Atheroprone fluid shear stress-regulated ALK1-Endoglin-SMAD signaling originates from early endosomes.

Paul-Lennard MendezLeon ObendorfJerome JatzlauWiktor BurdzinskiMaria ReichenbachVanasa NageswaranArash HaghikiaVerena StanglChristian HiepenPetra Knaus

Published in: BMC biology (2022)

We identified Endoglin to be essential in preventing excessive activation of SMAD1/5 under physiological flow conditions and Caveolin-1-positive early endosomes as a new flow-regulated signaling compartment for BMP9-ALK1-Endoglin signaling axis in atheroprone flow conditions.

Keyphrases

epithelial mesenchymal transition
advanced non small cell lung cancer
physical activity
bone marrow
body mass index
weight gain
signaling pathway
weight loss
tyrosine kinase