Affinage

BMPR1A

Bone morphogenetic protein receptor type-1A · UniProt P36894

Length
532 aa
Mass
60.2 kDa
Annotated
2026-04-28
100 papers in source corpus 47 papers cited in narrative 46 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BMPR1A (ALK3) is a type I BMP serine/threonine kinase receptor that transduces signals from multiple BMP/GDF ligands to control cell proliferation, survival, differentiation, and fate decisions across virtually every organ system, functioning through both canonical SMAD1/5/8–SMAD4 signaling and SMAD-independent effectors including p38 MAPK, mTORC1, and actin cytoskeleton reorganization (PMID:10814522, PMID:19733164, PMID:26657771, PMID:21613322). Upon BMP ligand binding, BMPR1A forms heteromeric complexes with BMPR2 (whose kinase activity is required for SMAD pathway activation) and can also homodimerize in a ligand-independent manner; its cell-surface abundance is regulated by HFE-mediated stabilization against ubiquitin-dependent degradation executed by USP15/SMAD6 and WWP2/LAPTM5 pathways, and by S-palmitoylation that controls receptor trafficking and localization (PMID:12829744, PMID:30227271, PMID:24904118, PMID:24850914, PMID:35842443, PMID:31772009). Tissue-specific conditional knockouts have established essential, non-redundant roles for BMPR1A in cardiac morphogenesis, hair follicle cycling, chondrogenesis (redundant with BMPR1B), lung epithelial branching, suture stem cell self-renewal, Müllerian duct regression, pancreatic beta-cell insulin secretion, uterine implantation, venous endothelial identity, and hepcidin regulation in iron homeostasis (PMID:11854453, PMID:15102710, PMID:15781876, PMID:16414041, PMID:12368913, PMID:17339028, PMID:26721398, PMID:30692543, PMID:30271947). In endothelial cells, BMPR1A prevents pathological endothelial-to-mesenchymal transition by inducing ID2–ZEB1 interaction to suppress TGFβ receptor 2 transcription, and its loss produces pulmonary arterial hypertension–like disease (PMID:36166408).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2000 Medium

    Establishing that BMPR1A specifically activates the BMP-restricted R-SMADs (SMAD1/5/8) answered the question of which intracellular effectors lie immediately downstream of this receptor and distinguished its signaling specificity from TGFβ type I receptors.

    Evidence Constitutively active ALK3 phosphorylated SMAD8 and induced SMAD8–SMAD4 nuclear translocation and BMP-responsive transcription; ALK5 did not, demonstrating pathway specificity in transfected cells

    PMID:10633078 PMID:10814522

    Open questions at the time
    • No endogenous confirmation of SMAD8-specific activation
    • Structural basis of receptor–SMAD specificity unknown
  2. 2002 High

    Tissue-specific knockouts revealed that BMPR1A is indispensable for two critical developmental processes—Müllerian duct regression (AMH signaling) and cardiac morphogenesis—establishing it as a pleiotropic developmental receptor rather than a functionally redundant type I BMP receptor.

    Evidence Conditional Bmpr1a deletion in Müllerian duct mesenchyme caused male uterine retention; cardiomyocyte-specific deletion caused trabecular, septal, and cushion defects with loss of TGFβ2 expression

    PMID:11854453 PMID:12368913

    Open questions at the time
    • Whether ALK2 or ALK6 can partially compensate in these tissues was not resolved
    • Identity of direct transcriptional targets was incomplete
  3. 2003 Medium

    Demonstration that BMPR2 kinase activity controls ALK3 surface distribution and that BMP stimulation rearranges receptor complexes established the model of ligand-induced heteromeric receptor reorganization as a prerequisite for SMAD pathway activation.

    Evidence Image correlation spectroscopy with kinase-dead BMPR2 mutants showed that BMPR2 kinase activity was required for BMP-2-induced ALK3 redistribution and SMAD activation

    PMID:12829744

    Open questions at the time
    • Stoichiometry of active signaling complexes not determined
    • Contribution of lipid raft partitioning not addressed
  4. 2004 High

    Placing WNT/β-catenin activation downstream of BMPR1A in hair follicles and kidney identified a recurring cross-talk module—BMP→WNT—that would be observed across multiple tissues, redefining BMPR1A as a morphogenetic pathway integrator.

    Evidence Conditional Bmpr1a deletion in epithelium abolished nuclear β-catenin in follicles; constitutively active ALK3 promoted β-catenin/SMAD1/SMAD4 complexes in kidney

    PMID:12736218 PMID:15084466 PMID:15102710

    Open questions at the time
    • Whether β-catenin–SMAD complexes form on chromatin versus cytoplasm was not resolved
    • Direct transcriptional targets of the combined complex were not identified
  5. 2005 High

    Double-knockout epistasis showed that BMPR1A and BMPR1B are functionally redundant during early chondrogenesis but that BMPR1A is uniquely required for AV valve morphogenesis, defining tissue contexts of redundancy versus specificity.

    Evidence Bmpr1a/Bmpr1b double knockout ablated Sox9/L-Sox5/Sox6 in cartilage precursors; AV-canal-specific Bmpr1a deletion disrupted valve leaflets and annulus fibrosus

    PMID:15781876 PMID:16037571

    Open questions at the time
    • How BMPR1A vs BMPR1B specificity is determined at the receptor level in non-redundant contexts remained unclear
  6. 2006 High

    Demonstrating that BMPR1A controls autocrine BMP-dependent survival and proliferation in lung epithelium and drives EMT in endocardial cells extended its function beyond differentiation to cell survival and mesenchymal transition.

    Evidence Epithelial Bmpr1a deletion caused apoptosis and branching failure even without mesenchyme; endocardial Alk3 deletion reduced AV canal EMT to ~20% of normal

    PMID:16414041 PMID:16959237

    Open questions at the time
    • Smad-independent survival pathways downstream of ALK3 in lung not identified
    • Whether EMT defect is cell-autonomous or partly paracrine was not fully resolved
  7. 2009 High

    Systematic comparison of receptor and Smad knockouts in lens ectoderm established that BMPR1A signals through both Smad-dependent (Sox2 maintenance) and Smad-independent (actin reorganization, FoxE3 expression) pathways, resolving a long-standing question about non-canonical BMP signaling.

