed/29866034

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Publication 2018 May:
A Hierarchical, Data-Driven
Approach to Modeling
Single-Cell Populations
Predicts Latent Causes of
Cell-To-Cell Variability.
https://www.ncbi.nlm.
snih.gov/pubmed/29730254

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Publication 2018 April: PKA-RII subunit phosphorylation precedes activation by cAMP and regulates activity termination.
https://www.ncbi.nlm.
nih.gov/pubmed/
29615473

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Publication 2017 July: Characterization of tumor-associated T-lymphocyte subsets and immune checkpoint molecules in head and neck squamous cell carcinoma. https://www.ncbi.nlm.
nih.gov /pubmed/
28574843

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Publication 2017 May: Crosstalk from cAMP to ERK1/2
emerges during postnatal
maturation of nociceptive neurons
and is maintained
during aging.
https://www.ncbi.nlm.
nih.gov/pubmed/28515230

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Publication 2017 May: HCS-Mikroskopie
– ein Schlüssel zu intrazellulären
Schmerzmechanismen
http://link.springer.com
/article/10.1007/s12268-017-0796-2

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Publication 2017 Feb: Ankyrin-rich membrane spanning protein as a novel modulator of transient receptor potential vanilloid 1-function in nociceptive neurons.
https://www.ncbi.nlm
.nih.gov/pubmed/
28182310

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Publication 2017 Jan: Synergistic regulation of serotonin and opioid signaling contributes to pain insensitivity in Nav1.7 knockout mice.
https://www.ncbi.nlm.
nih.gov/pubmed/
28074005

 

 

 

 

Intracellular Signaling Rules Over Pain Sensitization

Pain, who doesn’t know it? Well, but what is pain really? Even though pain is with us for long during evolution, our understanding of pain and also our abilities to counteract pain are still rather limited.

One problem central for the clinical practice is, that pain sensitivity is highly plastic and can change drastically. Patients are not in pain because they experience constantly strong physical insults. Instead, the pain sensitivity is altered. Thereby, for example, otherwise non- or only slightly-painful stimuli such as the pulsing of the arteries or body movements induce full-fledged pain.

My group is focused on the molecular and cellular mechanisms altering pain sensitivity. In contrast to many, we are neither focusing on sensitizing inputs such as extracellular mediators nor onto the ion channel based output structures. Instead, we are trying to understand, how the intracellular signaling machinery in between receptor input and ion channel output is coding for pain sensitivity.

The challenge is, that currently there are only few cellular correlates of pain sensitization known beyond ion channel mediated aspects. We therefore currently establish signaling finger prints for pain sensitization. We pursue this by having established as one of the first labs (if not the first lab) a quantitative automated microscopy approach for pain research. This now allows us to investigate the fully quantitative, single cell based analysis of signaling kinetics of endogenous signaling cascades in primary sensory neurons.

Investigating the cell biology of pain and using systems biological tools we continue to unravel novel aspects of pain, some of which we are already translating into novel clinical therapies.