---
_id: '6049'
abstract:
- lang: eng
text: 'In this article it is shown that large systems with many interacting units
endowing multiple phases display self-oscillations in the presence of linear feedback
between the control and order parameters, where an Andronov–Hopf bifurcation takes
over the phase transition. This is simply illustrated through the mean field Landau
theory whose feedback dynamics turn out to be described by the Van der Pol equation
and it is then validated for the fully connected Ising model following heat bath
dynamics. Despite its simplicity, this theory accounts potentially for a rich
range of phenomena: here it is applied to describe in a stylized way (i) excess
demand-price cycles due to strong herding in a simple agent-based market model;
(ii) congestion waves in queuing networks triggered by user feedback to delays
in overloaded conditions; and (iii) metabolic network oscillations resulting from
cell growth control in a bistable phenotypic landscape.'
article_number: '045002'
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Daniele
full_name: De Martino, Daniele
id: 3FF5848A-F248-11E8-B48F-1D18A9856A87
last_name: De Martino
orcid: 0000-0002-5214-4706
citation:
ama: 'De Martino D. Feedback-induced self-oscillations in large interacting systems
subjected to phase transitions. Journal of Physics A: Mathematical and Theoretical.
2019;52(4). doi:10.1088/1751-8121/aaf2dd'
apa: 'De Martino, D. (2019). Feedback-induced self-oscillations in large interacting
systems subjected to phase transitions. Journal of Physics A: Mathematical
and Theoretical. IOP Publishing. https://doi.org/10.1088/1751-8121/aaf2dd'
chicago: 'De Martino, Daniele. “Feedback-Induced Self-Oscillations in Large Interacting
Systems Subjected to Phase Transitions.” Journal of Physics A: Mathematical
and Theoretical. IOP Publishing, 2019. https://doi.org/10.1088/1751-8121/aaf2dd.'
ieee: 'D. De Martino, “Feedback-induced self-oscillations in large interacting systems
subjected to phase transitions,” Journal of Physics A: Mathematical and Theoretical,
vol. 52, no. 4. IOP Publishing, 2019.'
ista: 'De Martino D. 2019. Feedback-induced self-oscillations in large interacting
systems subjected to phase transitions. Journal of Physics A: Mathematical and
Theoretical. 52(4), 045002.'
mla: 'De Martino, Daniele. “Feedback-Induced Self-Oscillations in Large Interacting
Systems Subjected to Phase Transitions.” Journal of Physics A: Mathematical
and Theoretical, vol. 52, no. 4, 045002, IOP Publishing, 2019, doi:10.1088/1751-8121/aaf2dd.'
short: 'D. De Martino, Journal of Physics A: Mathematical and Theoretical 52 (2019).'
date_created: 2019-02-24T22:59:19Z
date_published: 2019-01-07T00:00:00Z
date_updated: 2023-08-24T14:49:23Z
day: '07'
ddc:
- '570'
department:
- _id: GaTk
doi: 10.1088/1751-8121/aaf2dd
ec_funded: 1
external_id:
isi:
- '000455379500001'
file:
- access_level: open_access
checksum: 1112304ad363a6d8afaeccece36473cf
content_type: application/pdf
creator: kschuh
date_created: 2019-04-19T12:18:57Z
date_updated: 2020-07-14T12:47:17Z
file_id: '6344'
file_name: 2019_IOP_DeMartino.pdf
file_size: 1804557
relation: main_file
file_date_updated: 2020-07-14T12:47:17Z
has_accepted_license: '1'
intvolume: ' 52'
isi: 1
issue: '4'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: 'Journal of Physics A: Mathematical and Theoretical'
publication_status: published
publisher: IOP Publishing
quality_controlled: '1'
scopus_import: '1'
status: public
title: Feedback-induced self-oscillations in large interacting systems subjected to
phase transitions
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 52
year: '2019'
...
---
_id: '6091'
abstract:
- lang: eng
text: Cortical networks are characterized by sparse connectivity, with synapses
found at only a subset of axo-dendritic contacts. Yet within these networks, neurons
can exhibit high connection probabilities, suggesting that cell-intrinsic factors,
not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a
factor that determines synapse density by mediating a cell-cell competition that
requires ephrin-B-EphB signaling. In a microisland culture system designed to
isolate cell-cell competition, we find that eB3 determines winning and losing
neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM)
genetic mouse model system in vivo the relative levels of eB3 control spine density
in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls
synapse density independently of action potential-driven activity. Our findings
illustrate a new class of competitive mechanism mediated by trans-synaptic organizing
proteins which control the number of synapses neurons receive relative to neighboring
neurons.
article_number: e41563
article_processing_charge: No
author:
- first_name: Nathan T.
full_name: Henderson, Nathan T.
last_name: Henderson
- first_name: Sylvain J.
full_name: Le Marchand, Sylvain J.
last_name: Le Marchand
- first_name: Martin
full_name: Hruska, Martin
last_name: Hruska
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Matthew B.
full_name: Dalva, Matthew B.
last_name: Dalva
citation:
ama: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. Ephrin-B3
controls excitatory synapse density through cell-cell competition for EphBs. eLife.
