Affinage

BMPR1A

Bone morphogenetic protein receptor type-1A · UniProt P36894

Length
532 aa
Mass
60.2 kDa
Annotated
2026-06-09
100 papers in source corpus 50 papers cited in narrative 50 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BMPR1A (ALK3) is a type I BMP receptor serine/threonine kinase that, upon ligand binding, phosphorylates receptor-SMADs (SMAD1/5/8) to drive their association with SMAD4, nuclear translocation, and BMP-responsive transcription (PMID:10814522, PMID:12857787). It functions within heteromeric receptor complexes: ALK3 undergoes ligand-independent homodimerization and forms ligand-dependent heterodimers with ALK2, and co-expression of the type II receptor BMPR2 is required for surface receptor rearrangement and SMAD activation (PMID:12829744, PMID:30227271). Receptor abundance and signaling output are tuned by post-translational control of receptor stability and trafficking — USP15 removes K48-linked polyubiquitin from ALK3 to stabilize it, HFE blocks ALK3 ubiquitination to raise cell-surface levels, the LAPTM5–WWP2 module ubiquitinates ALK3 for lysosomal degradation, and S-palmitoylation governs its membrane localization (PMID:24850914, PMID:24904118, PMID:31772009, PMID:35842443). Beyond canonical SMAD signaling, ALK3 engages SMAD-independent effectors including p38 MAPK and mTORC1 (PMID:26657771, PMID:21613322). Through these pathways ALK3 acts as a context-dependent hub across development and tissue homeostasis: it mediates AMH-induced Müllerian duct regression, cardiac valvulogenesis and ventricular morphogenesis, chondrogenesis (redundantly with BMPR1B, upstream of Sox9/L-Sox5/Sox6), skull suture stem-cell self-renewal, hair follicle and lung/kidney branching morphogenesis, and pancreatic beta-cell insulin secretion (PMID:12368913, PMID:11854453, PMID:15781876, PMID:17339028, PMID:33658353, PMID:18178801). Its downstream hierarchy repeatedly intersects WNT/β-catenin signaling and dedicated effector axes such as SMAD4–KLF15 in uterus, SOST/RANKL/OPG in bone, and ID2–ZEB1–TGFBR2 controlling endothelial-to-mesenchymal transition, with endothelial ALK3 maintaining venous identity via Ephb4 and protecting against PAH-like remodeling (PMID:26721398, PMID:27402532, PMID:36166408, PMID:30692543).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 2000 High

    Established that ALK3 is a BMP-specific (not TGFβ) type I receptor that phosphorylates R-SMADs to drive SMAD4 complex formation and BMP-responsive transcription, defining its core signaling output.

    Evidence Constitutively active receptor reporter assays, co-IP, and nuclear translocation assays for Smad8; constitutively active ALK3 in collecting duct cells with Smad1 readouts

    PMID:10633078 PMID:10814522

    Open questions at the time
    • Used constitutively active constructs rather than ligand-driven activation
    • Did not address selectivity among BMP ligands at the endogenous receptor
  2. 2002 High

    Conditional knockouts first revealed ALK3's in vivo tissue requirements, linking it to AMH-induced Müllerian duct regression and to cardiac morphogenesis through paracrine TGFβ2 induction.

    Evidence Tissue-specific Cre/lox deletion in Müllerian duct mesenchyme and cardiac myocytes with phenotypic and molecular analysis

    PMID:11854453 PMID:12368913

    Open questions at the time
    • Mechanism connecting ALK3 to TGFβ2 transcription not resolved
    • Receptor partners in these tissues not defined in vivo
  3. 2003 Medium

    Defined the receptor-complex requirements for signaling — that BMPRII kinase activity drives ALK3 surface rearrangement — and placed ALK3 upstream of WNT/β-catenin in renal tissue.

    Evidence Image correlation spectroscopy of surface clustering with kinase-inactive BMPRII; transgenic ALK3QD with SMAD1/β-catenin/SMAD4 co-IP and Tcf reporter

    PMID:12736218 PMID:12829744

    Open questions at the time
    • Surface clustering studied in overexpression systems
    • Physical basis of ALK3–β-catenin pathway convergence not structurally defined
  4. 2004 High

    Showed that epithelial ALK3 acts upstream of WNT/β-catenin activation in skin appendages, establishing a recurring BMP→WNT hierarchy in organogenesis.

