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. 2022 Oct 21;10:1045103. doi: 10.3389/fcell.2022.1045103

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Copyright © 2022 Setiawan, Kamarudin and Abd Ghafar.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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BMP4 signaling pathways and its’ regulatory mechanisms in stem cell differentiation: (A) Activation of smad-dependent pathway is initiated when BMP4 dimer binds to BMPR1/2 complex. This interaction activates the phosphorylation of receptor-associated SMADs (SMAD 1/5/8) by BMPR1 to produce R-smads. R-smads then recruit SMAD4 to form Co-smad and translocate into the nucleus leading to downstream signaling. (B) In smad-independent pathway, BMPR1 activates MAP kinase and acts as transcription factors inside the nucleus. Both pathways induce cell commitment and differentiation. (C) BMP4 signaling pathways are regulated by intracellular and extracellular antagonist molecules. Extracellular BMP antagonist (noggin, chordin, follistatin, gremlin and BAMBI) binds to BMP4 dimer ligand and prevent the interaction of BMP4 ligand with its BMP receptors leading to no activation of smad-dependent pathway. On the other hand, intracellular BMP antagonist, known as inhibitory smad (I-smad), shutdown the activated smad-dependent pathway by preventing the phosphorylation of r-smads and block the interaction between R-smads with Co-smads. This schematic was created with BioRender.com.