2019;8. doi:10.7554/eLife.41563
apa: Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L.,
& Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through
cell-cell competition for EphBs. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.41563
chicago: Henderson, Nathan T., Sylvain J. Le Marchand, Martin Hruska, Simon Hippenmeyer,
Liqun Luo, and Matthew B. Dalva. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/eLife.41563.
ieee: N. T. Henderson, S. J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, and
M. B. Dalva, “Ephrin-B3 controls excitatory synapse density through cell-cell
competition for EphBs,” eLife, vol. 8. eLife Sciences Publications, 2019.
ista: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. 2019.
Ephrin-B3 controls excitatory synapse density through cell-cell competition for
EphBs. eLife. 8, e41563.
mla: Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife, vol. 8, e41563, eLife
Sciences Publications, 2019, doi:10.7554/eLife.41563.
short: N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B.
Dalva, ELife 8 (2019).
date_created: 2019-03-10T22:59:20Z
date_published: 2019-02-21T00:00:00Z
date_updated: 2023-08-24T14:50:50Z
day: '21'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.41563
external_id:
isi:
- '000459380600001'
pmid:
- '30789343'
file:
- access_level: open_access
checksum: 7b0800d003f14cd06b1802dea0c52941
content_type: application/pdf
creator: dernst
date_created: 2019-03-11T16:15:37Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6098'
file_name: 2019_eLife_Henderson.pdf
file_size: 7260753
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ephrin-B3 controls excitatory synapse density through cell-cell competition
for EphBs
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2019'
...
---
_id: '6046'
abstract:
- lang: eng
text: Sudden stress often triggers diverse, temporally structured gene expression
responses in microbes, but it is largely unknown how variable in time such responses
are and if genes respond in the same temporal order in every single cell. Here,
we quantified timing variability of individual promoters responding to sublethal
antibiotic stress using fluorescent reporters, microfluidics, and time‐lapse microscopy.
We identified lower and upper bounds that put definite constraints on timing variability,
which varies strongly among promoters and conditions. Timing variability can be
interpreted using results from statistical kinetics, which enable us to estimate
the number of rate‐limiting molecular steps underlying different responses. We
found that just a few critical steps control some responses while others rely
on dozens of steps. To probe connections between different stress responses, we
then tracked the temporal order and response time correlations of promoter pairs
in individual cells. Our results support that, when bacteria are exposed to the
antibiotic nitrofurantoin, the ensuing oxidative stress and SOS responses are
part of the same causal chain of molecular events. In contrast, under trimethoprim,
the acid stress response and the SOS response are part of different chains of
events running in parallel. Our approach reveals fundamental constraints on gene
expression timing and provides new insights into the molecular events that underlie
the timing of stress responses.
acknowledged_ssus:
- _id: Bio
article_number: e8470
article_processing_charge: No
author:
- first_name: Karin
full_name: Mitosch, Karin
id: 39B66846-F248-11E8-B48F-1D18A9856A87
last_name: Mitosch
- first_name: Georg
full_name: Rieckh, Georg
id: 34DA8BD6-F248-11E8-B48F-1D18A9856A87
last_name: Rieckh
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Mitosch K, Rieckh G, Bollenbach MT. Temporal order and precision of complex
stress responses in individual bacteria. Molecular systems biology. 2019;15(2).
doi:10.15252/msb.20188470
apa: Mitosch, K., Rieckh, G., & Bollenbach, M. T. (2019). Temporal order and
precision of complex stress responses in individual bacteria. Molecular Systems
Biology. Embo Press. https://doi.org/10.15252/msb.20188470
chicago: Mitosch, Karin, Georg Rieckh, and Mark Tobias Bollenbach. “Temporal Order
and Precision of Complex Stress Responses in Individual Bacteria.” Molecular
Systems Biology. Embo Press, 2019. https://doi.org/10.15252/msb.20188470.