    Evidence Surface-epithelium conditional knockout with nuclear β-catenin and transcription-factor expression analysis; hair follicle conditional knockout

    PMID:15084466 PMID:15102710

    Open questions at the time
    • Direct molecular link from ALK3/SMAD to β-catenin nuclear entry not mapped
    • Ligand source in follicle not defined here
  5. 2005 High

    Genetic epistasis placed ALK3 (redundantly with BMPR1B) upstream of the Sox9/L-Sox5/Sox6 cartilage transcription program and defined distinct cardiac valve lineage requirements.

    Evidence Cartilage single/double conditional knockouts with Sox factor profiling; AV-canal myocyte conditional deletion with lineage tracing

    PMID:15781876 PMID:16037571

    Open questions at the time
    • Functional redundancy obscures ALK3-specific targets
    • Direct vs indirect regulation of Sox genes unresolved
  6. 2006 High

    Demonstrated autocrine ALK3 signaling controlling epithelial proliferation, survival, and EMT in lung and AV cushion, expanding its role to cell-fate and morphogenetic behaviors.

    Evidence Sftpc-cre and Tie1-Cre conditional knockouts with mesenchyme-free culture, genetic Bax rescue, and explant EMT assays

    PMID:16414041 PMID:16959237

    Open questions at the time
    • SMAD-dependent vs -independent contribution not separated
    • Downstream cell-cycle effectors only partially identified
  7. 2007 High

    Extended ALK3 function to endocrine and neural-progenitor contexts, linking BMP4–ALK3 to glucose-stimulated insulin secretion and to progenitor cell-cycle control governing oligodendrocyte fate.

    Evidence Beta-cell conditional KO with GTT, transgenic and pharmacological BMP4; olig1-progenitor conditional KO with cell counting and cell-cycle analysis

    PMID:17339028 PMID:17626200

    Open questions at the time
    • Direct transcriptional targets in beta cells not defined
    • Mechanism coupling ALK3 to cell-cycle length unresolved
  8. 2009 High

    Identified co-receptor and isoform selectivity: TβRIII retains ALK3 at the surface to enhance ID-1 signaling, and ALK3 (not ALK2/ALK6) is the preferred receptor for specific BMP transcriptional responses.

    Evidence Reciprocal co-IP with domain-mapping mutants and reporter assays; isoform-specific siRNA in gonadotroph cells with constitutively active receptors

    PMID:19211807 PMID:19726563

    Open questions at the time
    • Determinants of receptor-isoform preference not generalized across cell types
    • β-arrestin-independent retention mechanism incompletely defined
  9. 2010 High

    Conditional knockouts mapped ALK3 onto multiple WNT-linked developmental axes (epiblast Wnt3a→Dkk1, ureteric bud branching, palatal mesenchymal-epithelial crosstalk) and revealed opposing BMPR1A/BMPR1B effects via miR-21 in astrocytes.

    Evidence Sox2Cre/null and tissue-specific conditional KOs with WNT3A rescue, in situ hybridization, and miR-21 overexpression

    PMID:18178801 PMID:20130193 PMID:20211162 PMID:21185278

    Open questions at the time
    • Direct transcriptional intermediaries between ALK3 and Wnt ligand expression not identified
    • Mechanism of opposing receptor outputs on miR-21 unresolved
  10. 2011 High

    Showed ALK3 uses different effector branches in a tissue-specific manner — p38 MAPK for nephron progenitor markers versus pSMAD1/5/8 for Leydig cell formation — establishing branch selection as context-dependent.

    Evidence Intermediate mesoderm progenitor conditional KO with tissue-specific p38 and SMAD signaling readouts; osteoclast/osteoblast conditional KOs with histomorphometry

    PMID:21613322 PMID:21786321

    Open questions at the time
    • What dictates p38 vs SMAD branch selection unknown
    • Cell-type-intrinsic determinants of opposing bone outcomes undefined
  11. 2014 High

    Defined post-translational control of ALK3 abundance: USP15 deubiquitinates and stabilizes ALK3 while HFE blocks its ubiquitination to raise surface levels, both amplifying SMAD signaling, with HFE disease mutants losing this function.

