11979
2014
eng
107
8
article
1
2015-10-05
--
--
High abundance of BDNF within glutamatergic presynapses of cultured hippocampal neurons
In the mammalian brain, the neurotrophin brain-derived neurotrophic factor (BDNF) has emerged as a key factor for synaptic refinement, plasticity and learning. Although BDNF-induced signaling cascades are well known, the spatial aspects of the synaptic BDNF localization remained unclear. Recent data provide strong evidence for an exclusive presynaptic location and anterograde secretion of endogenous BDNF at synapses of the hippocampal circuit. In contrast, various studies using BDNF overexpression in cultured hippocampal neurons support the idea that postsynaptic elements and other dendritic structures are the preferential sites of BDNF localization and release. In this study we used rigorously tested anti-BDNF antibodies and achieved a dense labeling of endogenous BDNF close to synapses. Confocal microscopy showed natural BDNF close to many, but not all glutamatergic synapses, while neither GABAergic synapses nor postsynaptic structures carried a typical synaptic BDNF label. To visualize the BDNF distribution within the fine structure of synapses, we implemented super resolution fluorescence imaging by direct stochastic optical reconstruction microscopy (dSTORM). Two-color dSTORM images of neurites were acquired with a spatial resolution of ~20 nm. At this resolution, the synaptic scaffold proteins Bassoon and Homer exhibit hallmarks of mature synapses and form juxtaposed bars, separated by a synaptic cleft. BDNF imaging signals form granule-like clusters with a mean size of ~60 nm and are preferentially found within the fine structure of the glutamatergic presynapse. Individual glutamatergic presynapses carried up to 90% of the synaptic BDNF immunoreactivity, and only a minor fraction of BDNF molecules was found close to the postsynaptic bars. Our data proof that hippocampal neurons are able to enrich and store high amounts of BDNF in small granules within the mature glutamatergic presynapse, at a principle site of synaptic plasticity.
Frontiers in Cellular Neuroscience
10.3389/fncel.2014.00107
1662-5102
urn:nbn:de:bvb:20-opus-119793
Frontiers in Cellular Neuroscience 8:107. doi:10.3389/fncel.2014.00107
Thomas Andreska
Sarah Aufmkolk
Markus Sauer
Robert Blum
eng
uncontrolled
hippocampal neurons
eng
uncontrolled
synapse structure
eng
uncontrolled
presynapse
eng
uncontrolled
synaptic localization
eng
uncontrolled
BDNF
Humanphysiologie
open_access
Institut für Klinische Neurobiologie
Theodor-Boveri-Institut für Biowissenschaften
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/11979/056_Andreska_Frontieres_in_Cellular_Neuroscience.pdf
12640
2015
eng
3
10
article
1
2016-01-31
--
--
Hypotonic Activation of the Myo-Inositol Transporter SLC5A3 in HEK293 Cells Probed by Cell Volumetry, Confocal and Super-Resolution Microscopy
Swelling-activated pathways for myo-inositol, one of the most abundant organic osmolytes in mammalian cells, have not yet been identified. The present study explores the SLC5A3 protein as a possible transporter of myo-inositol in hyponically swollen HEK293 cells. To address this issue, we examined the relationship between the hypotonicity-induced changes in plasma membrane permeability to myo-inositol Pino [m/s] and expression/localization of SLC5A3. Pino values were determined by cell volumetry over a wide tonicity range (100–275 mOsm) in myo-inositol-substituted solutions. While being negligible under mild hypotonicity (200–275 mOsm), Pino grew rapidly at osmolalities below 200 mOsm to reach a maximum of ∼3 nm/s at 100–125 mOsm, as indicated by fast cell swelling due to myo-inositol influx. The increase in Pino resulted most likely from the hypotonicity-mediated incorporation of cytosolic SLC5A3 into the plasma membrane, as revealed by confocal fluorescence microscopy of cells expressing EGFP-tagged SLC5A3 and super-resolution imaging of immunostained SLC5A3 by direct stochastic optical reconstruction microscopy (dSTORM). dSTORM in hypotonic cells revealed a surface density of membrane-associated SLC5A3 proteins of 200–2000 localizations/μm2. Assuming SLC5A3 to be the major path for myo-inositol, a turnover rate of 80–800 myo-inositol molecules per second for a single transporter protein was estimated from combined volumetric and dSTORM data. Hypotonic stress also caused a significant upregulation of SLC5A3 gene expression as detected by semiquantitative RT-PCR and Western blot analysis. In summary, our data provide first evidence for swelling-mediated activation of SLC5A3 thus suggesting a functional role of this transporter in hypotonic volume regulation of mammalian cells.