    Evidence Conditional KO of Bmpr1a, Smad4, and Smad1/5 in lens showed that actin cytoskeleton reorganization and FoxE3 expression were Smad4-independent while Sox2 required canonical Smad signaling

    PMID:19733164

    Open questions at the time
    • Identity of the Smad-independent effector driving actin reorganization not determined
    • Whether p38 MAPK or other MAPKs mediate these non-canonical outputs in lens was untested
  8. 2010 High

    Discovery that BMPR1A and BMPR1B exert opposing effects on astrocytic hypertrophy through divergent post-transcriptional regulation of miR-21 demonstrated that closely related type I BMP receptors can antagonistically regulate the same downstream target in the same cell type.

    Evidence Conditional Bmpr1a ablation from GFAP+ cells reduced astrocytic hypertrophy; Bmpr1b null mice showed hyperactive astrocytes; both converged on opposing miR-21 regulation

    PMID:20130193

    Open questions at the time
    • Mechanism by which BMPR1A promotes versus BMPR1B suppresses miR-21 not elucidated
    • Whether this opposing mechanism operates outside CNS injury context is unknown
  9. 2011 Medium

    Lineage-specific use of different downstream effectors (p38 MAPK in kidney versus pSMAD1/5/8 in testis) by the same receptor resolved how a single receptor achieves diverse developmental outcomes in different tissues.

    Evidence Conditional Bmpr1a deletion in intermediate mesoderm progenitors showed p-p38 loss in metanephric mesenchyme and pSMAD1/5/8 loss in testis, with tissue-specific phenotypes

    PMID:21613322

    Open questions at the time
    • What determines the choice of downstream effector in each lineage is unknown
    • Single-lab finding without independent replication
  10. 2014 High

    Identification of HFE as a stabilizer and USP15/SMAD6 as a deubiquitylation-based regulator of ALK3 protein levels revealed that ALK3 surface abundance is actively controlled by ubiquitin-dependent turnover, linking iron homeostasis (HFE→ALK3→hepcidin) to receptor quality control.

    Evidence HFE inhibited ALK3 ubiquitination and increased cell-surface ALK3; HFE disease mutants (C282Y, H63D) failed this stabilization; USP15 removed K48-linked polyubiquitin from ALK3 via SMAD6 scaffolding

    PMID:24850914 PMID:24904118

    Open questions at the time
    • Whether HFE and USP15 act on the same or different ubiquitin chains on ALK3 is unclear
    • The E3 ligase responsible for basal ALK3 ubiquitination in hepatocytes was not identified at this point
  11. 2015 High

    Demonstrating that BMPR1A signals through mTORC1 for osteoblast protein anabolism, independent of Smad4, expanded the non-canonical signaling repertoire and explained how BMPR1A simultaneously suppresses preosteoblast proliferation while promoting osteoblast activity.

    Evidence Conditional KO and Smad4 KO comparison showed Smad4-independent proliferation control; mTORC1 inhibition abolished BMP2-induced anabolism gene expression in osteoblasts

    PMID:26657771

    Open questions at the time
    • How BMPR1A activates mTORC1 mechanistically (via PI3K, Akt, or other intermediates) was not defined
    • Whether mTORC1 signaling is relevant in non-skeletal BMPR1A contexts is unknown
  12. 2018 High

    In vivo genetic epistasis confirmed that HFE signals predominantly through ALK3 for hepcidin induction, and that ALK3 can form ligand-independent homodimers and ligand-dependent heterodimers with ALK2, establishing receptor complex diversity in iron regulation.

    Evidence AAV-HFE overexpression had no effect on hepcidin or pSmad1/5 in hepatocyte-specific Alk3 KO mice; Co-IP showed ALK3 homodimers without BMP and ALK2-ALK3 heterodimers requiring BMP2/BMP6

    PMID:30227271 PMID:30271947

    Open questions at the time
    • Whether ALK3 homodimers have signaling capacity without type II receptor engagement is unclear
    • Relative contribution of homodimer versus heterodimer to hepcidin regulation in vivo not quantified
  13. 2019 High

    Discovery of S-palmitoylation as a post-translational modification controlling BMPR1A localization, trafficking, and signaling output in neural stem cells introduced lipid modification as a regulatory layer governing receptor function and cell fate.

    Evidence Unbiased acylation screen in mouse NSCs identified BMPR1A palmitoylation; mutagenesis of palmitoylation sites altered BMPR1A localization, BMP signaling, and enhanced oligodendrogenesis in vivo

    PMID:31772009

    Open questions at the time
    • The palmitoyl acyltransferase(s) responsible for BMPR1A palmitoylation not identified
    • Whether palmitoylation status changes dynamically in response to BMP ligands is unknown
  14. 2022 High

    Identification of the LAPTM5–WWP2 axis as a pathway that sorts BMPR1A to lysosomes for degradation revealed a second, distinct ubiquitin-dependent degradation route (lysosomal rather than proteasomal) and linked BMPR1A turnover to metastatic cancer biology.

    Evidence Co-IP showed LAPTM5 recruits WWP2 to ubiquitinate BMPR1A; chloroquine rescued BMPR1A expression; LAPTM5-mediated BMPR1A degradation sustained cancer stemness and lung metastasis

    PMID:35842443

    Open questions at the time
    • Whether WWP2 and USP15/SMAD6 converge on the same ubiquitin sites on BMPR1A is unknown
    • In vivo relevance of LAPTM5-WWP2-BMPR1A axis beyond the metastasis model not tested
  15. 2023 High

    Discovery that BMPR1A induces ID2–ZEB1 physical interaction to sequester ZEB1 and suppress TGFβR2 transcription in endothelial cells provided a molecular mechanism by which BMP and TGFβ pathways are mutually antagonistic and explained how BMPR1A loss causes pathological EndoMT and pulmonary arterial hypertension.

    Evidence Conditional endothelial Bmpr1a deletion caused PAH-like EndoMT; Co-IP confirmed BMP-induced ID2–ZEB1 interaction; siRNA-LNP targeting Tgfbr2 rescued the phenotype

    PMID:36166408

    Open questions at the time
    • Whether ID2–ZEB1 sequestration operates in non-endothelial contexts is untested
    • Structural basis of the ID2–ZEB1 interaction is unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major open questions remain regarding the structural basis of BMPR1A's preferential use over other type I receptors in specific tissues, the identities of palmitoyl transferases and depalmitoylases regulating BMPR1A trafficking, and how cell-type-specific selection between canonical SMAD, p38 MAPK, mTORC1, and actin-remodeling outputs is determined.
  • No structural model of BMPR1A in a signaling-competent complex with type II receptor and ligand
  • Mechanism selecting between SMAD-dependent and SMAD-independent downstream pathways in different cell types is unresolved
  • Whether BMPR1A contributes to human Mendelian skeletal or cardiovascular disease beyond juvenile polyposis (not directly evidenced in this timeline) has limited direct genetic evidence