    Evidence Co-IP, K48-linkage ubiquitylation assays, RNAi, SMAD1 phospho assays, and in vivo mouse/Xenopus validation

    PMID:24850914 PMID:24904118

    Open questions at the time
    • E3 ligase opposing USP15 on ALK3 not identified here
    • Quantitative contribution of receptor turnover to physiological output unknown
  12. 2015 High

    Resolved SMAD-dependent vs -independent effector usage and defined dedicated downstream axes — Smad4–KLF15 in uterus and an mTORC1-dependent anabolic branch in osteoblasts — broadening ALK3's mechanistic repertoire.

    Evidence Multiple conditional KOs with Smad4 epistasis, KLF15 dual-pathway transcription analysis, mTORC1 assays with rapamycin, and lens-tissue receptor comparisons

    PMID:19733164 PMID:24898859 PMID:26657771 PMID:26721398

    Open questions at the time
    • Identity of Smad4-independent effectors suppressing preosteoblast proliferation incompletely defined
    • Mechanism coupling ALK3 to mTORC1 not mapped
  13. 2016 High

    Identified osteocyte and osteoclast BMPR1A targets (SOST/RANKL/OPG and connexin 43) that mediate cell-cell communication controlling bone mass.

    Evidence Dmp1-Cre osteocyte conditional KO with micro-CT and molecular profiling; osteoclast-osteoblast co-culture with Cx43 knockdown

    PMID:27402532 PMID:27649478

    Open questions at the time
    • Direct vs indirect regulation of SOST/RANKL not established
    • Cx43 regulation studied only in co-culture
  14. 2017 High

    Established BMPR1A as the dominant type I receptor for SMAD-dependent BMP signaling in cranial development, since only Bmpr1a loss abolishes pSmad1/5/9 and dose-dependently controls craniosynostosis.

    Evidence Systematic conditional KO and heterozygous rescue of Bmpr1a, Bmpr1b, Acvr1 in neural crest with pSmad quantification; endothelial-specific KO retinal angiogenesis comparison

    PMID:28232325 PMID:28641928

    Open questions at the time
    • Basis for ALK3 dominance over other type I receptors unresolved
    • Receptor-partner stoichiometry in vivo not defined
  15. 2018 High

    Clarified receptor-complex assembly and additional trafficking control: ligand-independent ALK3 homodimers and ligand-dependent ALK2-ALK3 heterodimers both signal, and IL-6 promotes ALK3 surface translocation to amplify SMAD/p38 output.

    Evidence Co-IP with/without ligand and hepatocyte double KO iron phenotyping; surface-translocation and signaling assays with IL-6; AML pathway and granulosa-cell siRNA studies

    PMID:28977600 PMID:29396550 PMID:30227271 PMID:30262802

    Open questions at the time
    • Functional differences between homodimeric and heterodimeric complexes not dissected
    • Direct BMPR1A binding vs intermediate signaling in AML not separated
  16. 2018 High

    Provided in vivo genetic proof that ALK3 is the required mediator of HFE-driven hepcidin induction, integrating receptor-stability regulation with systemic iron homeostasis.

    Evidence AAV-Hfe overexpression in hepatocyte-specific Alk3 KO vs control mice with hepcidin and pSmad1/5 readouts

    PMID:30271947

    Open questions at the time
    • Whether HFE acts solely through stabilization or also via complex assembly not resolved
  17. 2019 High

    Identified S-palmitoylation as a lipid modification controlling ALK3 membrane localization and signaling strength, with consequences for neural stem cell oligodendrogenesis, and defined a direct ALK3/SMAD1/5 transcriptional target (Ephb4) governing venous identity.

    Evidence Palmitoylation proteomic screen with acylation-site mutagenesis and in vivo lineage analysis; SMAD1/5 ChIP/enhancer and motif mutagenesis at the Ephb4 venous enhancer in mouse and zebrafish

    PMID:30692543 PMID:31772009

    Open questions at the time
    • Palmitoyl transferase/thioesterase enzymes acting on ALK3 not identified
    • Generality of Ephb4 regulation beyond venous endothelium untested
  18. 2021 High

    Established ALK3 as a determinant of adult stem-cell self-renewal, marking and maintaining suture stem cells, with loss causing precocious differentiation and craniosynostosis.

