Cdk5 controls lymphatic vessel development and function by phosphorylation of 
Foxc2

Liebl, Johanna; Zhang, Siwei; Moser, Markus; Agalarov, Yan; Demir, Cansaran Saygili; Hager, Bianca; Bibb, James A.; Adams, Ralf H.; Kiefer, Friedemann; Miura, Naoyuki; Petrova, Tatiana V.; Vollmar, Angelika M.; Zahler, Stefan

doi:10.1038/ncomms8274

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Cdk5 controls lymphatic vessel development and function by phosphorylation of Foxc2

MPS-Authors

/persons/resource/persons78420

Moser, Markus
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Liebl, J., Zhang, S., Moser, M., Agalarov, Y., Demir, C. S., Hager, B., et al. (2015). Cdk5 controls lymphatic vessel development and function by phosphorylation of Foxc2. NATURE COMMUNICATIONS, 6: 7274. doi:10.1038/ncomms8274.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0028-173E-9

Abstract

The lymphatic system maintains tissue fluid balance, and dysfunction of lymphatic vessels and valves causes human lymphedema syndromes. Yet, our knowledge of the molecular mechanisms underlying lymphatic vessel development is still limited. Here, we show that cyclin-dependent kinase 5 (Cdk5) is an essential regulator of lymphatic vessel development. Endothelial-specific Cdk5 knockdown causes congenital lymphatic dysfunction and lymphedema due to defective lymphatic vessel patterning and valve formation. We identify the transcription factor Foxc2 as a key substrate of Cdk5 in the lymphatic vasculature, mechanistically linking Cdk5 to lymphatic development and valve morphogenesis. Collectively, our findings show that Cdk5-Foxc2 interaction represents a critical regulator of lymphatic vessel development and the transcriptional network underlying lymphatic vascular remodeling.