PLoS One
10.1371/journal.pone.0119990
urn:nbn:de:bvb:20-opus-126408
PLoS ONE 10(3): e0119990. doi:10.1371/journal.pone.0119990
Joseph Andronic
Ryo Shirakashi
Simone U. Pickel
Katherine M. Westerling
Teresa Klein
Thorge Holm
Markus Sauer
Vladimir L. Sukhorukov
eng
uncontrolled
electrolytes
eng
uncontrolled
isotonic
eng
uncontrolled
membrane proteins
eng
uncontrolled
cell membranes
eng
uncontrolled
hypotonic
eng
uncontrolled
hypotonic solutions
eng
uncontrolled
tonicity
eng
uncontrolled
permeability
Datenverarbeitung; Informatik
Biowissenschaften; Biologie
open_access
Theodor-Boveri-Institut für Biowissenschaften
Förderzeitraum 2015
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/12640/Sukhurokov_journal.pone.0119990.pdf
30114
2022
eng
1
5
article
1
--
--
--
Unraveling the hidden temporal range of fast β2-adrenergic receptor mobility by time-resolved fluorescence
G-protein-coupled receptors (GPCRs) are hypothesized to possess molecular mobility over a wide temporal range. Until now the temporal range has not been fully accessible due to the crucially limited temporal range of available methods. This in turn, may lead relevant dynamic constants to remain masked. Here, we expand this dynamic range by combining fluorescent techniques using a spot confocal setup. We decipher mobility constants of β\(_{2}\)-adrenergic receptor over a wide time range (nanosecond to second). Particularly, a translational mobility (10 µm\(^{2}\)/s), one order of magnitude faster than membrane associated lateral mobility that explains membrane protein turnover and suggests a wider picture of the GPCR availability on the plasma membrane. And a so far elusive rotational mobility (1-200 µs) which depicts a previously overlooked dynamic component that, despite all complexity, behaves largely as predicted by the Saffman-Delbrück model.
Communications Biology
10.1038/s42003-022-03106-4
urn:nbn:de:bvb:20-opus-301140
@articleBalakrishnan.2022, author = Balakrishnan, Ashwin and Hemmen, Katherina and Choudhury, Susobhan and Krohn, Jan-Hagen and Jansen, Kerstin and Friedrich, Mike and Beliu, Gerti and Sauer, Markus and Lohse, Martin J. and Heinze, Katrin G., year = 2022, title = Unraveling the hidden temporal range of fast β2-adrenergic receptor mobility by time-resolved fluorescence, pages = 176, volume = 5, number = 1, journal = Communications biology, doi = 10.1038/s42003-022-03106-4,
md5:b91bf3e582bbbcef85de712c917780fd
2023-01-24T14:33:20+00:00
/tmp/phpUy5lQq
bibtex
63cfec30b3d502.87062320
Communications Biology 2022, 5(1):176. DOI: 10.1038/s42003-022-03106-4
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Ashwin Balakrishnan
Katherina Hemmen
Susobhan Choudhury
Jan-Hagen Krohn
Kerstin Jansen
Mike Friedrich
Gerti Beliu
Markus Sauer
Martin J. Lohse
Katrin G. Heinze
eng
uncontrolled
G-protein-coupled receptors
eng
uncontrolled
molecular mobility
eng
uncontrolled
temporal range
Biowissenschaften; Biologie
open_access
Theodor-Boveri-Institut für Biowissenschaften
Rudolf-Virchow-Zentrum
Förderzeitraum 2022
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/30114/Communications_Balakrishnan.pdf
15936
2017
eng
17627
7
article
1
2018-03-20
--
--
Antibacterial activity of ceramide and ceramide analogs against pathogenic Neisseria