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0060089 molecular transducer activity 4 GO:0098772 molecular function regulator activity 3
Localization
GO:0005886 plasma membrane 6
Pathway
R-HSA-1266738 Developmental Biology 10 R-HSA-162582 Signal Transduction 10 R-HSA-1640170 Cell Cycle 3 R-HSA-1430728 Metabolism 2
Partners
BMPR2HFESMAD1SMAD4SMAD6TGFBR3USP15WWP2
Complex memberships
ALK2-ALK3 heterodimerBMPR1A-BMPR2 heteromeric receptor complexSMAD1/5/8-SMAD4 signaling complex

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 BMPR1A (ALK3) is identified as the type I receptor required for AMH/MIS-induced Müllerian duct regression in male sexual development; targeted disruption of Bmpr1a in Müllerian duct mesenchymal cells causes retention of oviducts and uteri in males, demonstrating BMPR1A mediates AMH signaling in vivo. Conditional knockout (Cre/lox), genetic epistasis Nature genetics High 12368913
2002 Cardiac myocyte-specific deletion of ALK3/BMPR1A causes defects in trabeculae, compact myocardium, interventricular septum, and endocardial cushion; ALK3 is specifically required for TGFβ2 expression in cardiac muscle, identifying a paracrine signaling axis for cushion morphogenesis. Conditional knockout (Cre/lox), immunohistochemistry, gene expression analysis Proceedings of the National Academy of Sciences of the United States of America High 11854453
2003 BMP4 signals through ALK3/BMPR1A and SMAD5 in spermatogonia; BMP4 stimulation induces Smad4/5 nuclear translocation and formation of a DNA-binding complex with p300/CBP, and exerts mitogenic and differentiative effects including induction of Kit expression in undifferentiated spermatogonia. Cell culture, nuclear translocation assay, [3H]thymidine incorporation, RT-PCR Journal of cell science Medium 12857787
2003 Constitutively active ALK3 receptor promotes formation of β-catenin/SMAD1/SMAD4 molecular complexes in kidney tissue, and functional cooperativity between ALK3 and β-catenin-dependent signaling pathways was demonstrated in vivo using ALK3(QD) transgenic mice. Transgenic mouse model, Co-immunoprecipitation, β-catenin reporter assay Development (Cambridge, England) Medium 12736218
2003 Co-expression of BMP type II receptor (BMPR2) influences aggregation and distribution of ALK3/BMPR1A at the cell surface; BMP-2 stimulation rearranges receptor complexes, and kinase activity of BMPR2 is required for this rearrangement and for activation of the SMAD pathway downstream of ALK3. Image correlation spectroscopy, constitutively active and kinase-dead receptor constructs, cell surface receptor distribution analysis Journal of cell science Medium 12829744
2004 Epithelial BMPR1A is required for hair follicle differentiation and cycling; conditional knockout causes failure of hair shaft and inner root sheath differentiation with loss of Msx1, Msx2, Foxn1, and Gata3 expression; nuclear β-catenin is absent in mutant follicles, placing WNT pathway activation downstream of BMPR1A signaling. Conditional knockout (Cre/lox), gene expression analysis, β-catenin localization Development (Cambridge, England) High 15084466 15102710
2000 Constitutively active ALK3/BMPR1A (ALK-3) phosphorylates Smad8 and induces its interaction with Smad4, nuclear translocation of Smad8, and cooperative transcriptional activation of BMP-responsive promoter Xvent2; ALK-5 (TGFβ type I receptor) does not activate Smad8, demonstrating specificity. In vitro transfection, co-immunoprecipitation, reporter assay, dominant-negative constructs Biochemical and biophysical research communications Medium 10814522
2005 BMPR1A and BMPR1B are functionally redundant during early chondrogenesis; double conditional knockout mice develop severe chondrodysplasia with absence of Sox9, L-Sox5, and Sox6 expression in precartilaginous condensations, increased apoptosis, and decreased proliferation, placing BMP signaling through these receptors upstream of Sox transcription factors. Double conditional knockout (Cre/lox), gene expression analysis, histology Proceedings of the National Academy of Sciences of the United States of America High 15781876
2005 ALK3/BMPR1A in AV canal myocardium is required for development of AV valves and annulus fibrosus; lineage analysis showed AV canal myocytes contribute to specific leaflets, and deletion of Alk3 in these cells causes defects in the same leaflets and disrupted annulus fibrosus leading to ventricular pre-excitation. Conditional knockout (Cre/lox), lineage tracing, ECG analysis Circulation research High 16037571
2006 Autocrine BMP signaling through BMPR1A in distal lung epithelium regulates proliferation, survival, and morphogenetic behavior; deletion of Bmpr1a in epithelium causes apoptosis, reduced proliferation, and failure of secondary budding in mesenchyme-free culture, with phenotype not rescued by deletion of pro-apoptotic Bax alone. Conditional knockout (Cre/lox), Bax double mutant epistasis, mesenchyme-free culture in Matrigel Developmental biology High 16414041
2006 Endocardial/endothelial Alk3 deletion severely impairs epithelial-mesenchymal transformation (EMT) in the AV canal, reducing mesenchymal cell number to ~20% of normal; Alk3 also regulates growth/survival of AV cushion mesenchymal cells through regulation of Smad activation and subcellular localization and cell-cycle regulators. Conditional knockout (Cre/lox), in vitro explant assays, section studies Developmental biology High 16959237
2007 BMPR1a signaling in olig1-expressing progenitors regulates oligodendrocyte lineage commitment and calbindin-positive interneuron specification in the dorsal cortex by controlling cell cycle length in subventricular zone progenitors. Conditional knockout (Cre/lox), cell counting, BrdU incorporation The Journal of neuroscience Medium 17626200
2007 BMP4-BMPR1A signaling in pancreatic beta cells is required for glucose-stimulated insulin secretion (GSIS); conditional attenuation of BMPR1A signaling in beta cells decreases expression of genes for insulin gene expression, proinsulin processing, glucose sensing, and insulin exocytosis, causing diabetes; transgenic BMP4 overexpression enhances GSIS. Conditional knockout/transgenic mice, glucose tolerance tests, gene expression analysis, systemic BMP4 administration Cell metabolism High 17339028
2007 Deletion of Bmpr1a in vascular smooth muscle cells attenuates pulmonary vascular remodeling; siRNA knockdown of Bmpr1a in pulmonary arterial smooth muscle cells reduces serum-induced proliferation, and knockdown in pericytes increases resistance to apoptosis, explaining decreased muscularization and vessel loss in hypoxia. Conditional knockout (Cre/lox), siRNA knockdown in cultured cells, proliferation and apoptosis assays Circulation research Medium 18079409
2008 ALK3/BMPR1A in the ureteric bud lineage controls renal collecting duct branching morphogenesis; Alk3 deficiency leads to abnormal ureteric bud branching, dysplastic renal phenotype with abnormal β-catenin and c-MYC expression in medullary tubules. Conditional knockout (Cre/lox), histology, gene expression analysis Journal of the American Society of Nephrology High 18178801