    Evidence SuSC-specific conditional KO with ex vivo stem cell culture, lineage analysis, and human SuSC surface-marker characterization

    PMID:33658353

    Open questions at the time
    • Downstream effectors of ALK3 in stem-cell maintenance not defined
    • Ligand source in the suture niche unspecified
  19. 2022 High

    Defined a lysosomal degradation route — LAPTM5 recruiting WWP2 to ubiquitinate and degrade BMPR1A — that suppresses BMP signaling and promotes cancer stemness and organotropic metastasis.

    Evidence Co-IP of LAPTM5-WWP2-BMPR1A trimeric complex, ubiquitylation assays, chloroquine rescue, and in vivo metastasis models

    PMID:35842443

    Open questions at the time
    • Signal triggering LAPTM5-mediated sorting unknown
    • Relationship to proteasomal/USP15 regulation not integrated
  20. 2023 High

    Revealed ALK3's protective role in adult vasculature and brain: it restrains EndoMT through an ID2-ZEB1-TGFBR2 axis to prevent PAH-like remodeling and induces deep quiescence in pallial neural stem cells.

    Evidence Endothelial inducible conditional KO with ID2-ZEB1 co-IP, lineage tracing, and Tgfbr2 siRNA rescue; scRNA-seq with Bmpr1a manipulation in postnatal V-SVZ

    PMID:36166408 PMID:37146152

    Open questions at the time
    • How ALK3 activation drives ID2 to outcompete ZEB1 not mechanistically detailed
    • Effectors of quiescence induction downstream of ALK3 incompletely defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single receptor selects among SMAD-dependent, p38 MAPK, and mTORC1 branches, and how the competing ubiquitination, deubiquitination, palmitoylation, and lysosomal-sorting machineries are integrated to set context-specific signaling thresholds, remains unresolved.
  • No unifying model for effector-branch selection
  • Quantitative interplay of post-translational regulators not reconstituted
  • Structural basis of complex assembly with type II receptors and co-receptors undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0016740 transferase activity 2 GO:0060089 molecular transducer activity 2 GO:0140657 ATP-dependent activity 1
Localization
GO:0005886 plasma membrane 4 GO:0005764 lysosome 1
Pathway
R-HSA-1266738 Developmental Biology 5 R-HSA-392499 Metabolism of proteins 4 R-HSA-162582 Signal Transduction 3
Partners
ALK2/ACVR1BMPR2HFELAPTM5SMAD4TGFBR3USP15WWP2

