Christina Seebode
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Christina Seebode has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Hugo Murua Escobar
Clinic for Hematology, Oncology and Palliative Care, Rostock University Medical Center, University of Rostock, Rostock, Germany
1 shared publication - Janin Edelkamp
Monasterium Laboratory Skin and Hair Research Solutions GmbH, Münster, Germany
1 shared publication - Lars Boeckmann
Clinic and Policlinic for Dermatology, Venereology and Allergology, University Medical Center Rostock, Rostock, Germany
1 shared publication - Marie Christine Martens
Clinic and Policlinic for Dermatology and Venerology, University Medical Center Rostock, 18057 Rostock, Germany
1 shared publication - Mirijam Schäfer
Clinic and Polyclinic for Dermatology and Venereology, University Medical Center Rostock, 18057 Rostock, Germany
1 shared publication - Ole Jung
Clinic and Policlinic for Dermatology and Venereology, University Medical Center Rostock, Rostock, Germany
1 shared publication
Latest Publications
- Open Access
- 18 May 2021
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 22 (10) , 5293
Generation and Characterization of a CRISPR/Cas9-Mediated SNAP29 Knockout in Human Fibroblasts
Loss-of-function mutations in the synaptosomal-associated protein 29 (SNAP29) lead to the rare autosomal recessive neurocutaneous cerebral dysgenesis, neuropathy, ichthyosis, and keratoderma (CEDNIK) syndrome. SNAP29 is a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein. So far, it has been shown to be involved in membrane fusion, epidermal differentiation, formation of primary cilia, and autophagy. Recently, we reported the successful generation of two mouse models for the human CEDNIK syndrome. The aim of this investigation was the generation of a CRISPR/Cas9-mediated SNAP29 knockout (KO) in an immortalized human cell line to further investigate the role of SNAP29 in cellular homeostasis and signaling in humans independently of animal models. Comparison of different methods of delivery for CRISPR/Cas9 plasmids into the cell revealed that lentiviral transduction is more efficient than transfection methods. Here, we reported to the best of our knowledge the first successful generation of a CRISPR/Cas9-mediated SNAP29 KO in immortalized human MRC5Vi fibroblasts (c.169_196delinsTTCGT) via lentiviral transduction.
- 18 May 2021
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 22 (10) , 5293
Open AccessGeneration and Characterization of a CRISPR/Cas9-Mediated SNAP29 Knockout in Human Fibroblasts
Loss-of-function mutations in the synaptosomal-associated protein 29 (SNAP29) lead to the rare autosomal recessive neurocutaneous cerebral dysgenesis, neuropathy, ichthyosis, and keratoderma (CEDNIK) syndrome. SNAP29 is a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein. So far, it has been shown to be involved in membrane fusion, epidermal differentiation, formation of primary cilia, and autophagy. Recently, we reported the successful generation of two mouse models for the human CEDNIK syndrome. The aim of this investigation was the generation of a CRISPR/Cas9-mediated SNAP29 knockout (KO) in an immortalized human cell line to further investigate the role of SNAP29 in cellular homeostasis and signaling in humans independently of animal models. Comparison of different methods of delivery for CRISPR/Cas9 plasmids into the cell revealed that lentiviral transduction is more efficient than transfection methods. Here, we reported to the best of our knowledge the first successful generation of a CRISPR/Cas9-mediated SNAP29 KO in immortalized human MRC5Vi fibroblasts (c.169_196delinsTTCGT) via lentiviral transduction.