2008 BMP-2/ALK3 and HGF operate in parallel downstream pathways during renal collecting duct morphogenesis; HGF rescues BMP-2/ALK3 inhibition without blocking Smad1 phosphorylation, Smad1/Smad4 complex formation, or Smad1 nuclear translocation, indicating integration occurs at transcriptional or post-transcriptional levels. Stable cell line with constitutively active ALK3, Smad1 phosphorylation assay, reporter assay, tubule formation assay Journal of cell science Medium 10633078
2008 Prenatal deletion of Alk3 in lung epithelium disrupts distal airway formation, reduces surfactant secretion, and perturbs canonical Wnt signaling through reduced Wnt inhibitory factor-1 expression, placing ALK3 upstream of Wnt signaling in lung development. Inducible conditional knockout (Cre/lox), gene expression analysis, marker staining The American journal of pathology Medium 18258849
2009 TβRIII (TGFβ type III receptor) differentially modulates ALK3 and ALK6 subcellular trafficking: TβRIII associates with ALK3 primarily through extracellular domains and causes cell surface retention of ALK3 independently of β-arrestin2, whereas TβRIII/ALK6 interaction requires both extracellular and cytoplasmic domains and promotes ALK6 internalization, resulting in distinct downstream signaling. Co-immunoprecipitation, subcellular localization/internalization assays, reporter assay, mutagenesis Molecular biology of the cell High 19726563
2009 BMPR1A is the preferred BMP2 type I receptor in gonadotroph (LbetaT2) cells for regulating Fshb transcription; knockdown of endogenous BMPR1A, but not ACVR1 or BMPR1B, significantly impairs BMP2/activin A synergism on Fshb promoter activity and SMAD1/5 phosphorylation. siRNA knockdown, reporter assay, pharmacological inhibition, SMAD phosphorylation assay Biology of reproduction Medium 19211807
2009 Bmpr1a and Acvr1 in lens ectoderm regulate cell survival and proliferation respectively; they control lens formation through both Smad-dependent and Smad-independent pathways—FoxE3 expression, αA-crystallin, and placode proliferation are regulated in a Smad4-independent manner, while Sox2 maintenance requires canonical Smad signaling; Smad-independent BMP receptor signaling reorganizes the actin cytoskeleton to drive lens invagination. Conditional knockout (Cre/lox), Smad4/1/5 knockout comparisons, actin cytoskeleton analysis Developmental biology High 19733164
2010 BMPR1a and BMPR1b exert opposing effects on astrocytic hypertrophy after spinal cord injury; conditional ablation of BMPR1a from GFAP+ cells causes defective astrocytic hypertrophy, while BMPR1b null mice develop hyperactive reactive astrocytes; both receptors regulate astrocytic size through opposing posttranscriptional regulation of microRNA-21, with overexpression of miR-21 causing dramatic cell size reduction. Conditional knockout (Cre/lox), double knockout epistasis, miR-21 overexpression, cell size measurement The Journal of neuroscience High 20130193
2010 Bmpr1a signaling in the epiblast regulates anterior visceral endoderm (AVE) migration by inducing Wnt3/Wnt3a expression to maintain WNT signaling in the visceral endoderm, which establishes the anterior Dkk1 expression domain required for directional AVE migration; epiblast-specific Bmpr1a deletion causes random AVE migration and circumferential Dkk1 expression. Conditional knockout (Cre/lox), WNT3A rescue experiment in embryo culture, gene expression analysis Developmental biology High 20211162
2010 Bmpr1a signaling in palatal mesenchyme regulates cell proliferation in the primary and anterior secondary palate; loss of Bmpr1a reduces Msx1 and Fgf10 expression in mesenchyme and Shh in epithelium, indicating BMPR1A controls mesenchymal-epithelial interactions during palatal outgrowth. Conditional knockout (Cre/lox), gene expression analysis, cell proliferation assay Developmental biology High 21185278
2011 Conditional deletion of Bmpr1a in differentiated osteoclasts increases osteoblastic bone formation (increased bone formation rates), indicating BMPR1A signaling in osteoclasts negatively regulates coupling to osteoblasts; osteoblast-specific deletion of Bmpr1a had opposite effect with decreased bone formation rate. Conditional knockout (Cre/lox), bone histomorphometry, bone marker analysis Journal of bone and mineral research High 21786321
2011 Alk3 in intermediate mesoderm progenitors controls nephron number via phospho-p38 MAPK signaling (in metanephric mesenchyme) and androgen production via phospho-SMAD1/5/8 signaling (in testis), demonstrating lineage-specific signaling effectors downstream of ALK3. Conditional knockout (Cre/lox), signaling pathway analysis (pSMAD and p-p38), histology Development (Cambridge, England) Medium 21613322
2013 BMP15 suppresses progesterone production in human granulosa cells via ALK3-mediated SMAD1/5/8 phosphorylation leading to downregulation of StAR; siRNA-mediated depletion of ALK3 reverses BMP15-induced SMAD1/5/8 phosphorylation and StAR suppression. siRNA knockdown, pharmacological inhibition (dorsomorphin, DMH-1), SMAD phosphorylation assay, progesterone measurement Molecular endocrinology High 24140593
2013 ALK3/BMPR1A is required for blastocyst attachment and uterine implantation; conditional knockout in uterus causes increased microvilli density, maintained apical polarity, elevated E2 response, and unopposed epithelial proliferation; mechanistically, BMPR1A-SMAD4 signaling and progesterone receptor cooperatively regulate Klf15 to inhibit uterine epithelial proliferation. Conditional knockout (Cre/lox), gene expression analysis, in vivo fertility assay Proceedings of the National Academy of Sciences of the United States of America High 26721398
2014 HFE protein interacts with ALK3/BMPR1A, inhibiting ALK3 ubiquitination and proteasomal degradation, thereby increasing ALK3 protein expression and cell surface accumulation; this leads to enhanced SMAD1/5/8 phosphorylation and hepcidin expression; HH-associated HFE mutants (C282Y, H63D) fail to increase ALK3 cell-surface expression. Co-immunoprecipitation, ubiquitination assay, cell surface biotinylation, HFE mutant analysis, Hfe knockout mice Blood High 24904118
2014 USP15 is a deubiquitylating enzyme that interacts with SMAD6 and ALK3/BMPR1A; USP15 deubiquitylates ALK3, reducing K48-linked polyubiquitylation and preventing proteasomal degradation, thereby enhancing BMP-induced SMAD1 phosphorylation and transcription of BMP target genes; loss of USP15 inhibits BMP-induced osteoblast differentiation. Co-immunoprecipitation, ubiquitination assay (K48-linkage specific), siRNA knockdown, osteoblast differentiation assay, Xenopus embryo experiments Open biology High 24850914
2014 miR-885-3p inhibits BMP/Smad/Id1-mediated angiogenesis by directly targeting BMPR1A; overexpression or silencing of BMPR1A affects Smad1/5/8 phosphorylation and Id1 expression in a Smad-dependent manner, controlling angiogenesis. miRNA target validation (luciferase), siRNA/overexpression, SMAD phosphorylation assay, in vivo xenograft Oncogene Medium 24882581
2015 BMP4 and BMP7 suppress StAR expression and progesterone production in human granulosa-lutein cells via ALK3 and SMAD1/5/8-SMAD4 signaling; siRNA knockdown of ALK3 (but not ALK2 or ALK6) reverses BMP4/7-induced SMAD1/5/8 phosphorylation and StAR suppression; SMAD4 knockdown abolishes the effect. siRNA knockdown (receptor-specific), pharmacological inhibitors, SMAD phosphorylation assay, progesterone measurement Endocrinology High 26302112