ieee: K. Mitosch, G. Rieckh, and M. T. Bollenbach, “Temporal order and precision
of complex stress responses in individual bacteria,” Molecular systems biology,
vol. 15, no. 2. Embo Press, 2019.
ista: Mitosch K, Rieckh G, Bollenbach MT. 2019. Temporal order and precision of
complex stress responses in individual bacteria. Molecular systems biology. 15(2),
e8470.
mla: Mitosch, Karin, et al. “Temporal Order and Precision of Complex Stress Responses
in Individual Bacteria.” Molecular Systems Biology, vol. 15, no. 2, e8470,
Embo Press, 2019, doi:10.15252/msb.20188470.
short: K. Mitosch, G. Rieckh, M.T. Bollenbach, Molecular Systems Biology 15 (2019).
date_created: 2019-02-24T22:59:18Z
date_published: 2019-02-14T00:00:00Z
date_updated: 2023-08-24T14:49:53Z
day: '14'
department:
- _id: GaTk
doi: 10.15252/msb.20188470
external_id:
isi:
- '000459628300003'
pmid:
- '30765425'
intvolume: ' 15'
isi: 1
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/30765425
month: '02'
oa: 1
oa_version: Submitted Version
pmid: 1
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
grant_number: RGP0042/2013
name: Revealing the fundamental limits of cell growth
publication: Molecular systems biology
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Temporal order and precision of complex stress responses in individual bacteria
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 15
year: '2019'
...
---
_id: '6105'
abstract:
- lang: eng
text: " Hosts can alter their strategy towards pathogens during their lifetime;
that is, they can show phenotypic plasticity in immunity or life history. Immune
priming is one such example, where a previous encounter with a pathogen confers
enhanced protection upon secondary challenge, resulting in reduced pathogen load
(i.e., resistance) and improved host survival. However, an initial encounter might
also enhance tolerance, particularly to less virulent opportunistic pathogens
that establish persistent infections. In this scenario, individuals are better
able to reduce the negative fecundity consequences that result from a high pathogen
burden. Finally, previous exposure may also lead to life‐history adjustments,
such as terminal investment into reproduction.\r\n Using different Drosophila
melanogaster host genotypes and two bacterial pathogens, Lactococcus lactis and
Pseudomonas entomophila, we tested whether previous exposure results in resistance
or tolerance and whether it modifies immune gene expression during an acute‐phase
infection (one day post‐challenge). We then asked whether previous pathogen exposure
affects chronic‐phase pathogen persistence and longer‐term survival (28 days post‐challenge).\r\n
\ We predicted that previous exposure would increase host resistance to an early
stage bacterial infection while it might come at a cost to host fecundity tolerance.
We reasoned that resistance would be due in part to stronger immune gene expression
after challenge. We expected that previous exposure would improve long‐term survival,
that it would reduce infection persistence, and we expected to find genetic variation
in these responses.\r\n We found that previous exposure to P. entomophila weakened
host resistance to a second infection independent of genotype and had no effect
on immune gene expression. Fecundity tolerance showed genotypic variation but
was not influenced by previous exposure. However, L. lactis persisted as a chronic
infection, whereas survivors cleared the more pathogenic P. entomophila infection.\r\n
\ To our knowledge, this is the first study that addresses host tolerance to
bacteria in relation to previous exposure, taking a multi‐faceted approach to
address the topic. Our results suggest that previous exposure comes with transient
costs to resistance during the early stage of infection in this host–pathogen
system and that infection persistence may be bacterium‐specific.\r\n"
article_processing_charge: No
article_type: original
author:
- first_name: Megan
full_name: Kutzer, Megan
id: 29D0B332-F248-11E8-B48F-1D18A9856A87
last_name: Kutzer
orcid: 0000-0002-8696-6978
- first_name: Joachim
full_name: Kurtz, Joachim
last_name: Kurtz
- first_name: Sophie A.O.
full_name: Armitage, Sophie A.O.
last_name: Armitage
citation:
ama: Kutzer M, Kurtz J, Armitage SAO. A multi-faceted approach testing the effects
of previous bacterial exposure on resistance and tolerance. Journal of Animal
Ecology. 2019;88(4):566-578. doi:10.1111/1365-2656.12953
apa: Kutzer, M., Kurtz, J., & Armitage, S. A. O. (2019). A multi-faceted approach
testing the effects of previous bacterial exposure on resistance and tolerance.
