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Article ; Online: The SARS-CoV-2 main protease M

Wenzel, Jan / Lampe, Josephine / Müller-Fielitz, Helge / Schuster, Raphael / Zille, Marietta / Müller, Kristin / Krohn, Markus / Körbelin, Jakob / Zhang, Linlin / Özorhan, Ümit / Neve, Vanessa / Wagner, Julian U G / Bojkova, Denisa / Shumliakivska, Mariana / Jiang, Yun / Fähnrich, Anke / Ott, Fabian / Sencio, Valentin / Robil, Cyril /

Pfefferle, Susanne / Sauve, Florent / Coêlho, Caio Fernando Ferreira / Franz, Jonas / Spiecker, Frauke / Lembrich, Beate / Binder, Sonja / Feller, Nina / König, Peter / Busch, Hauke / Collin, Ludovic / Villaseñor, Roberto / Jöhren, Olaf / Altmeppen, Hermann C / Pasparakis, Manolis / Dimmeler, Stefanie / Cinatl, Jindrich / Püschel, Klaus / Zelic, Matija / Ofengeim, Dimitry / Stadelmann, Christine / Trottein, François / Nogueiras, Ruben / Hilgenfeld, Rolf / Glatzel, Markus / Prevot, Vincent / Schwaninger, Markus

Nature neuroscience

2021 Volume 24, Issue 11, Page(s) 1522–1533

Abstract: ... We obtained evidence that brain endothelial cells are infected and that the main protease of SARS-CoV-2 (M ...

Abstract	Coronavirus disease 2019 (COVID-19) can damage cerebral small vessels and cause neurological symptoms. Here we describe structural changes in cerebral small vessels of patients with COVID-19 and elucidate potential mechanisms underlying the vascular pathology. In brains of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected individuals and animal models, we found an increased number of empty basement membrane tubes, so-called string vessels representing remnants of lost capillaries. We obtained evidence that brain endothelial cells are infected and that the main protease of SARS-CoV-2 (M
MeSH term(s)	Animals ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/pathology ; Brain/metabolism ; Brain/pathology ; Chlorocebus aethiops ; Coronavirus 3C Proteases/genetics ; Coronavirus 3C Proteases/metabolism ; Cricetinae ; Female ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Male ; Mesocricetus ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microvessels/metabolism ; Microvessels/pathology ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism ; Vero Cells
Chemical Substances	Intracellular Signaling Peptides and Proteins ; NEMO protein, mouse ; Coronavirus 3C Proteases (EC 3.4.22.28)
Language	English
Publishing date	2021-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-021-00926-1
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Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 67: Show issues

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Article ; Online: Inducing Z-DNA overcomes immune checkpoint blockade resistance.

Jiao, Huipeng / Pasparakis, Manolis

Cell research

2022 Volume 32, Issue 10, Page(s) 871–872

MeSH term(s)	DNA, Z-Form ; Immune Checkpoint Inhibitors ; Immunotherapy ; Programmed Cell Death 1 Receptor
Chemical Substances	DNA, Z-Form ; Immune Checkpoint Inhibitors ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2022-07-30
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	1319303-x
ISSN	1748-7838 ; 1001-0602
ISSN (online)	1748-7838
ISSN	1001-0602
DOI	10.1038/s41422-022-00705-y
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Zs.A 5283: Show issues

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Article: Metabolic cost of osmoregulation by the gastro-intestinal tract in marine teleost fish.

Little, A / Pasparakis, C / Stieglitz, J / Grosell, M

Frontiers in physiology

2023 Volume 14, Page(s) 1163153

Abstract: Introduction: ...

Abstract	Introduction:
Language	English
Publishing date	2023-04-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2023.1163153
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Article ; Online: IKKε and TBK1 prevent RIPK1 dependent and independent inflammation.

Eren, Remzi Onur / Kaya, Göksu Gökberk / Schwarzer, Robin / Pasparakis, Manolis

Nature communications

2024 Volume 15, Issue 1, Page(s) 130

Abstract: TBK1 and IKKε regulate multiple cellular processes including anti-viral type-I interferon responses, metabolism and TNF receptor signaling. However, the relative contributions and potentially redundant functions of IKKε and TBK1 in cell death, ... ...