2015 Physiological BMPR1A signaling in osteoblast lineage exerts dual function: it suppresses trabecular bone formation by restricting preosteoblast proliferation (through effectors beyond Smad4, since Smad4 deletion had minor effect), while also promoting osteoblast activity and periosteal bone growth through mTORC1 signaling; inhibition of mTORC1 abolishes BMP2-induced protein anabolism genes in vitro. Conditional knockout (Cre/lox), inducible Cre, Smad4 knockout comparison, mTORC1 inhibition in vitro Development (Cambridge, England) High 26657771
2016 BMP signaling through BMPR1A in osteocytes suppresses SOST (sclerostin) and RANKL, and increases Wnt/β-catenin signaling; osteocyte-specific Bmpr1a deletion causes dramatic increase in bone mass with decreased osteoclast numbers, establishing that BMPR1A in osteocytes controls bone remodeling by simultaneously inhibiting RANKL (reducing osteoclastogenesis) and inhibiting SOST (activating Wnt). Conditional knockout (Cre/lox), molecular analysis of Sost/RANKL/OPG/β-catenin, serum protein analysis, bone histomorphometry Bone High 27402532
2016 BMP signaling through BMPR1A in osteoclasts negatively regulates osteoblast mineralization through suppression of connexin 43 (Cx43/GJA1); co-culture of osteoblasts with BMPR1A-deficient osteoclasts promotes osteoblast mineralization; knockdown of Gja1 in mutant osteoclasts reduces this effect, identifying Cx43-mediated gap junction communication as the coupling mechanism. Co-culture assay, gene knockdown, mineralization assay Journal of cellular biochemistry Medium 27649478
2017 BMP signaling mediated by ALK3/BMPR1A in venous endothelial cells controls venous identity via SMAD1/SMAD5; perturbation of ALK3/BMPR1A in mice and zebrafish results in loss of Ephb4 (venous-specific gene) expression; a venous endothelium-specific Ephb4 enhancer shows enriched SMAD1/5 binding with required SMAD binding motifs. Conditional knockout (zebrafish and mouse), enhancer analysis, ChIP/SMAD binding motif analysis Nature communications High 30692543
2017 BmpR1A is the major type I BMP receptor for BMP-Smad signaling in neural crest cells during skull development; pSmad1/5/9 levels are undetectable in Bmpr1a homozygous null cells but not in Bmpr1b or Acvr1 null cells; heterozygous loss of Bmpr1a (but not Bmpr1b or Acvr1) rescues craniosynostosis in constitutively active BmpR1A mice, demonstrating dosage-sensitive, preferential signaling through BMPR1A. Conditional knockout, constitutively active receptor, genetic rescue experiments, pSmad analysis Developmental biology High 28641928
2017 Endothelial ALK2/ACVR1 and ALK3/BMPR1A both provide essential function for BMP-induced retinal angiogenesis in coordination with BMPR2; endothelial-specific deletion of either Alk2 or Alk3 causes delay in radial vascular expansion similar to BMPR2 deletion, identifying ALK2 and ALK3 as critical type I receptors for proangiogenic BMP signaling. Inducible endothelial-specific conditional knockout (Cre/lox), retinal vascular analysis Arteriosclerosis, thrombosis, and vascular biology High 28232325
2018 HFE signals predominantly via ALK3 to induce hepcidin in vivo; HFE overexpression in control mice increases hepcidin and pSmad1/5 levels, while HFE overexpression in hepatocyte-specific Alk3-deficient mice has no effect on hepcidin, pSmad1/5 levels, or blood parameters. AAV-mediated HFE overexpression in Alk3 conditional knockout mice, hepcidin measurement, pSmad analysis Communications biology High 30271947
2018 ALK3 undergoes ligand-independent homodimerization, whereas ALK2-ALK3 heterodimer formation is BMP ligand-dependent (BMP2 or BMP6); both ALK3-ALK3 and ALK2-ALK3 receptor complexes functionally induce hepcidin expression in Huh7 cells. Co-immunoprecipitation in presence/absence of BMP ligands, hepcidin reporter assay Free radical biology & medicine Medium 30227271
2018 IL-6 potentiates BMP-2-induced osteogenic and adipogenic differentiation by promoting cell surface translocation of BMPR1A, which amplifies BMPR1A-mediated BMP/Smad and p38 MAPK pathways respectively in human BMSCs. Cell surface translocation assay, SMAD and MAPK pathway activation assays, differentiation assays Cell death & disease Medium 29396550
2018 BMP4 controls ΔNp73 expression through BMPR1A, which directly induces NANOG expression and stem-like features in AML leukemic cells; BMPR1A transcript is increased in AML samples and further upregulated by BMP4, and high BMPR1A expression correlates with patient outcome. Gene expression analysis, functional stem cell assays (ALDH, functional assays), correlation analysis Cell death & disease Medium 30262802
2019 BMPR1a is S-palmitoylated in mouse neural stem cells; genetic manipulation of S-acylated sites affects BMPR1a localization and trafficking, alters BMP signaling, and modulates NSC fate—defective palmitoylation of BMPR1a leads to enhanced oligodendrogenesis in mouse brain. Unbiased acylation screen, site-directed mutagenesis of palmitoylation sites, subcellular localization assay, in vivo NSC manipulation Proceedings of the National Academy of Sciences of the United States of America High 31772009
2020 BMPR1A is necessary for chondrogenesis and osteogenesis (signaled through BMPR1A-BMPR2 dimerization), while BMPR1B signaling prevents chondrocyte hypertrophy; GDF5 mutants with decreased BMPR1A affinity show minimal chondrogenic/osteogenic activity; stronger BMPR1B-BMPR2 dimerization reduces hypertrophic differentiation. GDF5 mutants with altered receptor affinity, receptor dimerization assay, chondrogenic/osteogenic differentiation assays Journal of cell science Medium 32764110
2021 BMPR1A is essential for suture stem cell (SuSC) self-renewal; SuSC-specific disruption of Bmpr1a causes precocious differentiation leading to craniosynostosis initiated at the suture midline; BMPR1A was identified as a cell surface marker of human SuSCs, and SuSCs maintained stemness ex vivo without losing osteogenic ability. Conditional knockout, ex vivo SuSC culture system, human cell marker identification Science translational medicine High 33658353
2022 LAPTM5 promotes lung-specific metastasis by recruiting WWP2 E3 ubiquitin ligase, which binds to BMPR1A and mediates its lysosomal sorting, ubiquitination, and degradation; BMPR1A expression is restored by lysosomal inhibitor chloroquine, and LAPTM5-mediated BMPR1A degradation blocks BMP signaling to sustain cancer stem cell-like traits. Co-immunoprecipitation, ubiquitination assay, lysosomal inhibitor treatment, conditional KO, lineage tracing Nature communications High 35842443
2023 BMPR1A activation in endothelial cells induces physical interaction between ID2 and ZEB1, sequestering ZEB1 to attenuate Tgfbr2 transcription, thereby reducing EC sensitivity to TGFβ and preventing excessive endothelial-to-mesenchymal transition (EndoMT); endothelial Bmpr1a deletion causes PAH-like symptoms via excessive EndoMT, rescued by endothelial targeting of siRNA against Tgfbr2. Conditional knockout, lineage tracing, Co-IP (ID2-ZEB1 interaction), siRNA-LNP therapeutic rescue, ChIP/transcription analysis Cardiovascular research High 36166408