Evidence

Reading pass · 50 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 BMPR1A (ALK3) is required in mesenchymal cells of the Müllerian duct as a type I receptor for AMH-induced Müllerian duct regression during male sexual development; conditional disruption of Bmpr1a in mesenchyme leads to retention of oviducts and uteri in males. Conditional knockout (Cre/lox) with tissue-specific deletion in Müllerian duct mesenchyme; phenotypic analysis of male reproductive tract Nature genetics High 12368913
2002 Cardiac myocyte-specific deletion of ALK3 (BMPR1A) causes defects in trabeculae, compact myocardium, interventricular septum, and endocardial cushion at mid-gestation; ALK3 is specifically required for expression of TGFβ2 in cardiac muscle, linking ALK3 signaling to a paracrine mediator of cushion morphogenesis. Cardiac myocyte-specific Cre/lox conditional knockout; phenotypic and molecular analysis including TGFβ2 expression Proceedings of the National Academy of Sciences of the United States of America High 11854453
2004 Epithelial BMPR1A is required for tooth morphogenesis and for differentiation of the hair shaft and inner root sheath in postnatal follicles; loss of BMPR1A in epithelium results in absence of nuclear β-catenin, placing WNT pathway activation downstream of BMPR1A signaling in postnatal follicles. Cre-mediated conditional knockout in surface epithelium; expression analysis of transcriptional regulators (Msx1, Msx2, Foxn1, Gata3, Lef1) and nuclear β-catenin localization Development (Cambridge, England) High 15102710
2004 BMPR1A signaling in hair follicle cells is essential for inner root sheath differentiation and for hair follicle cycling/renewal in adult skin. Hair follicle cell-specific conditional knockout (Cre/loxP); histological and molecular analysis Development (Cambridge, England) High 15084466
2005 BMPR1A and BMPR1B are functionally redundant during early chondrogenesis; double conditional knockout mice develop severe generalized chondrodysplasia with absent Sox9, L-Sox5, and Sox6 expression in condensations, increased apoptosis, decreased proliferation, and loss of cartilage-specific extracellular matrix proteins. Cartilage-specific single and double conditional knockouts; skeletal analysis, expression profiling of Sox transcription factors Proceedings of the National Academy of Sciences of the United States of America High 15781876
2005 ALK3 (BMPR1A) is required in AV canal myocardium for development of the tricuspid mural and posterior leaflets, mitral septal leaflet, and annulus fibrosus; lineage analysis showed AV canal myocytes contribute directly to these structures. Cre/lox conditional deletion targeted to AV canal cardiac myocytes; lineage tracing; electrophysiological and histological analysis Circulation research High 16037571
2006 Autocrine BMP/BMPR1A signaling in distal lung epithelium regulates proliferation, survival, and morphogenetic behavior; deletion of Bmpr1a in epithelium reduces proliferation and causes apoptosis, and mutant epithelium fails secondary budding in mesenchyme-free culture; Bmp4 epithelial deletion phenocopies this. Sftpc-cre conditional knockout; mesenchyme-free epithelial cultures in Matrigel; genetic rescue with Bax null background Developmental biology High 16414041
2006 Endocardial/endothelial-specific deletion of Alk3 severely impairs epithelial-mesenchymal transformation (EMT) in the AV canal; Alk3 regulates expression/activation/subcellular localization of Smads and cell-cycle regulators in AV cushion mesenchymal cells. Tie1-Cre endothelial conditional knockout; in vivo section studies and in vitro explant assays quantifying mesenchymal cell number Developmental biology High 16959237
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 involved in insulin transcription, proinsulin processing, glucose sensing, and exocytosis, causing diabetes. Beta cell-specific conditional knockout; glucose tolerance tests; transgenic BMP4 overexpression; systemic BMP4 administration Cell metabolism High 17339028
2007 BMPR1a signaling in olig1-expressing progenitors suppresses oligodendrocyte lineage commitment and specification of calbindin-positive interneurons in the dorsomedial cortex, at least in part through regulation of subventricular zone progenitor cell cycle length. Cre/loxP conditional knockout in olig1-expressing cells; cell counting of oligodendrocyte populations at multiple postnatal timepoints; cell cycle analysis The Journal of neuroscience : the official journal of the Society for Neuroscience High 17626200
2000 Constitutively active BMP type I receptors ALK3 (BMPR1A) and ALK6 (as well as ALK2) phosphorylate Smad8, inducing Smad8 interaction with Smad4, nuclear translocation of Smad8, and cooperative transcriptional activation of the BMP-responsive Xvent2 promoter; TGFβ type I receptor ALK5 does not phosphorylate Smad8. In vitro reporter assays with constitutively active receptor constructs; co-immunoprecipitation; nuclear translocation assays; alkaline phosphatase induction assay Biochemical and biophysical research communications High 10814522
