The Role of ZIP13 in Connective Tissue Development
Author Information
Author(s): Fukada Toshiyuki, Civic Natacha, Furuichi Tatsuya, Shimoda Shinji, Mishima Kenji, Higashiyama Hiroyuki, Idaira Yayoi, Asada Yoshinobu, Kitamura Hiroshi, Yamasaki Satoru, Hojyo Shintaro, Nakayama Manabu, Ohara Osamu, Koseki Haruhiko, dos Santos Heloisa G., Bonafe Luisa, Ha-Vinh Russia, Zankl Andreas, Unger Sheila, Kraenzlin Marius E., Beckmann Jacques S., Saito Ichiro, Rivolta Carlo, Ikegawa Shiro, Superti-Furga Andrea, Hirano Toshio
Primary Institution: Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan
Hypothesis
The zinc transporter SLC39A13/ZIP13 is crucial for connective tissue development and its involvement in BMP/TGF-β signaling pathways.
Conclusion
The study reveals that SLC39A13/ZIP13 is essential for connective tissue development, linking zinc metabolism to BMP/TGF-β signaling.
Supporting Evidence
- ZIP13 knockout mice showed defects in bone and connective tissue development.
- Homozygosity for a SLC39A13 mutation was found in patients with a unique variant of Ehlers-Danlos syndrome.
- ZIP13 is involved in BMP and TGF-β signaling pathways, crucial for connective tissue development.
- Reduced expression of genes essential for osteoblast and chondrocyte differentiation was observed in ZIP13 deficient mice.
- ZIP13 regulates intracellular zinc distribution, affecting signaling pathways in connective tissue cells.
Takeaway
ZIP13 helps our body make strong connective tissues, like skin and bones, by managing zinc levels and signaling pathways.
Methodology
The study used Slc39a13 knockout mice to investigate the role of ZIP13 in connective tissue development and signaling pathways.
Limitations
The study primarily focuses on a mouse model, which may not fully replicate human conditions.
Digital Object Identifier (DOI)
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