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Bmpr1a and Bmpr1b have overlapping functions and are essential for chondrogenesis in vivo. Proceedings of the National Academy of Sciences of the United States of America 339 15781876
2002 Requirement of Bmpr1a for Müllerian duct regression during male sexual development. Nature genetics 336 12368913
2004 Epithelial Bmpr1a regulates differentiation and proliferation in postnatal hair follicles and is essential for tooth development. Development (Cambridge, England) 311 15102710
2002 Endocardial cushion and myocardial defects after cardiac myocyte-specific conditional deletion of the bone morphogenetic protein receptor ALK3. Proceedings of the National Academy of Sciences of the United States of America 231 11854453
2004 The prevalence of MADH4 and BMPR1A mutations in juvenile polyposis and absence of BMPR2, BMPR1B, and ACVR1 mutations. Journal of medical genetics 199 15235019
2001 Germline mutations in BMPR1A/ALK3 cause a subset of cases of juvenile polyposis syndrome and of Cowden and Bannayan-Riley-Ruvalcaba syndromes. American journal of human genetics 185 11536076
2003 Developmental expression of BMP4/ALK3/SMAD5 signaling pathway in the mouse testis: a potential role of BMP4 in spermatogonia differentiation. Journal of cell science 167 12857787
2002 Germline SMAD4 or BMPR1A mutations and phenotype of juvenile polyposis. Annals of surgical oncology 131 12417513
2010 BMPR1a and BMPR1b signaling exert opposing effects on gliosis after spinal cord injury. The Journal of neuroscience : the official journal of the Society for Neuroscience 129 20130193
2002 Juvenile polyposis: massive gastric polyposis is more common in MADH4 mutation carriers than in BMPR1A mutation carriers. Human genetics 128 12136244
2006 Evidence that autocrine signaling through Bmpr1a regulates the proliferation, survival and morphogenetic behavior of distal lung epithelial cells. Developmental biology 126 16414041
2007 BMP4-BMPR1A signaling in beta cells is required for and augments glucose-stimulated insulin secretion. Cell metabolism 116 17339028
2005 Alk3/Bmpr1a receptor is required for development of the atrioventricular canal into valves and annulus fibrosus. Circulation research 113 16037571
2008 Large genomic deletions of SMAD4, BMPR1A and PTEN in juvenile polyposis. Gut 100 18178612
2010 Granulosa cell-expressed BMPR1A and BMPR1B have unique functions in regulating fertility but act redundantly to suppress ovarian tumor development. Molecular endocrinology (Baltimore, Md.) 96 20363875
2006 Contiguous gene deletion within chromosome arm 10q is associated with juvenile polyposis of infancy, reflecting cooperation between the BMPR1A and PTEN tumor-suppressor genes. American journal of human genetics 93 16685657
2008 The rate of germline mutations and large deletions of SMAD4 and BMPR1A in juvenile polyposis. Clinical genetics 89 18823382
2014 HFE interacts with the BMP type I receptor ALK3 to regulate hepcidin expression. Blood 86 24904118
2010 Bmpr1a signaling plays critical roles in palatal shelf growth and palatal bone formation. Developmental biology 84 21185278
2004 BMPR1A signaling is necessary for hair follicle cycling and hair shaft differentiation in mice. Development (Cambridge, England) 81 15084466
2009 Temporal regulation of BMP2, BMP6, BMP15, GDF9, BMPR1A, BMPR1B, BMPR2 and TGFBR1 mRNA expression in the oocyte, granulosa and theca cells of developing preovulatory follicles in the pig. Reproduction (Cambridge, England) 79 19359354
2013 BMP15 suppresses progesterone production by down-regulating StAR via ALK3 in human granulosa cells. Molecular endocrinology (Baltimore, Md.) 75 24140593
2006 Essential functions of Alk3 during AV cushion morphogenesis in mouse embryonic hearts. Developmental biology 75 16959237
2017 Unintended targeting of Dmp1-Cre reveals a critical role for Bmpr1a signaling in the gastrointestinal mesenchyme of adult mice. Bone research 73 28163952
2011 Conditional deletion of Bmpr1a in differentiated osteoclasts increases osteoblastic bone formation, increasing volume of remodeling bone in mice. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 71 21786321
2009 The type I BMP receptors, Bmpr1a and Acvr1, activate multiple signaling pathways to regulate lens formation. Developmental biology 65 19733164
2009 Adipose tissue expression and genetic variants of the bone morphogenetic protein receptor 1A gene (BMPR1A) are associated with human obesity. Diabetes 64 19502417
2021 BMPR1A maintains skeletal stem cell properties in craniofacial development and craniosynostosis. Science translational medicine 61 33658353
2013 Synthesis and structure-activity relationships of a novel and selective bone morphogenetic protein receptor (BMP) inhibitor derived from the pyrazolo[1.5-a]pyrimidine scaffold of dorsomorphin: the discovery of ML347 as an ALK2 versus ALK3 selective MLPCN probe. Bioorganic & medicinal chemistry letters 61 23639540
2015 Dual function of Bmpr1a signaling in restricting preosteoblast proliferation and stimulating osteoblast activity in mouse. Development (Cambridge, England) 60 26657771
2019 Venous identity requires BMP signalling through ALK3. Nature communications 57 30692543
2015 Uterine ALK3 is essential during the window of implantation. Proceedings of the National Academy of Sciences of the United States of America 57 26721398
2006 Mapping of hereditary mixed polyposis syndrome (HMPS) to chromosome 10q23 by genomewide high-density single nucleotide polymorphism (SNP) scan and identification of BMPR1A loss of function. Journal of medical genetics 57 16525031
