Loss of ADAMTS3 activity causes Hennekam lymphangiectasia–lymphedema syndrome 3

By P. Brouillard, Laura Dupont, R. Helaers, R. Coulie, G. Tiller, J. Peeden, A. Colige, M. Vikkula. 2017

105 citations recorded by the source corpus.

Subfields: Genetics, Oncology, Physiology

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. S. Apte
2. S. Zhong
3. R. Khalil
4. T. Mead

In Oncology

1. S. Zhong
2. S. Apte
3. R. Khalil

In Physiology

1. R. Khalil

Citations in the corpus

• A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “ADAMTS-3 also participates in triggering VEGFR-3 signaling, a cornerstone for the differentiation and function of lymphatic endothelial cells [129], and loss of ADAMTS-3 activity has been associated with Hennekam lymphangiectasia-lymphedema syndrome [130].”
• ADAMTS proteins in human disorders (2018, background): “ADAMTS3 and primary lymphedema—The most recent incrimination of an ADAMTS protease in a Mendelian disorder occurred via identification of recessive ADAMTS3 mutations in Hennekam lymphangiectasia-lymphedema syndrome 3 [30].”