Abstract	TBK1 and IKKε regulate multiple cellular processes including anti-viral type-I interferon responses, metabolism and TNF receptor signaling. However, the relative contributions and potentially redundant functions of IKKε and TBK1 in cell death, inflammation and tissue homeostasis remain poorly understood. Here we show that IKKε compensates for the loss of TBK1 kinase activity to prevent RIPK1-dependent and -independent inflammation in mice. Combined inhibition of IKKε and TBK1 kinase activities caused embryonic lethality that was rescued by heterozygous expression of kinase-inactive RIPK1. Adult mice expressing kinase-inactive versions of IKKε and TBK1 developed systemic inflammation that was induced by both RIPK1-dependent and -independent mechanisms. Combined inhibition of IKKε and TBK1 kinase activities in myeloid cells induced RIPK1-dependent cell death and systemic inflammation mediated by IL-1 family cytokines. Tissue-specific studies showed that IKKε and TBK1 were required to prevent cell death and inflammation in the intestine but were dispensable for liver and skin homeostasis. Together, these findings revealed that IKKε and TBK1 exhibit tissue-specific functions that are important to prevent cell death and inflammation and maintain tissue homeostasis.
MeSH term(s)	Animals ; Mice ; I-kappa B Kinase/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Phosphorylation ; Cytokines/metabolism ; Inflammation
Chemical Substances	I-kappa B Kinase (EC 2.7.11.10) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Cytokines
Language	English
Publishing date	2024-01-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44372-y
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Article ; Conference proceedings: A Mavs-induced type I IFN pathway contributes to non-viral liver injury upon hepatic autophagy impairment

Schneider, Farina / Lüdde, Tom / Pasparakis, Manolis / Kondylis, Evangelos

Zeitschrift für Gastroenterologie

2024 Volume 62, Issue 01

Event/congress	40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber, Haus der Technik e.V., Essen, 2024-01-26
Language	German
Publishing date	2024-01-01
Publisher	Georg Thieme Verlag
Publishing place	Stuttgart ; New York
Document type	Article ; Conference proceedings
ZDB-ID	201387-3
ISSN	1439-7803 ; 0044-2771 ; 0172-8504
ISSN (online)	1439-7803
ISSN	0044-2771 ; 0172-8504
DOI	10.1055/s-0043-1777503
Database	Thieme publisher's database

In stock of ZB MED Cologne/Königswinter

Zs.A 111: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.A 111/X: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Polymer coated gold nanoshells for combinational photochemotherapy of pancreatic cancer with gemcitabine.

Emamzadeh, Mina / Pasparakis, George

Scientific reports

2021 Volume 11, Issue 1, Page(s) 9404

Abstract: Pancreatic cancer is one of the most lethal malignancies with limited therapeutic options and dismal prognosis. Gemcitabine is the front-line drug against pancreatic cancer however with limited improvement of therapeutic outcomes. In this study we ... ...

Abstract	Pancreatic cancer is one of the most lethal malignancies with limited therapeutic options and dismal prognosis. Gemcitabine is the front-line drug against pancreatic cancer however with limited improvement of therapeutic outcomes. In this study we envisaged the integration of GEM with gold nanoshells which constitute an interesting class of nanomaterials with excellent photothermal conversion properties. Nanoshells were coated with thiol-capped poly(ethylene glycol) methacrylate polymers of different molecular weight via Au-S attachment. It was found that the molecular weight of the polymers affects the in vitro performance of the formulations; more importantly we demonstrate that the EC
MeSH term(s)	Antimetabolites, Antineoplastic/administration & dosage ; Cell Line, Tumor ; Deoxycytidine/administration & dosage ; Deoxycytidine/analogs & derivatives ; Drug Screening Assays, Antitumor ; Gold ; Humans ; Nanoshells/chemistry ; Pancreatic Neoplasms/drug therapy ; Photochemotherapy ; Polymers ; Gemcitabine
Chemical Substances	Antimetabolites, Antineoplastic ; Polymers ; Deoxycytidine (0W860991D6) ; Gold (7440-57-5) ; Gemcitabine
Language	English
Publishing date	2021-04-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-88909-x
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Article ; Online: Physiological Responses of Fish to Oil Spills.