2020 Disease expression in juvenile polyposis syndrome: a retrospective survey on a cohort of 221 European patients and comparison with a literature-derived cohort of 473 SMAD4/BMPR1A pathogenic variant carriers. Genetics in medicine : official journal of the American College of Medical Genetics 55 32398773
2013 Expression of the BMP receptor Alk3 in the second heart field is essential for development of the dorsal mesenchymal protrusion and atrioventricular septation. Circulation research 55 23584254
2003 Elevated SMAD1/beta-catenin molecular complexes and renal medullary cystic dysplasia in ALK3 transgenic mice. Development (Cambridge, England) 55 12736218
2014 MicroRNA-885-3p inhibits the growth of HT-29 colon cancer cell xenografts by disrupting angiogenesis via targeting BMPR1A and blocking BMP/Smad/Id1 signaling. Oncogene 51 24882581
2007 BMPR1a signaling determines numbers of oligodendrocytes and calbindin-expressing interneurons in the cortex. The Journal of neuroscience : the official journal of the Society for Neuroscience 51 17626200
2013 Prevalence of germline PTEN, BMPR1A, SMAD4, STK11, and ENG mutations in patients with moderate-load colorectal polyps. Gastroenterology 50 23399955
2000 Mouse smad8 phosphorylation downstream of BMP receptors ALK-2, ALK-3, and ALK-6 induces its association with Smad4 and transcriptional activity. Biochemical and biophysical research communications 50 10814522
2018 P2RY1/ALK3-Expressing Cells within the Adult Human Exocrine Pancreas Are BMP-7 Expandable and Exhibit Progenitor-like Characteristics. Cell reports 48 29490276
2007 Abnormal conduction and morphology in the atrioventricular node of mice with atrioventricular canal targeted deletion of Alk3/Bmpr1a receptor. Circulation 46 17998461
2022 Exosomal miR-143-3p derived from follicular fluid promotes granulosa cell apoptosis by targeting BMPR1A in polycystic ovary syndrome. Scientific reports 45 35288625
2014 USP15 targets ALK3/BMPR1A for deubiquitylation to enhance bone morphogenetic protein signalling. Open biology 44 24850914
2008 BMP receptor ALK3 controls collecting system development. Journal of the American Society of Nephrology : JASN 44 18178801
2003 Effect of the distribution and clustering of the type I A BMP receptor (ALK3) with the type II BMP receptor on the activation of signalling pathways. Journal of cell science 44 12829744
2008 Prenatal lung epithelial cell-specific abrogation of Alk3-bone morphogenetic protein signaling causes neonatal respiratory distress by disrupting distal airway formation. The American journal of pathology 43 18258849
2018 IL-6 potentiates BMP-2-induced osteogenesis and adipogenesis via two different BMPR1A-mediated pathways. Cell death & disease 42 29396550
2007 Smooth muscle protein 22alpha-mediated patchy deletion of Bmpr1a impairs cardiac contractility but protects against pulmonary vascular remodeling. Circulation research 42 18079409
2015 Deletion of the BMP receptor BMPR1a impairs mammary tumor formation and metastasis. Oncotarget 40 26274893
2014 miR-656 inhibits glioma tumorigenesis through repression of BMPR1A. Carcinogenesis 40 24480809
2016 Targeted disruption of BMP signaling through type IA receptor (BMPR1A) in osteocyte suppresses SOST and RANKL, leading to dramatic increase in bone mass, bone mineral density and mechanical strength. Bone 39 27402532
2017 Alk2/ACVR1 and Alk3/BMPR1A Provide Essential Function for Bone Morphogenetic Protein-Induced Retinal Angiogenesis. Arteriosclerosis, thrombosis, and vascular biology 38 28232325
2022 Lysosomal protein transmembrane 5 promotes lung-specific metastasis by regulating BMPR1A lysosomal degradation. Nature communications 37 35842443
2016 Ginsenosides Rg3 attenuates glucocorticoid-induced osteoporosis through regulating BMP-2/BMPR1A/Runx2 signaling pathway. Chemico-biological interactions 37 27387537
2009 The transforming growth factor-beta type III receptor mediates distinct subcellular trafficking and downstream signaling of activin-like kinase (ALK)3 and ALK6 receptors. Molecular biology of the cell 36 19726563
2000 BMP-2/ALK3 and HGF signal in parallel to regulate renal collecting duct morphogenesis. Journal of cell science 36 10633078
2014 Intramuscular adipogenesis is inhibited by myo-endothelial progenitors with functioning Bmpr1a signalling. Nature communications 35 24898859
2015 BMP4 and BMP7 Suppress StAR and Progesterone Production via ALK3 and SMAD1/5/8-SMAD4 in Human Granulosa-Lutein Cells. Endocrinology 34 26302112
2020 BMPR1A is necessary for chondrogenesis and osteogenesis, whereas BMPR1B prevents hypertrophic differentiation. Journal of cell science 32 32764110
2018 A new signaling cascade linking BMP4, BMPR1A, ΔNp73 and NANOG impacts on stem-like human cell properties and patient outcome. Cell death & disease 32 30262802
2005 Vessels' morphology in SMAD4 and BMPR1A-related juvenile polyposis. American journal of medical genetics. Part A 32 16152648
2020 BMPR1A and BMPR1B Missense Mutations Cause Primary Ovarian Insufficiency. The Journal of clinical endocrinology and metabolism 31 31769494
2009 Bone morphogenetic protein 2 signals via BMPR1A to regulate murine follicle-stimulating hormone beta subunit transcription. Biology of reproduction 31 19211807
2019 Assessment of structurally and functionally high-risk nsSNPs impacts on human bone morphogenetic protein receptor type IA (BMPR1A) by computational approach. Computational biology and chemistry 30 30884445
