Refine
Has Fulltext
- yes (11)
Is part of the Bibliography
- yes (11)
Document Type
- Journal article (11)
Language
- English (11)
Keywords
- AKT-signaling (1)
- B-cell lymphoma (1)
- CD30 (1)
- COX2 expression (1)
- CTNNB1 (1)
- Cushing’s disease (1)
- Cushing’s syndrome (1)
- DNA methylation (1)
- KRAS (1)
- MEK/ERK-signaling (1)
- NR3C1 (1)
- NRF2 (1)
- PLEKHG5 (1)
- RNA (1)
- Salmonella (1)
- Schwann cells (1)
- Tdp-43 (1)
- USP8 (1)
- acetylcholine (1)
- amplicon sequencing (1)
- amyotrophic lateral sclerosis (1)
- autophagy (1)
- axonal transcriptome (1)
- blood (1)
- brush cells (1)
- cutaneous T-cell-lymphoma (1)
- epigenetics (1)
- gene expression (1)
- genomic imprinting (1)
- glucocorticoid excess (1)
- hypercortisolism (1)
- immune response (1)
- infectious disease (1)
- large cell transformation (1)
- melanoma malignancy (1)
- motor axons (1)
- mucociliary clearance (1)
- multiple myeloma (1)
- mycosis fungoides (1)
- myelin (1)
- nicotinamide (1)
- panel sequencing (1)
- polymerase chain reaction (1)
- primary cutaneous follicular B-cell lymphoma (1)
- sequence alignment (1)
- single‐cell RNA‐seq (1)
- sperm (1)
- targeted sequencing (1)
- taste (1)
Institute
- Pathologisches Institut (4)
- Klinik und Poliklinik für Dermatologie, Venerologie und Allergologie (3)
- Medizinische Klinik und Poliklinik II (3)
- Comprehensive Cancer Center Mainfranken (2)
- Institut für Humangenetik (2)
- Institut für Klinische Neurobiologie (2)
- Institut für Anatomie und Zellbiologie (1)
- Institut für Molekulare Infektionsbiologie (1)
- Institut für Virologie und Immunbiologie (1)
- Institut für diagnostische und interventionelle Radiologie (Institut für Röntgendiagnostik) (1)
EU-Project number / Contract (GA) number
- 259867 (1)
Inflammation and dysregulation of the immune system are hallmarks of several neurodegenerative diseases. An activated immune response is considered to be the cause of myelin breakdown in demyelinating disorders. In the peripheral nervous system (PNS), myelin can be degraded in an autophagy-dependent manner directly by Schwann cells or by macrophages, which are modulated by T-lymphocytes. Here, we show that the NF-κB activator Pleckstrin homology containing family member 5 (Plekhg5) is involved in the regulation of both Schwann cell autophagy and recruitment of T-lymphocytes in peripheral nerves during motoneuron disease. Plekhg5-deficient mice show defective axon/Schwann cell units characterized by myelin infoldings in peripheral nerves. Even at late stages, Plekhg5-deficient mice do not show any signs of demyelination and inflammation. Using RNAseq, we identified a transcriptional signature for an impaired immune response in sciatic nerves, which manifested in a reduced number of CD4\(^+\) and CD8\(^+\) T-cells. These findings identify Plekhg5 as a promising target to impede myelin breakdown in demyelinating PNS disorders.