Grosell, Martin / Pasparakis, Christina

Annual review of marine science

2020 Volume 13, Page(s) 137–160

Abstract: Millions of tons of oil are spilled in aquatic environments every decade, and this oil has the potential to greatly impact fish populations. Here, we review available information on the physiological effects of oil and polycyclic aromatic hydrocarbons on ...

Abstract	Millions of tons of oil are spilled in aquatic environments every decade, and this oil has the potential to greatly impact fish populations. Here, we review available information on the physiological effects of oil and polycyclic aromatic hydrocarbons on fish. Oil toxicity affects multiple biological systems, including cardiac function, cholesterol biosynthesis, peripheral and central nervous system function, the stress response, and osmoregulatory and acid-base balance processes. We propose that cholesterol depletion may be a significant contributor to impacts on cardiac, neuronal, and synaptic function as well as reduced cortisol production and release. Furthermore, it is possible that intracellular calcium homeostasis-a part of cardiotoxic and neuronal function that is affected by oil exposure-may be related to cholesterol depletion. A detailed understanding of oil impacts and affected physiological processes is emerging, but knowledge of their combined effects on fish in natural habitats is largely lacking. We identify key areas deserving attention in future research.
MeSH term(s)	Animals ; Ecosystem ; Fishes/physiology ; Heart/drug effects ; Nervous System/drug effects ; Oxidative Stress/drug effects ; Petroleum/analysis ; Petroleum/toxicity ; Petroleum Pollution/analysis ; Polycyclic Aromatic Hydrocarbons/analysis ; Polycyclic Aromatic Hydrocarbons/toxicity ; Water Pollutants, Chemical/analysis ; Water Pollutants, Chemical/toxicity
Chemical Substances	Petroleum ; Polycyclic Aromatic Hydrocarbons ; Water Pollutants, Chemical
Language	English
Publishing date	2020-08-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2458404-6
ISSN	1941-0611 ; 1941-1405
ISSN (online)	1941-0611
ISSN	1941-1405
DOI	10.1146/annurev-marine-040120-094802
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Article ; Online: Role of the cardiovascular system in ammonia excretion in early life stages of zebrafish (

Wang, Y / Pasparakis, C / Grosell, M

American journal of physiology. Regulatory, integrative and comparative physiology

2021 Volume 321, Issue 3, Page(s) R377–R384

Abstract: The purpose of this study was to investigate if the cardiovascular system is important for ammonia excretion in the early life stages of zebrafish. Morpholino knockdowns of cardiac troponin T (TNNT2) or vascular endothelial growth factor A (VEGFA) ... ...

Abstract	The purpose of this study was to investigate if the cardiovascular system is important for ammonia excretion in the early life stages of zebrafish. Morpholino knockdowns of cardiac troponin T (TNNT2) or vascular endothelial growth factor A (VEGFA) provided morphants with nonfunctional circulation. At the embryonic stage [30-36 h postfertilization (hpf)], ammonia excretion was not constrained by a lack of cardiovascular function. At 2 days postfertilization (dpf) and 4 dpf, morpholino knockdowns of TNNT2 or VEGFA significantly reduced ammonia excretion in all morphants. Expression of
MeSH term(s)	Animals ; Cardiovascular System/metabolism ; Cation Transport Proteins/genetics ; Gills/metabolism ; Membrane Glycoproteins/metabolism ; Membrane Transport Proteins/metabolism ; Urea/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Zebrafish/metabolism ; Zebrafish Proteins/metabolism ; Urea Transporters
Chemical Substances	Cation Transport Proteins ; Membrane Glycoproteins ; Membrane Transport Proteins ; Vascular Endothelial Growth Factor A ; Zebrafish Proteins ; Urea (8W8T17847W)
Language	English
Publishing date	2021-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00284.2020
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Uc I Zs.89: Show issues

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Article ; Online: NEMO- and RelA-dependent NF-κB signaling promotes small cell lung cancer.