Certain fatty acids and sphingoid bases found at mucosal surfaces are known to have antibacterial activity and are thought to play a more direct role in innate immunity against bacterial infections. Herein, we analysed the antibacterial activity of sphingolipids, including the sphingoid base sphingosine as well as short-chain C\(_{6}\) and long-chain C\(_{16}\)-ceramides and azido-functionalized ceramide analogs against pathogenic Neisseriae. Determination of the minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) demonstrated that short-chain ceramides and a ω-azido-functionalized C\(_{6}\)-ceramide were active against Neisseria meningitidis and N. gonorrhoeae, whereas they were inactive against Escherichia coli and Staphylococcus aureus. Kinetic assays showed that killing of N. meningitidis occurred within 2 h with ω–azido-C\(_{6}\)-ceramide at 1 X the MIC. Of note, at a bactericidal concentration, ω–azido-C\(_{6}\)-ceramide had no significant toxic effect on host cells. Moreover, lipid uptake and localization was studied by flow cytometry and confocal laser scanning microscopy (CLSM) and revealed a rapid uptake by bacteria within 5 min. CLSM and super-resolution fluorescence imaging by direct stochastic optical reconstruction microscopy demonstrated homogeneous distribution of ceramide analogs in the bacterial membrane. Taken together, these data demonstrate the potent bactericidal activity of sphingosine and synthetic short-chain ceramide analogs against pathogenic Neisseriae.
Scientific Reports
10.1038/s41598-017-18071-w
urn:nbn:de:bvb:20-opus-159367
Scientific Reports 7:17627 (2017). DOI: 10.1038/s41598-017-18071-w
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Jérôme Becam
Tim Walter
Anne Burgert
Jan Schlegel
Markus Sauer
Jürgen Seibel
Alexandra Schubert-Unkmeir
eng
uncontrolled
ceramide analogs
eng
uncontrolled
Neisseria
eng
uncontrolled
ceramide
Mikroorganismen, Pilze, Algen
open_access
Institut für Hygiene und Mikrobiologie
Theodor-Boveri-Institut für Biowissenschaften
Institut für Organische Chemie
Förderzeitraum 2017
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/15936/Becam_Scientific_Reports.pdf
26168
2021
eng
1
article
1
2022-03-24
--
--
Fourier Ring Correlation and anisotropic kernel density estimation improve deep learning based SMLM reconstruction of microtubules
Single-molecule super-resolution microscopy (SMLM) techniques like dSTORM can reveal biological structures down to the nanometer scale. The achievable resolution is not only defined by the localization precision of individual fluorescent molecules, but also by their density, which becomes a limiting factor e.g., in expansion microscopy. Artificial deep neural networks can learn to reconstruct dense super-resolved structures such as microtubules from a sparse, noisy set of data points. This approach requires a robust method to assess the quality of a predicted density image and to quantitatively compare it to a ground truth image. Such a quality measure needs to be differentiable to be applied as loss function in deep learning. We developed a new trainable quality measure based on Fourier Ring Correlation (FRC) and used it to train deep neural networks to map a small number of sampling points to an underlying density. Smooth ground truth images of microtubules were generated from localization coordinates using an anisotropic Gaussian kernel density estimator. We show that the FRC criterion ideally complements the existing state-of-the-art multiscale structural similarity index, since both are interpretable and there is no trade-off between them during optimization. The TensorFlow implementation of our FRC metric can easily be integrated into existing deep learning workflows.
