Gabriele Siegel

ORCID: 0000-0002-9501-7061
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About
Contact & Profiles
Research Areas
  • MicroRNA in disease regulation
  • Circular RNAs in diseases
  • RNA Research and Splicing
  • Neuroscience and Neuropharmacology Research
  • RNA regulation and disease
  • Alzheimer's disease research and treatments
  • Genetics and Neurodevelopmental Disorders
  • Genomics and Rare Diseases
  • Retinal Diseases and Treatments
  • Immunotherapy and Immune Responses
  • Retinal Development and Disorders
  • Ocular Oncology and Treatments
  • Macrophage Migration Inhibitory Factor
  • Ion channel regulation and function
  • Cancer-related gene regulation
  • Retinopathy of Prematurity Studies
  • Mechanisms of cancer metastasis
  • Ubiquitin and proteasome pathways
  • Neural dynamics and brain function
  • Drug Transport and Resistance Mechanisms
  • RNA modifications and cancer
  • Neurogenesis and neuroplasticity mechanisms
  • Cellular transport and secretion
  • Receptor Mechanisms and Signaling
  • Congenital heart defects research

University of Zurich
2013-2025

Philipps University of Marburg
2015

Heidelberg University
2007-2011

University Hospital Heidelberg
2007-2011

University at Buffalo, State University of New York
2004-2009

Schiller International University
2006

Friedrich Schiller University Jena
2004

Alzheimer's disease (AD) is characterized by cerebral deposition of β-amyloid (Aβ) peptides, which are generated from amyloid precursor protein (APP) β- and γ-secretases. APP the secretases membrane associated, but whether trafficking controls Aβ levels unclear. Here, we performed an RNAi screen all human Rab-GTPases, regulate trafficking, complemented with a Rab-GTPase-activating screen, present road map membrane-trafficking events regulating production. We identify Rab11 Rab3 as key...

10.1016/j.celrep.2013.12.005 article EN cc-by-nc-nd Cell Reports 2013-12-01

Alzheimer's disease is characterized by intracerebral deposition of β-amyloid (Aβ). While Aβ40 the most abundant form, neurotoxicity mainly mediated Aβ42. Sequential cleavage amyloid precursor protein (APP) β- and γ-secretases gives rise to full-length Aβ (Aβ1-x) N-terminally truncated Aβ′ (Aβ11-x) whereas α- leads shorter p3 peptides (Aβ17-x). We uncovered significantly higher ratios 42- versus 40-ending variants for than secreted mouse neurons human induced pluripotent stem cell...

10.1016/j.celrep.2017.05.034 article EN cc-by-nc-nd Cell Reports 2017-06-01

Of the around 7,000 known rare diseases worldwide, disease-modifying treatments are available for fewer than 5%, leaving millions of individuals without specialized therapeutic strategies. In recent years, antisense oligonucleotides (ASOs) have shown promise as individualized genetic interventions diseases. However, there is currently no consensus on which disease-causing DNA variants suitable candidates this type therapy. The Patient Identification Working Group N=1 Collaborative (N1C),...

10.1101/2024.09.27.24314122 preprint EN cc-by medRxiv (Cold Spring Harbor Laboratory) 2024-09-28

Animal models of focal ischemic infarcts reveal an impaired GABAergic (gamma-aminobutyric acid) neurotransmission. GABA, the main inhibitory neurotransmitter, is primarily taken up by specific sodium-dependent transporters. As these transporters play a crucial role in maintaining levels GABA concentration, they may be functionally involved processes. We investigated whether mRNA and protein expression GAT-1, dominant neuronal transporter, altered after cortical infarct induced...

10.1002/cne.20282 article EN The Journal of Comparative Neurology 2004-08-31
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