Koerner, Lioba / Schmiel, Marcel / Yang, Tsun-Po / Peifer, Martin / Buettner, Reinhard / Pasparakis, Manolis

Cell death and differentiation

2023 Volume 30, Issue 4, Page(s) 938–951

Abstract: Small cell lung cancer (SCLC) is an aggressive type of lung cancer driven by combined loss of the tumor suppressors RB1 and TP53. SCLC is highly metastatic and despite good initial response to chemotherapy patients usually relapse, resulting in poor ... ...

Abstract	Small cell lung cancer (SCLC) is an aggressive type of lung cancer driven by combined loss of the tumor suppressors RB1 and TP53. SCLC is highly metastatic and despite good initial response to chemotherapy patients usually relapse, resulting in poor survival. Therefore, better understanding of the mechanisms driving SCLC pathogenesis is required to identify new therapeutic targets. Here we identified a critical role of the IKK/NF-κB signaling pathway in SCLC development. Using a relevant mouse model of SCLC, we found that ablation of NEMO/IKKγ, the regulatory subunit of the IKK complex that is essential for activation of canonical NF-κB signaling, strongly delayed the onset and growth of SCLC resulting in considerably prolonged survival. In addition, ablation of the main NF-κB family member p65/RelA also delayed the onset and growth of SCLC and prolonged survival, albeit to a lesser extent than NEMO. Interestingly, constitutive activation of IKK/NF-κB signaling within the tumor cells did not exacerbate the pathogenesis of SCLC, suggesting that endogenous NF-κB levels are sufficient to fully support tumor development. Moreover, TNFR1 deficiency did not affect the development of SCLC, showing that TNF signaling does not play an important role in this tumor type. Taken together, our results revealed that IKK/NF-κB signaling plays an important role in promoting SCLC, identifying the IKK/NF-κB pathway as a promising therapeutic target.
MeSH term(s)	Animals ; Mice ; I-kappa B Kinase/genetics ; I-kappa B Kinase/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Lung Neoplasms/genetics ; NF-kappa B/metabolism ; Signal Transduction ; Small Cell Lung Carcinoma/genetics
Chemical Substances	I-kappa B Kinase (EC 2.7.11.10) ; Intracellular Signaling Peptides and Proteins ; NEMO protein, mouse ; NF-kappa B ; Rela protein, mouse
Language	English
Publishing date	2023-01-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-023-01112-5
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Zs.A 4230: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 80: Show issues

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Article ; Online: Smooth muscle cell specific NEMO deficiency inhibits atherosclerosis in ApoE

Imai, Takashi / Van, Trieu-My / Pasparakis, Manolis / Polykratis, Apostolos

Scientific reports

2022 Volume 12, Issue 1, Page(s) 12538

Abstract: The development of atherosclerotic plaques is the result of a chronic inflammatory response coordinated by stromal and immune cellular components of the vascular wall. While endothelial cells and leukocytes are well-recognised mediators of inflammation ... ...

Abstract	The development of atherosclerotic plaques is the result of a chronic inflammatory response coordinated by stromal and immune cellular components of the vascular wall. While endothelial cells and leukocytes are well-recognised mediators of inflammation in atherosclerosis, the role of smooth muscle cells (SMCs) remains incompletely understood. Here we aimed to address the role of canonical NF-κB signalling in SMCs in the development of atherosclerosis. We investigated the role of NF-κB signalling in SMCs in atherosclerosis by employing SMC-specific ablation of NEMO, an IKK complex subunit that is essential for canonical NF-κB activation, in ApoE
MeSH term(s)	Animals ; Apolipoproteins E/metabolism ; Atherosclerosis/pathology ; Endothelial Cells/metabolism ; Inflammation/pathology ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Smooth Muscle/metabolism ; NF-kappa B/metabolism ; Plaque, Atherosclerotic/pathology
Chemical Substances	Apoe protein, mouse ; Apolipoproteins E ; Intracellular Signaling Peptides and Proteins ; NEMO protein, mouse ; NF-kappa B
Language	English
Publishing date	2022-07-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-16737-8
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