Frontiers in Bioinformatics
10.3389/fbinf.2021.752788
urn:nbn:de:bvb:20-opus-261686
publish
Frontiers in Bioinformatics (2021) 1:752788. https://doi.org/10.3389/fbinf.2021.752788
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Andreas Berberich
Andreas Kurz
Sebastian Reinhard
Torsten Johann Paul
Paul Ray Burd
Markus Sauer
Philip Kollmannsberger
eng
uncontrolled
dSTORM
eng
uncontrolled
deep learning–artificial neural network (DL-ANN)
eng
uncontrolled
single molecule localization microscopy
eng
uncontrolled
microtubule cytoskeleton
eng
uncontrolled
super-resolution
Biowissenschaften; Biologie
open_access
Institut für Theoretische Physik und Astrophysik
Theodor-Boveri-Institut für Biowissenschaften
Center for Computational and Theoretical Biology
Förderzeitraum 2021
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/26168/fbinf-01-752788.pdf
31358
2023
eng
8
24
article
1
--
2023-04-14
--
Azido-ceramides, a tool to analyse SARS-CoV-2 replication and inhibition — SARS-CoV-2 is inhibited by ceramides
Recently, we have shown that C6-ceramides efficiently suppress viral replication by trapping the virus in lysosomes. Here, we use antiviral assays to evaluate a synthetic ceramide derivative α-NH2-ω-N3-C6-ceramide (AKS461) and to confirm the biological activity of C6-ceramides inhibiting SARS-CoV-2. Click-labeling with a fluorophore demonstrated that AKS461 accumulates in lysosomes. Previously, it has been shown that suppression of SARS-CoV-2 replication can be cell-type specific. Thus, AKS461 inhibited SARS-CoV-2 replication in Huh-7, Vero, and Calu-3 cells up to 2.5 orders of magnitude. The results were confirmed by CoronaFISH, indicating that AKS461 acts comparable to the unmodified C6-ceramide. Thus, AKS461 serves as a tool to study ceramide-associated cellular and viral pathways, such as SARS-CoV-2 infections, and it helped to identify lysosomes as the central organelle of C6-ceramides to inhibit viral replication.
International Journal of Molecular Sciences
1422-0067
10.3390/ijms24087281
urn:nbn:de:bvb:20-opus-313581
2023-05-05T10:53:15+00:00
sword
swordwue
attachment; filename=deposit.zip
8bdd280ef909181ae72683e6d4825fae
International Journal of Molecular Sciences (2023) 24:8, 7281. https://doi.org/10.3390/ijms24087281
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Daniela Brenner
Nina Geiger
Jan Schlegel
Viktoria Diesendorf
Louise Kersting
Julian Fink
Linda Stelz
Sibylle Schneider-Schaulies
Markus Sauer
Jochen Bodem
Jürgen Seibel
eng
uncontrolled
ceramides
eng
uncontrolled
SARS-CoV-2
eng
uncontrolled
azido-ceramides
eng
uncontrolled
sphingolipids
Medizin und Gesundheit
open_access
Institut für Virologie und Immunbiologie
Theodor-Boveri-Institut für Biowissenschaften
Institut für Organische Chemie
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/31358/ijms-24-07281.pdf
29749
2022
eng
23
14
article
1
--
2022-11-24
--
Glucose and inositol transporters, SLC5A1 and SLC5A3, in glioblastoma cell migration
(1) Background: The recurrence of glioblastoma multiforme (GBM) is mainly due to invasion of the surrounding brain tissue, where organic solutes, including glucose and inositol, are abundant. Invasive cell migration has been linked to the aberrant expression of transmembrane solute-linked carriers (SLC). Here, we explore the role of glucose (SLC5A1) and inositol transporters (SLC5A3) in GBM cell migration. (2) Methods: Using immunofluorescence microscopy, we visualized the subcellular localization of SLC5A1 and SLC5A3 in two highly motile human GBM cell lines. We also employed wound-healing assays to examine the effect of SLC inhibition on GBM cell migration and examined the chemotactic potential of inositol. (3) Results: While GBM cell migration was significantly increased by extracellular inositol and glucose, it was strongly impaired by SLC transporter inhibition. In the GBM cell monolayers, both SLCs were exclusively detected in the migrating cells at the monolayer edge. In single GBM cells, both transporters were primarily localized at the leading edge of the lamellipodium. Interestingly, in GBM cells migrating via blebbing, SLC5A1 and SLC5A3 were predominantly detected in nascent and mature blebs, respectively. (4) Conclusion: We provide several lines of evidence for the involvement of SLC5A1 and SLC5A3 in GBM cell migration, thereby complementing the migration-associated transportome. Our findings suggest that SLC inhibition is a promising approach to GBM treatment.
