A5048553020- Amyotrophic Lateral Sclerosis Research
- Neurogenetic and Muscular Disorders Research
- RNA Research and Splicing
- Pancreatic function and diabetes
- Neurological diseases and metabolism
- Epigenetics and DNA Methylation
- Hematopoietic Stem Cell Transplantation
- T-cell and B-cell Immunology
- Histone Deacetylase Inhibitors Research
- Autophagy in Disease and Therapy
- Monoclonal and Polyclonal Antibodies Research
- Immune Cell Function and Interaction
- Prion Diseases and Protein Misfolding
- Sirtuins and Resveratrol in Medicine
- vaccines and immunoinformatics approaches
- Genetics and Neurodevelopmental Disorders
- ATP Synthase and ATPases Research
- Photosynthetic Processes and Mechanisms
- Mitochondrial Function and Pathology
- Immunotherapy and Immune Responses
University of Rostock
2020-2024
University Medical Center
2024
German Center for Neurodegenerative Diseases
2023
Jena University Hospital
2018
University of Michigan
2015
Goethe University Frankfurt
2014
Max Planck Institute of Biophysics
2009
Indian Institute of Science Bangalore
2007
Abstract MicroRNAs (miRNAs) are a subset of small non-coding single-stranded RNA molecules involved in the regulation post-transcriptional gene expression variety transcript targets. Therefore altered miRNA may result dysregulation key genes and biological pathways that has been reported with onset progression neurodegenerative diseases, such as Amyotrophic lateral sclerosis (ALS). ALS is marked by progressive degeneration motor neurons (MNs) present spinal cord, brain stem cortex. Although...
Intronic hexanucleotide repeat expansions (HREs) in C9ORF72 are the most frequent genetic cause of amyotrophic lateral sclerosis, a devastating, incurable motoneuron (MN) disease. The mechanism by which HREs trigger pathogenesis remains elusive. discovery repeat-associated non-ATG (RAN) translation dipeptide proteins (DPRs) from along with reduced exonic expression suggests gain toxic functions (GOFs) through DPRs versus loss (LOFs). Through multiparametric high-content (HC) live profiling...
Amyotropic lateral sclerosis (ALS) is a lethally progressive and irreversible neurodegenerative disease marked by apparent death of motor neurons present in the spinal cord, brain stem cortex. While more gene mutants being established for genetic ALS, vast majority suffer from sporadic ALS (>90%). It has been challenging, thus, to model which one reason why underlying pathophysiology remains elusive stalled development therapeutic strategies this neuron disease. To further unravel these...
Amyotrophic Lateral Sclerosis (ALS) is a progressive and fatal neurodegenerative disease marked by death of motor neurons (MNs) present in the spinal cord, brain stem cortex. Despite extensive research, reason for neurodegeneration still not understood. To generate novel hypotheses putative underlying molecular mechanisms, we used human induced pluripotent cell (hiPSCs)-derived from SOD1- TARDBP (TDP-43 protein)-mutant-ALS patients healthy controls to perform high-throughput RNA-sequencing...
Amyotrophic lateral sclerosis (ALS) is one of the most dreadful neurodegenerative diseases leading to death within 1–5 years after symptom onset. The majority ALS cases are sporadic (sALS), while remaining 5–10% familial (fALS). Genetic discoveries have identified ALS-causative mutations in more than 30 genes so far (Chia et al., 2018). Indeed, four common observed Europe hexanucleotide expansion repeat Chromosome 9 Open Reading Frame 72 (C9ORF72), Cu-Zn superoxide dismutase 1 (SOD1)),...
Amyotrophic lateral sclerosis (ALS) is a fatal, adult-onset disease marked by progressive degeneration of motor neurons (MNs) present in the spinal cord, brain stem and cortex. Death most patients usually occurs within 2-4 years after symptoms onset. Despite promising progress delineating underlying mechanisms, such as disturbed proteostasis, DNA/RNA metabolism, splicing or proper nucleocytoplasmic shuttling, there are no effective therapies for vast majority cases. A reason this might be...
Mutations in the gene
Recent research has demonstrated significant aberrant activation of the innate immune system in ALS model systems due to mutations SOD1, TARDBP and C9orf72 through stimulation TBK1-IRF3 pathway. This pathway can be activated, for example, by cGAS-STING-dependent sensing cytosolic DNA that accumulates as a result chronic damage defective mitochondria, both which have been identified early pathology FUS-ALS spinal motor neurons (sMNs). Therefore, we analysed pathways isogenic non-isogenic...
Abstract Structural and biophysical studies have established that the recognition of antigenic peptide-MHC complexes (pMHC) by T-cell receptors (TCR) involves conformational changes in so-called CDR loops, which define binding interface TCR. This plasticity is believed to underlie receptors' cross-reactivity, a key feature given vast diversity antigens limited repertoire. It remains unclear, however, whether this induced upon specific pMHC, or it an intrinsic characteristic loops. To gain...
A key step in rational vaccine development is to understand how antigens are recognized by their receptors. Several crystal structures of MHC/HLA molecules now available. We report a structural bioinformatics study peptide- HLA complexes derive features that generate recognition specificity, useful for guiding the design process. Keywords: Epitope prediction, protein-peptide interaction, class-I, design,