Journal of Animal Ecology. Wiley. https://doi.org/10.1111/1365-2656.12953
chicago: Kutzer, Megan, Joachim Kurtz, and Sophie A.O. Armitage. “A Multi-Faceted
Approach Testing the Effects of Previous Bacterial Exposure on Resistance and
Tolerance.” Journal of Animal Ecology. Wiley, 2019. https://doi.org/10.1111/1365-2656.12953.
ieee: M. Kutzer, J. Kurtz, and S. A. O. Armitage, “A multi-faceted approach testing
the effects of previous bacterial exposure on resistance and tolerance,” Journal
of Animal Ecology, vol. 88, no. 4. Wiley, pp. 566–578, 2019.
ista: Kutzer M, Kurtz J, Armitage SAO. 2019. A multi-faceted approach testing the
effects of previous bacterial exposure on resistance and tolerance. Journal of
Animal Ecology. 88(4), 566–578.
mla: Kutzer, Megan, et al. “A Multi-Faceted Approach Testing the Effects of Previous
Bacterial Exposure on Resistance and Tolerance.” Journal of Animal Ecology,
vol. 88, no. 4, Wiley, 2019, pp. 566–78, doi:10.1111/1365-2656.12953.
short: M. Kutzer, J. Kurtz, S.A.O. Armitage, Journal of Animal Ecology 88 (2019)
566–578.
date_created: 2019-03-17T22:59:15Z
date_published: 2019-04-01T00:00:00Z
date_updated: 2023-08-25T08:04:53Z
day: '01'
ddc:
- '570'
department:
- _id: SyCr
doi: 10.1111/1365-2656.12953
ec_funded: 1
external_id:
isi:
- '000467994800007'
file:
- access_level: open_access
checksum: 405cde15120de26018b3bd0dfa29986c
content_type: application/pdf
creator: dernst
date_created: 2019-03-18T07:43:06Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6107'
file_name: 2019_JournalAnimalEcology_Kutzer.pdf
file_size: 1460662
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 88'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 566-578
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Journal of Animal Ecology
publication_identifier:
eissn:
- '13652656'
issn:
- '00218790'
publication_status: published
publisher: Wiley
quality_controlled: '1'
related_material:
record:
- id: '9806'
relation: research_data
status: public
scopus_import: '1'
status: public
title: A multi-faceted approach testing the effects of previous bacterial exposure
on resistance and tolerance
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 88
year: '2019'
...
---
_id: '6088'
abstract:
- lang: eng
text: P-Glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) are two
efflux transporters at the blood–brain barrier (BBB), which effectively restrict
brain distribution of diverse drugs, such as tyrosine kinase inhibitors. There
is a crucial need for pharmacological ABCB1 and ABCG2 inhibition protocols for
a more effective treatment of brain diseases. In the present study, seven marketed
drugs (osimertinib, erlotinib, nilotinib, imatinib, lapatinib, pazopanib, and
cyclosporine A) and one nonmarketed drug (tariquidar), with known in vitro ABCB1/ABCG2
inhibitory properties, were screened for their inhibitory potency at the BBB in
vivo. Positron emission tomography (PET) using the model ABCB1/ABCG2 substrate
[11C]erlotinib was performed in mice. Tested inhibitors were administered as i.v.
bolus injections at 30 min before the start of the PET scan, followed by a continuous
i.v. infusion for the duration of the PET scan. Five of the tested drugs increased
total distribution volume of [11C]erlotinib in the brain (VT,brain) compared to
vehicle-treated animals (tariquidar, + 69%; erlotinib, + 19% and +23% for the
21.5 mg/kg and the 43 mg/kg dose, respectively; imatinib, + 22%; lapatinib, +
25%; and cyclosporine A, + 49%). For all drugs, increases in [11C]erlotinib brain
distribution were lower than in Abcb1a/b(−/−)Abcg2(−/−) mice (+149%), which suggested
that only partial ABCB1/ABCG2 inhibition was reached at the mouse BBB. The plasma
concentrations of the tested drugs at the time of the PET scan were higher than
clinically achievable plasma concentrations. Some of the tested drugs led to significant
increases in blood radioactivity concentrations measured at the end of the PET
scan (erlotinib, + 103% and +113% for the 21.5 mg/kg and the 43 mg/kg dose, respectively;
imatinib, + 125%; and cyclosporine A, + 101%), which was most likely caused by
decreased hepatobiliary excretion of radioactivity. Taken together, our data suggest
that some marketed tyrosine kinase inhibitors may be repurposed to inhibit ABCB1
and ABCG2 at the BBB. From a clinical perspective, moderate increases in brain
delivery despite the administration of high i.v. doses as well as peripheral drug–drug
interactions due to transporter inhibition in clearance organs question the translatability
of this concept.