Cancers
2072-6694
10.3390/cancers14235794
urn:nbn:de:bvb:20-opus-297498
2022-12-15T14:05:29+00:00
sword
swordwue
attachment; filename=deposit.zip
a8a961907ee50b87631a62c07b37ba32
Cancers (2022) 14:23, 5794. https://doi.org/10.3390/cancers14235794
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Philippa K. Brosch
Tessa Korsa
Danush Taban
Patrick Eiring
Sascha Hildebrand
Julia Neubauer
Heiko Zimmermann
Markus Sauer
Ryo Shirakashi
Cholpon S. Djuzenova
Dmitri Sisario
Vladimir L. Sukhorukov
eng
uncontrolled
volume regulation
eng
uncontrolled
transportome
eng
uncontrolled
phlorizin
Medizin und Gesundheit
open_access
Klinik und Poliklinik für Strahlentherapie
Theodor-Boveri-Institut für Biowissenschaften
Import
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/29749/cancers-14-05794-v3.pdf
17657
2018
eng
815
9
article
1
2019-02-13
--
--
The neutral sphingomyelinase 2 is required to polarize and sustain T Cell receptor signaling
By promoting ceramide release at the cytosolic membrane leaflet, the neutral sphingomyelinase 2 (NSM) is capable of organizing receptor and signalosome segregation. Its role in T cell receptor (TCR) signaling remained so far unknown. We now show that TCR-driven NSM activation is dispensable for TCR clustering and initial phosphorylation, but of crucial importance for further signal amplification. In particular, at low doses of TCR stimulatory antibodies, NSM is required for Ca\(^{2+}\) mobilization and T cell proliferation. NSM-deficient T cells lack sustained CD3ζ and ZAP-70 phosphorylation and are unable to polarize and stabilize their microtubular system. We identified PKCζ as the key NSM downstream effector in this second wave of TCR signaling supporting dynamics of microtubule-organizing center (MTOC). Ceramide supplementation rescued PKCζ membrane recruitment and MTOC translocation in NSM-deficient cells. These findings identify the NSM as essential in TCR signaling when dynamic cytoskeletal reorganization promotes continued lateral and vertical supply of TCR signaling components: CD3ζ, Zap70, and PKCζ, and functional immune synapses are organized and stabilized via MTOC polarization.
Frontiers in Immunology
10.3389/fimmu.2018.00815
urn:nbn:de:bvb:20-opus-176572
Frontiers in Immunology 2018, Volume 9, Article 815. DOI: 10.3389/fimmu.2018.00815
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Charlene Börtlein
Annette Draeger
Roman Schoenauer
Alexander Kuhlemann
Markus Sauer
Sybille Schneider-Schaulies
Elita Avota
eng
uncontrolled
neutral sphingomyelinase 2
eng
uncontrolled
T cells
eng
uncontrolled
ceramides
eng
uncontrolled
PKCζ,
eng
uncontrolled
the microtubule-organizing center
Medizin und Gesundheit
open_access
Institut für Virologie und Immunbiologie
Theodor-Boveri-Institut für Biowissenschaften
Förderzeitraum 2018
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/17657/Boertlein_Froniters_in_Immunology.pdf
29944
2022
eng
16
article
1
--
2022-12-14
--
Endogenous tagging of Unc-13 reveals nanoscale reorganization at active zones during presynaptic homeostatic potentiation
Introduction
Neurotransmitter release at presynaptic active zones (AZs) requires concerted protein interactions within a dense 3D nano-hemisphere. Among the complex protein meshwork the (M)unc-13 family member Unc-13 of Drosophila melanogaster is essential for docking of synaptic vesicles and transmitter release.
Methods
We employ minos-mediated integration cassette (MiMIC)-based gene editing using GFSTF (EGFP-FlAsH-StrepII-TEV-3xFlag) to endogenously tag all annotated Drosophila Unc-13 isoforms enabling visualization of endogenous Unc-13 expression within the central and peripheral nervous system.
Results and discussion
Electrophysiological characterization using two-electrode voltage clamp (TEVC) reveals that evoked and spontaneous synaptic transmission remain unaffected in unc-13\(^{GFSTF}\) 3rd instar larvae and acute presynaptic homeostatic potentiation (PHP) can be induced at control levels. Furthermore, multi-color structured-illumination shows precise co-localization of Unc-13\(^{GFSTF}\), Bruchpilot, and GluRIIA-receptor subunits within the synaptic mesoscale. Localization microscopy in combination with HDBSCAN algorithms detect Unc-13\(^{GFSTF}\) subclusters that move toward the AZ center during PHP with unaltered Unc-13\(^{GFSTF}\) protein levels.
