Bone morphogenetic protein (BMP) type I receptor that is involved in a wide variety of biological processes, including bone, heart, cartilage, nervous, and reproductive system development and regulation (PubMed:10479450, PubMed:15531373, PubMed:21945937). As a type I receptor, forms heterotetrameric receptor complexes with the type II receptors AMHR2, ACVR2A ors ACVR2B. Upon binding of ligands such as BMP7 or BMP9 to the heteromeric complexes, type II receptors transphosphorylate ACVR1 intracellular domain. In turn, ACVR1 kinase domain is activated and subsequently phosphorylates SMAD1/5/8 proteins that transduce the signal. In addition to its role in mediating BMP pathway-specific signaling, suppresses TGFbeta/activin pathway signaling by interfering with the binding of activin to its type II receptor. Besides canonical SMAD signaling, can activate non-canonical pathways such as p38 mitogen-activated protein kinases/MAPKs (PubMed:25413979, PubMed:10479450, PubMed:15531373, PubMed:21945937) (By similarity). ATP + L-threonyl-[receptor-protein] = ADP + H(+) + O-phospho-L-threonyl-[receptor-protein] ATP + L-seryl-[receptor-protein] = ADP + H(+) + O-phospho-L-seryl-[receptor-protein] Interacts with FKBP1A. Interacts with FCHO1. Interacts with CLU. Interacts with type II receptors AMHR2 and ACVR2A. Interacts with BMP7. Interacts with BMP9. Interacts with BMP6. Highly expressed in bone during developmental stages (PubMed:21945937). Expressed in normal parenchymal cells, endothelial cells, fibroblasts and tumor-derived epithelial cells. Highly expressed in the node and midline and weakly expressed in 8.5 dpc embryos and in the lateral plate mesoderm. Deletion mutants show a recessive embryonic lethality. At 7.0 dpc, mutant embryos did not show any special abnormalities except a smaller size. However, at 8.0 dpc, mesoderm formation is initiated but its development is arrested around the mid/late streak stage (PubMed:10479450). In an osteoblast-specific manner loss of BMP signaling via ACVR1 directs osteoblasts to increase endogenous bone mass (PubMed:21945937). Additionally, mice lacking ACVR1 in cartilage show reduced SMAD responses, but also decreased p38 MAPK activation (PubMed:25413979). Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. TGFB receptor subfamily.