Cell News 01/2017
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MEETING REPORT
The workshop on “G protein-coupled receptors” was introduced
by Daniel Legler (Kreuzlingen, Switzerland) who demonstrated
the importance of CCR7 (C-C chemokine receptor type 7) and
its ligands, the cytokines CCL19 and CCL21 for migration of
adaptive immune cells. Following CCR7-CCL19/CCL21-mediated
signaling pathways, Prof. Legler pointed out that imbalanced
regulations of these complexes contribute to pathophysiolog-
ical developments such as chronic inflammation, autoimmune
diseases, and tumorigenesis.
Reinhold Förster (Hannover) addressed his keynote talk in the
workshop “Signaling in Infection and Inflammation”. He focused
on homing of immune cells to the lymph node. Following in-
tra-lymphatic vessel injection in vivo, Prof. Förster demonstrated
T cell migration in afferent lymphatic vessels to enter the outer
lymph node sinus and relocate from the sub-capsular sinus to
the lymph node parenchyma which also depends on functional
G protein-coupled receptor signaling in T cells.
Tobias Dansen (Utrecht, The Netherlands) presented a keynote
talk in the workshop „Receptor and Redox Signaling“ where-
by he introduced the pathways of reversible oxidation upon
bridging and disrupting specific thiol side chains in appropriate
receptors and proteins. For example, the formation of reversible
disulfide-dependent protein-protein interactions and accompa-
nying conformational changes serve as a signaling pathway in
addition or alternative to phosphorylation cascades.
In the workshop “Differentiation, Stress and Death” Ute Moll
(New York/Göttingen) focused on new functional aspects of p53
family proteins including the structural homologues p63 and
p73. In her keynote lecture Prof. Moll highlighted effects on p53
activation during cellular stress such as hypoxia, oxidative stress
and generation of reactive oxygen species (ROS), telomere attri-
tion, replicative senescence, or DNA damage. Activation of p53
occurs after disruption of MDM2 and MDM4 interactions and
a paralleled Ser15 and Ser20 phosphorylation of p53 via ATM/
ATR and CHK1/CHK2 kinases, respectively. Regulatory responses
of activated p53 include cell cycle arrest with subsequent DNA
repair, senescence and apoptosis. Moreover, p53 activation
stimulates signaling within the tumor microenvironment, inhib-
its invasion and metastasis, activates autophagy, and inhibits the
reprogramming of differentiated cells back to stem cells (retrodif-
ferentiation) among others.
All keynote lectures were followed by a number of short talks
selected from the submitted abstracts. Here, the mixture of pre-
sentations given by group leaders, post-doctoral fellows and also a
number of PhD students was highly appreciated as a unique feature
of the STS meetings.
As one of the traditions during these meetings since 2010, the STS
honors an outstanding scientist in the field of signal transduction
research to conclude the workshop program with a “Honorary
Medal Lecture”. The STS/CCS Honorary Medal was introduced by
the STS in cooperation with the open access journal “Cell Commu-
nication and Signaling” (CCS). Following Tony Pawson (
) in 2010,
Tony Hunter in 2011, Carl-Henrik Heldin in 2012, Klaus Rajewsky in
2013, the Nobel prize winner Jules Hoffmann in 2014, Mina Bissell
in 2015, it was Tak Wah Mak from Toronto, Canada, who received
the 2016 STS/CCS Honorary medal. The laudatio was given by Klaus
Pfeffer (Düsseldorf), one of Prof. Mak’s former postdocs.
Prof. Mak was honored with the STS/CCS medal for his seminal
and pioneering immunological and cell biological research work.
He was the lead scientist of the group that cloned the genes of
the human T cell receptor (TCR), and thus unraveled the molecular
basis of cellular immunity. In order to address individual signaling
steps in lymphocyte activation and differentiation, his laboratory
generated a whole set of mouse strains lacking various surface
receptors or kinases, phosphatases or adapter proteins involved in
signal transduction through the TCR complex. A second major focus
of Prof. Mak’s work is the biology of programmed cell death. His
laboratory significantly contributed to our present understanding of
the bifunctionality of death receptors and the control of apoptot-
ic pathways in different cellular entities by caspases or adapter
proteins. More recently, Prof. Mak has devoted his research to
investigating the pathogenesis of cancer. As a new and promising
concept to identify potential targets for novel cancer therapeutics,
he focuses on understanding mechanisms of “metabolic transfor-
mation”. This Honorary Medal Lecture was very much appreciated
by the audience.
Another important aspect of the STS joint meeting has always
been the support of young scientists. At the occasion of the
20
th
anniversary meeting, the STS grant committee selected 15
Bachelor/Master or MD/PhD students to receive travel grants
of 3,750.--
€
in total to support their meeting attendance.
Ten travel grants were provided by the STS and additional five
travel awards were sponsored by industrial partners. The 2016
STS Science Award of 1,000.--
€
, sponsored again by BIOMOL
GmbH was received by Melanie Brinkmann (Braunschweig), who
presented data on the murine cytomegalovirus protein M35 as a
novel negative regulator of type I interferon response. Moreover,
all participants selected by the chair people for poster presentation
Travel grants awarded to young scientists at the STS meeting 2016