Frontiers in Cellular Neuroscience
1662-5102
10.3389/fncel.2022.1074304
urn:nbn:de:bvb:20-opus-299440
2023-01-18T06:19:17+00:00
sword
swordwue
attachment; filename=deposit.zip
b2865a404dcc65a1e7608966b766fbf7
Frontiers in Cellular Neuroscience (2022) 16:1074304. doi:10.3389/fncel.2022.1074304
false
true
Sven Dannhäuser
Achmed Mrestani
Florian Gundelach
Martin Pauli
Fabian Komma
Philip Kollmannsberger
Markus Sauer
Manfred Heckmann
Mila M. Paul
eng
uncontrolled
active zone
eng
uncontrolled
Unc-13
eng
uncontrolled
MiMIC
eng
uncontrolled
presynaptic homeostasis
eng
uncontrolled
nanoarchitecture
eng
uncontrolled
localization microscopy
eng
uncontrolled
STORM
eng
uncontrolled
HDBSCAN
Medizin und Gesundheit
open_access
Physiologisches Institut
Klinik und Poliklinik für Psychiatrie, Psychosomatik und Psychotherapie
Klinik und Poliklinik für Unfall-, Hand-, Plastische und Wiederherstellungschirurgie (Chirurgische Klinik II)
Theodor-Boveri-Institut für Biowissenschaften
Import
Center for Computational and Theoretical Biology
Förderzeitraum 2022
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/29944/fncel-16-1074304.pdf
20181
2019
eng
1294
10
article
1
2020-03-16
--
--
Measles virus infection fosters dendritic cell motility in a 3D environment to enhance transmission to target cells in the respiratory epithelium
Transmission of measles virus (MV) from dendritic to airway epithelial cells is considered as crucial to viral spread late in infection. Therefore, pathways and effectors governing this process are promising targets for intervention. To identify these, we established a 3D respiratory tract model where MV transmission by infected dendritic cells (DCs) relied on the presence of nectin-4 on H358 lung epithelial cells. Access to recipient cells is an important prerequisite for transmission, and we therefore analyzed migration of MV-exposed DC cultures within the model. Surprisingly, enhanced motility toward the epithelial layer was observed for MV-infected DCs as compared to their uninfected siblings. This occurred independently of factors released from H358 cells indicating that MV infection triggered cytoskeletal remodeling associated with DC polarization enforced velocity. Accordingly, the latter was also observed for MV-infected DCs in collagen matrices and was particularly sensitive to ROCK inhibition indicating infected DCs preferentially employed the amoeboid migration mode. This was also implicated by loss of podosomes and reduced filopodial activity both of which were retained in MV-exposed uninfected DCs. Evidently, sphingosine kinase (SphK) and sphingosine-1-phosphate (S1P) as produced in response to virus-infection in DCs contributed to enhanced velocity because this was abrogated upon inhibition of sphingosine kinase activity. These findings indicate that MV infection promotes a push-and-squeeze fast amoeboid migration mode via the SphK/S1P system characterized by loss of filopodia and podosome dissolution. Consequently, this enables rapid trafficking of virus toward epithelial cells during viral exit.
Frontiers in Immunology
10.3389/fimmu.2019.01294
urn:nbn:de:bvb:20-opus-201818
Frontiers in Immunology 2019, 10:1294. doi: 10.3389/fimmu.2019.01294
false
true
CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International
Shaghayegh Derakhshani
Andreas Kurz
Lukasz Japtok
Fabian Schumacher
Lisa Pilgram
Maria Steinke
Burkhard Kleuser
Markus Sauer
Sibylle Schneider-Schaulies
Elita Avota
eng
uncontrolled
dendritic cell
eng
uncontrolled
cell migration
eng
uncontrolled
measles virus
eng
uncontrolled
3D tissue model
eng
uncontrolled
sphingosine-1-phosphate
Medizin und Gesundheit
open_access
Institut für Virologie und Immunbiologie
Theodor-Boveri-Institut für Biowissenschaften
Lehrstuhl für Tissue Engineering und Regenerative Medizin
Förderzeitraum 2019
Universität Würzburg
https://opus.bibliothek.uni-wuerzburg.de/files/20181/Avota_fimmu-10-01294.pdf