Author

M. Bader

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Physiology· 2 Animal Behavior & Cognition· 1 Cell Biology· 1 Microbiology· 1 Pharmacology & Toxicology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 5 Organism:mouse· 5 Research Focus:host-pathogen & immune response· 4 Assay:proteomics· 3 Research Focus:cell type annotation· 2 Organism:human· 2 Organism:rat· 2 Assay:behavioral assay· 1

Frequent Co-Authors

N. Alenina· 3 shared A. F. Rodrigues· 2 shared L. Rodrigues-Ribeiro· 2 shared T. Verano-Braga· 2 shared A. A. Peluso· 1 shared A. C. Ventris-Godoy· 1 shared A. d. A. Silva· 1 shared A. D. de Kloet· 1 shared

Activity by Year

2020-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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3 shared papersPhysiology

N. Alenina

Mutual co-authors in cluster

Author profile →

6 papers

Recent·Most cited

Identification and characterization of alamandine-(1-5), a new component of the Renin-Angiotensin System with unique properties

M. T. S. Dias, S. C. d. A. Goncalves, F. A. da Silva, L. Rodrigues-Ribeiro, K. S. Ferraz, S. Scalzo, M. F Itaborahy, N. P. Soares, D. A. Alves Pereira, P. A. S. Vaz de Castro, J. B. R. Dutra, C. F. Barros, U. F. Vieira-Machado, I. Feng, A. C. Ventris-Godoy, , Ville

This study identifies and characterizes alamandine-(1-5), a new RAS component with unique biological activities and increased plasma concentration in nephropathic patients.

bioRxiv · Apr 27, 2024 · PreprintPhysiology

Angiotensin-(1-5) is a Potent Endogenous Angiotensin AT2-Receptor Agonist

I. M. Souza-Silva, A. A. Peluso, K. Elsaafien, A. L. Nazarova, K. B. Assersen, L. Rodrigues-Ribeiro, M. Mohammed, A. F. Rodrigues, A. Nawrocki, L. A. Johansen, P. Jensen, A. D. de Kloet, E. G. Krause, M. DelBorgo, I. Maslov, , U. M. Steckelings

This study identifies angiotensin-(1-5) as a potent endogenous agonist of the AT2-receptor, showing its ability to increase nitric oxide release and lower blood pressure through AT2R-mediated mechanisms.

bioRxiv · Apr 5, 2024 · PreprintPharmacology & Toxicology

The lncRNA landscape of cardiac resident macrophages and identification of Schlafenlnc as a regulator of macrophage migratory function

A. Dueck, L. Althaus, K. Heise, D. Esfandyari, S. Bayguen, R. P. Brandes, J. Gagneur, N. Jae, P. Knolle, M. S. Leisegang, L. Maegdefessel, T. Meitinger, D. Niessing, N. Petzold, D. Ramanujam, , S. Engelhardt

The paper identifies lncRNAs in cardiac resident macrophages and shows Schlafenlnc regulates macrophage migration.

bioRxiv · Nov 30, 2022 · PreprintCell Biology

Constitutive depletion of brain serotonin differentially affects rats' social and cognitive abilities

L. Alonso, P. Peeva, S. Stasko, M. Bader, N. Alenina, Y. Winter, M. Rivalan

This study shows that serotonin depletion in rats affects social and cognitive behaviors differently, revealing complex behavioral changes in social contexts but normal cognitive performance in classical tests.

bioRxiv · Sep 23, 2021Animal Behavior & Cognition

Quantifying the impact of gut microbiota on inflammation and hypertensive organ damage

E. G. Avery, H. Bartolomaeus, A. Rauch, C.-Y. Chen, G. N'diaye, U. Loeber, T. U. Bartolomaeus, R. Fritsche-Guenther, A. F. Rodrigues, D. Tsvetkov, M. Todiras, J.-K. Park, L. Marko, A. Maifeld, M. Bader, , N. Wilck

This study quantifies how gut microbiota affects inflammation and organ damage in hypertension using germ-free and colonized mice, finding the kidney is more susceptible to microbial influence.

bioRxiv · Sep 17, 2021Microbiology

Myogenic Vasoconstriction Requires Canonical Gq/11 Signaling of Angiotensin II Type 1a Receptor in Murine Vasculature

Y. Cui, M. Kassmann, S. Nickel, C. Zhang, N. Alenina, Y. M. Anistan, J. Schleifenbaum, M. Bader, D. G. Welsh, Y. Huang, M. Gollasch

This study shows that myogenic vasoconstriction in mice depends on Gq/11 signaling through AT1aR, not β-arrestin-mediated pathways.

bioRxiv · Sep 9, 2020 · PreprintPhysiology