His primary scientific interests are in Cell biology, Membrane protein, Cilium, Genetics and Nephronophthisis. His Cell biology research includes elements of Molecular biology and Podocin, Podocyte. His studies in Membrane protein integrate themes in fields like Transport protein, Mechanosensation, Ion channel, Slit diaphragm and Cell polarity.
Bernhard Schermer interconnects Ciliopathies and Microtubule in the investigation of issues within Cilium. His Nephronophthisis research is multidisciplinary, incorporating elements of Cystic kidney disease and Pathology. Bernhard Schermer works mostly in the field of Cystic kidney disease, limiting it down to topics relating to Wnt signaling pathway and, in certain cases, Endocrinology, Internal medicine, Xenopus, Situs inversus and Polydactyly, as a part of the same area of interest.
Bernhard Schermer focuses on Cell biology, Podocyte, Internal medicine, Cilium and Kidney. His Cell biology research incorporates elements of Molecular biology, Transcription factor, Slit diaphragm and Membrane protein. His Transcription factor research is multidisciplinary, relying on both Regulation of gene expression, Cancer research and Interactome.
His Internal medicine study typically links adjacent topics like Endocrinology. In his work, Cystic kidney disease, Cystic kidney and Wnt signaling pathway is strongly intertwined with Nephronophthisis, which is a subfield of Cilium. Polycystic kidney disease is a subfield of Genetics that Bernhard Schermer investigates.
The scientist’s investigation covers issues in Cell biology, Kidney, Podocyte, Proteome and Cancer research. Specifically, his work in Cell biology is concerned with the study of Cilium. His Kidney research also works with subjects such as
His Podocyte research incorporates themes from Autophagy, Glomerulosclerosis, Kidney disorder and RHOA. His study in Proteome is interdisciplinary in nature, drawing from both Renal replacement therapy, Proteomics and Transplantation, Kidney transplantation. His study looks at the relationship between Cancer research and topics such as Hippo signaling, which overlap with Compound heterozygosity and Missense mutation.
His primary areas of investigation include Cell biology, Proteome, Podocyte, Population and Polymerase chain reaction. Bernhard Schermer combines subjects such as RNA and Interactome with his study of Cell biology. His RNA research includes themes of Translation, Messenger RNA and Binding site.
His research investigates the connection with Proteome and areas like Transcriptome which intersect with concerns in Filamin, Glomerulosclerosis, Proteomics, Slit diaphragm and Proteostasis. Bernhard Schermer has included themes like Diabetic nephropathy, Enzyme replacement therapy, Fabry disease and PI3K/AKT/mTOR pathway, Signal transduction in his Podocyte study. His work carried out in the field of Polymerase chain reaction brings together such families of science as Real-time polymerase chain reaction and Computational biology.
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A mammalian microRNA expression atlas based on small RNA library sequencing.
Pablo Landgraf;Mirabela Rusu;Robert Sheridan;Alain Sewer;Alain Sewer.
Inversin, the gene product mutated in nephronophthisis type II, functions as a molecular switch between Wnt signaling pathways
Matias Simons;Joachim Gloy;Athina Ganner;Axel Bullerkotte.
Nature Genetics (2005)
Mutations in INVS encoding inversin cause nephronophthisis type 2, linking renal cystic disease to the function of primary cilia and left-right axis determination.
Edgar A. Otto;Bernhard Schermer;Tomoko Obara;John F. O'Toole.
Nature Genetics (2003)
Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling.
Tobias B. Huber;Björn Hartleben;Jeong Kim;Miriam Schmidts.
Molecular and Cellular Biology (2003)
Mutations in a novel gene, NPHP3, cause adolescent nephronophthisis, tapeto-retinal degeneration and hepatic fibrosis
Heike Olbrich;Manfred Fliegauf;Julia Hoefele;Andreas Kispert.
Nature Genetics (2003)
Exome Capture Reveals ZNF423 and CEP164 Mutations, Linking Renal Ciliopathies to DNA Damage Response Signaling
Moumita Chaki;Rannar Airik;Amiya K. Ghosh;Rachel H. Giles.
Podocyte-Specific Deletion of Dicer Alters Cytoskeletal Dynamics and Causes Glomerular Disease
Scott J. Harvey;George Jarad;Jeanette Cunningham;Seth Goldberg.
Journal of The American Society of Nephrology (2008)
Loss of Nephrocystin-3 Function Can Cause Embryonic Lethality, Meckel-Gruber-like Syndrome, Situs Inversus, and Renal-Hepatic-Pancreatic Dysplasia
Carsten Bergmann;Manfred Fliegauf;Nadina Ortiz Brüchle;Valeska Frank.
American Journal of Human Genetics (2008)
Podocin and MEC-2 bind cholesterol to regulate the activity of associated ion channels.
Tobias B. Huber;Bernhard Schermer;Roman Ulrich Müller;Martin Höhne.
Proceedings of the National Academy of Sciences of the United States of America (2006)
Trafficking of TRPP2 by PACS proteins represents a novel mechanism of ion channel regulation.
Michael Köttgen;Thomas Benzing;Thomas Simmen;Robert Tauber.
The EMBO Journal (2005)
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