2018 Transcriptional and translational abundance of Bone morphogenetic protein (BMP) 2, 4, 6, 7 and their receptors BMPR1A, 1B and BMPR2 in buffalo ovarian follicle and the role of BMP4 and BMP7 on estrogen production and survival of cultured granulosa cells. Research in veterinary science 30 29684814
2017 ALK2/ALK3-BMPR2/ACVR2A Mediate BMP2-Induced Downregulation of Pentraxin 3 Expression in Human Granulosa-Lutein Cells. Endocrinology 29 28977600
2009 Hereditary mixed polyposis syndrome due to a BMPR1A mutation. Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland 29 19438883
2010 Bmpr1a is required for proper migration of the AVE through regulation of Dkk1 expression in the pre-streak mouse embryo. Developmental biology 28 20211162
2009 Myoblast sensitivity and fibroblast insensitivity to osteogenic conversion by BMP-2 correlates with the expression of Bmpr-1a. BMC musculoskeletal disorders 27 19442313
2021 Targeting local lymphatics to ameliorate heterotopic ossification via FGFR3-BMPR1a pathway. Nature communications 26 34282140
2020 BMP Ligand Trap ALK3-Fc Attenuates Osteogenesis and Heterotopic Ossification in Blast-Related Lower Extremity Trauma. Stem cells and development 26 33256557
2017 BmpR1A is a major type 1 BMP receptor for BMP-Smad signaling during skull development. Developmental biology 26 28641928
2017 Bone morphogenetic protein signaling through ACVR1 and BMPR1A negatively regulates bone mass along with alterations in bone composition. Journal of structural biology 26 29175363
2016 Loss of BMP signaling through BMPR1A in osteoblasts leads to greater collagen cross-link maturation and material-level mechanical properties in mouse femoral trabecular compartments. Bone 26 27113526
2013 Germline Mutations in the Polyposis-Associated Genes BMPR1A, SMAD4, PTEN, MUTYH and GREM1 Are Not Common in Individuals with Serrated Polyposis Syndrome. PloS one 26 23805267
2010 Discovery of the BMPR1A promoter and germline mutations that cause juvenile polyposis. Human molecular genetics 26 20843829
2019 MiR-15b-5p is Involved in Doxorubicin-Induced Cardiotoxicity via Inhibiting Bmpr1a Signal in H9c2 Cardiomyocyte. Cardiovascular toxicology 25 30535663
2016 BMP Signaling Mediated by BMPR1A in Osteoclasts Negatively Regulates Osteoblast Mineralization Through Suppression of Cx43. Journal of cellular biochemistry 25 27649478
2014 Alk3 mediated Bmp signaling controls the contribution of epicardially derived cells to the tissues of the atrioventricular junction. Developmental biology 25 25300579
2016 Differential requirement of bone morphogenetic protein receptors Ia (ALK3) and Ib (ALK6) in early embryonic patterning and neural crest development. BMC developmental biology 24 26780949
2011 BMPR1A is a candidate gene for congenital heart defects associated with the recurrent 10q22q23 deletion syndrome. European journal of medical genetics 24 22067610
2014 Critical role of Bmpr1a in mandibular condyle growth. Connective tissue research 23 25158185
2023 BMPR1A promotes ID2-ZEB1 interaction to suppress excessive endothelial to mesenchymal transition. Cardiovascular research 22 36166408
2019 Palmitoylation of BMPR1a regulates neural stem cell fate. Proceedings of the National Academy of Sciences of the United States of America 22 31772009
2016 Enrichment of Adipose-Derived Stromal Cells for BMPR1A Facilitates Enhanced Adipogenesis. Tissue engineering. Part A 22 26585335
2015 Somatic alterations in juvenile polyps from BMPR1A and SMAD4 mutation carriers. Genes, chromosomes & cancer 22 26171675
2012 BMP-6 and BMPR-1a are up-regulated in the growth plate of the fractured tibia. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 22 23097200
2023 Single-cell analysis of the postnatal dorsal V-SVZ reveals a role for Bmpr1a signaling in silencing pallial germinal activity. Science advances 21 37146152
2018 ALK3 undergoes ligand-independent homodimerization and BMP-induced heterodimerization with ALK2. Free radical biology & medicine 21 30227271
2011 Alk3 controls nephron number and androgen production via lineage-specific effects in intermediate mesoderm. Development (Cambridge, England) 21 21613322
2004 Loss of heterozygosity on 10q and mutational status of PTEN and BMPR1A in colorectal primary tumours and metastases. British journal of cancer 21 15026806
2007 Deficient Alk3-mediated BMP signaling causes prenatal omphalocele-like defect. Biochemical and biophysical research communications 19 17588538
2018 Knockdown of Bone Morphogenetic Proteins Type 1a Receptor (BMPR1a) in Breast Cancer Cells Protects Bone from Breast Cancer-Induced Osteolysis by Suppressing RANKL Expression. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 18 29495003
2015 Bmpr1a Signaling in Cartilage Development and Endochondral Bone Formation. Vitamins and hormones 18 26279380
2003 Identification of a novel BMPR1A germline mutation in a Korean juvenile polyposis patient without SMAD4 mutation. Clinical genetics 18 12630959
2022 BMP7-based peptide agonists of BMPR1A protect the left ventricle against pathological remodeling induced by pressure overload. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 16 35616049
2020 Loss of BMP signaling mediated by BMPR1A in osteoblasts leads to differential bone phenotypes in mice depending on anatomical location of the bones. Bone 16 32360900
2018 The hemochromatosis protein HFE signals predominantly via the BMP type I receptor ALK3 in vivo. Communications biology 16 30271947
2021 mTOR inhibitors reduce enteropathy, intestinal bleeding and colectomy rate in patients with juvenile polyposis of infancy with PTEN-BMPR1A deletion. Human molecular genetics 15 33822054