article_processing_charge: No
author:
- first_name: Alexander
full_name: Traxl, Alexander
last_name: Traxl
- first_name: Severin
full_name: Mairinger, Severin
last_name: Mairinger
- first_name: Thomas
full_name: Filip, Thomas
last_name: Filip
- first_name: Michael
full_name: Sauberer, Michael
last_name: Sauberer
- first_name: Johann
full_name: Stanek, Johann
last_name: Stanek
- first_name: Stefan
full_name: Poschner, Stefan
last_name: Poschner
- first_name: Walter
full_name: Jäger, Walter
last_name: Jäger
- first_name: Viktoria
full_name: Zoufal, Viktoria
last_name: Zoufal
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
- first_name: Nicolas
full_name: Tournier, Nicolas
last_name: Tournier
- first_name: Martin
full_name: Bauer, Martin
last_name: Bauer
- first_name: Thomas
full_name: Wanek, Thomas
last_name: Wanek
- first_name: Oliver
full_name: Langer, Oliver
last_name: Langer
citation:
ama: Traxl A, Mairinger S, Filip T, et al. Inhibition of ABCB1 and ABCG2 at the
mouse blood-brain barrier with marketed drugs to improve brain delivery of the
model ABCB1/ABCG2 substrate [11C]erlotinib. Molecular Pharmaceutics. 2019;16(3):1282-1293.
doi:10.1021/acs.molpharmaceut.8b01217
apa: Traxl, A., Mairinger, S., Filip, T., Sauberer, M., Stanek, J., Poschner, S.,
… Langer, O. (2019). Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier
with marketed drugs to improve brain delivery of the model ABCB1/ABCG2 substrate
[11C]erlotinib. Molecular Pharmaceutics. American Chemical Society. https://doi.org/10.1021/acs.molpharmaceut.8b01217
chicago: Traxl, Alexander, Severin Mairinger, Thomas Filip, Michael Sauberer, Johann
Stanek, Stefan Poschner, Walter Jäger, et al. “Inhibition of ABCB1 and ABCG2 at
the Mouse Blood-Brain Barrier with Marketed Drugs to Improve Brain Delivery of
the Model ABCB1/ABCG2 Substrate [11C]Erlotinib.” Molecular Pharmaceutics.
American Chemical Society, 2019. https://doi.org/10.1021/acs.molpharmaceut.8b01217.
ieee: A. Traxl et al., “Inhibition of ABCB1 and ABCG2 at the mouse blood-brain
barrier with marketed drugs to improve brain delivery of the model ABCB1/ABCG2
substrate [11C]erlotinib,” Molecular Pharmaceutics, vol. 16, no. 3. American
Chemical Society, pp. 1282–1293, 2019.
ista: Traxl A, Mairinger S, Filip T, Sauberer M, Stanek J, Poschner S, Jäger W,
Zoufal V, Novarino G, Tournier N, Bauer M, Wanek T, Langer O. 2019. Inhibition
of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed drugs to improve
brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib. Molecular Pharmaceutics.
16(3), 1282–1293.
mla: Traxl, Alexander, et al. “Inhibition of ABCB1 and ABCG2 at the Mouse Blood-Brain
Barrier with Marketed Drugs to Improve Brain Delivery of the Model ABCB1/ABCG2
Substrate [11C]Erlotinib.” Molecular Pharmaceutics, vol. 16, no. 3, American
Chemical Society, 2019, pp. 1282–93, doi:10.1021/acs.molpharmaceut.8b01217.
short: A. Traxl, S. Mairinger, T. Filip, M. Sauberer, J. Stanek, S. Poschner, W.
Jäger, V. Zoufal, G. Novarino, N. Tournier, M. Bauer, T. Wanek, O. Langer, Molecular
Pharmaceutics 16 (2019) 1282–1293.
date_created: 2019-03-10T22:59:19Z
date_published: 2019-03-04T00:00:00Z
date_updated: 2023-08-25T08:02:51Z
day: '04'
department:
- _id: GaNo
doi: 10.1021/acs.molpharmaceut.8b01217
external_id:
isi:
- '000460600400031'
pmid:
- '30694684'
intvolume: ' 16'
isi: 1
issue: '3'
language:
- iso: eng
month: '03'
oa_version: None
page: 1282-1293
pmid: 1
publication: Molecular Pharmaceutics
publication_status: published
publisher: American Chemical Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed
drugs to improve brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 16
year: '2019'
...