Thebone morphogenetic protein receptor, type IA also known asBMPR1A is aprotein which in humans is encoded by theBMPR1Agene. BMPR1A has also been designated asCD292 (cluster of differentiation 292).[5]
The bone morphogenetic protein (BMP) receptors are a family of transmembraneserine/threonine kinases that include the type I receptors BMPR1A (this protein) andBMPR1B and the type II receptorBMPR2. These receptors are also closely related to the activin receptors,ACVR1 andACVR2. The ligands of these receptors are members of theTGF beta superfamily. TGF-betas and activins transduce their signals through the formation of heterodimeric complexes with 2 different types of serine (threonine) kinase receptors: type I receptors of about 50-55 kD and type II receptors of about 70-80 kD. Type II receptors bind ligands in the absence of type I receptors, but they require their respective type I receptors for signaling, whereas type I receptors require their respective type II receptors for ligand binding.[5]
BMP's repressWNT signaling to maintain stable stem cell populations. BMPR1A null mice died at embryonic day 8.0 withoutmesoderm specification, demonstrating its vital role ingastrulation.[6] It has been demonstrated in experiments using dominant negative BMPR1A chick embryos that BMPR1A plays a role inapoptosis andadipocyte development.[6] Using constitutively active forms of BMPR1A, it has been shown that BMPR1A plays a role incell differentiation.[6] Signals transduced by the BMPR1A receptor are not essential forosteoblast formation or proliferation; however, BMPR1A is necessary for theextracellular matrix deposition by osteoblasts.[6] In the chick embryo, BMPR1A receptors are found in low levels in limb budmesenchyme, a differing location to BMPR1B, supporting the differing roles they play in osteogenesis.[7]
BMPR1A,SMAD4 andPTEN are responsible forjuvenile polyposis syndrome,juvenile intestinal polyposis andCowden's disease.
BMPR1A has been shown tointeract with: