Fig. 2: Schematic overview of SMAD-(in)dependent bone morphogenetic protein (BMP) signalling pathway (oversimplification). | npj Genomic Medicine

Fig. 2: Schematic overview of SMAD-(in)dependent bone morphogenetic protein (BMP) signalling pathway (oversimplification).

From: SMAD6-deficiency in human genetic disorders

Fig. 2: Schematic overview of SMAD-(in)dependent bone morphogenetic protein (BMP) signalling pathway (oversimplification).

Upon BMP ligand binding, specific type I and type II receptors form a heterotetrameric complex. The type II receptor phosphorylates the type I receptor, which, in turn, phosphorylates Smad1, Smad5, and Smad8 (canonical BMP signalling). Phosphorylated Smads propagate the signal via complex formation with Smad4 and translocates into the nucleus, where it regulates the expression of BMP-responsive target genes. In addition to Smad activation, activated BMP receptor complexes initiates several intracellular pathways to modulate BMP-dependent cellular responses like PI3-kinase, ERK, RhoA, and MAPK/JNK. Canonical BMP signalling is intracellularly inhibited by inhibitory Smads (Smad6, Smad7) and E3 ubiquitin ligases like Smurf1 and Smurf2. Created with BioRender.com. The figure was exported under a paid subscription.

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