2003 Co-expression of BMP type II receptor (BMPRII) influences aggregation and distribution of ALK3 at the cell surface; BMP-2 stimulation rearranges receptor complexes; co-expression of BMPRII with constitutively active ALK3 is required for Smad pathway activation; kinase activity of BMPRII is needed for ALK3 rearrangement. Image correlation spectroscopy; cell surface receptor clustering analysis in COS7 and A431 cells; kinase-inactive BMPRII mutant experiments Journal of cell science Medium 12829744
2003 Expression of constitutively active ALK3 (ALK3QD) in transgenic mice causes renal medullary cystic dysplasia; ALK3 signaling promotes formation of SMAD1/β-catenin/SMAD4 molecular complexes in dysplastic renal tissue, indicating functional cooperativity between ALK3 and WNT/β-catenin pathways in kidney. Transgenic mouse model with ALK3QD; histological analysis; co-immunoprecipitation of SMAD1/β-catenin/SMAD4 complexes; Tcf-lacZ reporter assay Development (Cambridge, England) Medium 12736218
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 the transcriptional coactivator p300/CBP, and drives both mitogenic and differentiative effects including Kit expression in undifferentiated spermatogonia. Cell culture of spermatogonia with BMP4; immunofluorescence for nuclear translocation; DNA-binding complex analysis; [3H]thymidine incorporation; Kit expression assay Journal of cell science Medium 12857787
2008 ALK3 (BMPR1A) controls ureteric bud branching morphogenesis in vivo; ureteric bud-specific deletion of Alk3 causes abnormal primary branching pattern, followed by fewer branches, and postnatal renal dysplasia with abnormal β-catenin and c-MYC expression in medullary tubules. Ureteric bud-specific conditional knockout (Alk3-UB-/-); renal morphological analysis at multiple developmental stages; molecular marker analysis Journal of the American Society of Nephrology : JASN High 18178801
2008 Prenatal abrogation of Alk3 in lung epithelial cells impairs distal airway formation, reduces cell proliferation and differentiation, disrupts surfactant secretion, and perturbs canonical Wnt signaling possibly through reduced Wnt inhibitory factor-1 expression. Inducible epithelial-specific conditional knockout (SPC-rtTA/TetO-Cre x Alk3-flox); analysis at multiple developmental timepoints; Wnt pathway marker expression The American journal of pathology High 18258849
2009 TβRIII (betaglycan) differentially modulates ALK3 and ALK6 subcellular trafficking and downstream signaling: TβRIII associates with ALK3 primarily through extracellular domains and causes cell surface retention of ALK3 (independent of β-arrestin2), specifically enhancing ALK3-mediated ID-1 upregulation; in contrast, TβRIII/ALK6 interaction requires cytoplasmic domains and promotes ALK6 internalization. Co-immunoprecipitation; cell surface retention assays; reporter gene assays (XVent2, 3GC2); domain deletion mutants; β-arrestin2 mutant TβRIII Molecular biology of the cell High 19726563
2009 BMPR1A and ACVR1 (type I BMP receptors) activate multiple signaling pathways to regulate lens formation; BMPR1A specifically regulates cell survival, while ACVR1 regulates proliferation; for most lens development processes (placode proliferation, FoxE3 expression, αA-crystallin, lens invagination), BMP receptor signaling acts in a Smad-independent manner; only maintaining high Sox2 levels requires canonical Smad4-dependent signaling. Conditional knockout of Bmpr1a, Acvr1, Smad4, Smad1, Smad5 in lens ectoderm; cellular and molecular phenotypic analysis; epistasis analysis Developmental biology High 19733164
2010 BMPR1a and BMPR1b exert opposing effects on astrocytic hypertrophy after spinal cord injury; BMPR1a ablation in GFAP+ cells leads to defective astrocytic hypertrophy, while BMPR1b null mice develop hyperactive reactive astrocytes; the two receptors oppositely regulate posttranscriptional levels of astrocytic microRNA-21, which controls astrocyte size. Conditional knockout (GFAP-Cre); BMPR1b global knockout; double knockout rescue; in vitro astrocyte culture; microRNA-21 overexpression experiments The Journal of neuroscience : the official journal of the Society for Neuroscience High 20130193
2010 Bmpr1a is required in the epiblast to maintain Wnt signaling in the visceral endoderm, which in turn establishes the anterior Dkk1 expression domain needed for directional AVE migration; Bmpr1a in epiblast induces Wnt3/Wnt3a expression, thereby maintaining WNT signaling that restricts Dkk1 to the anterior proximal visceral endoderm. Bmpr1a null and epiblast-specific conditional knockout (Sox2Cre); WNT3A rescue experiments in embryo culture; in situ hybridization for Dkk1 and Cer1 Developmental biology High 20211162
2010 Granulosa cell-expressed BMPR1A and BMPR1B act redundantly to suppress ovarian tumor development; BMPR1A single conditional knockout females are subfertile with reduced ovulation; double Bmpr1a/Bmpr1b mutants develop granulosa cell tumors with increased TGFβ and hedgehog signaling, similar to Smad1/Smad5 double knockouts. Single and double granulosa cell-specific conditional knockouts; tumor phenotype analysis; pathway marker analysis (TGFβ, hedgehog) Molecular endocrinology (Baltimore, Md.) High 20363875
2010 Bmpr1a signaling in palatal mesenchyme is required for cell proliferation in the primary and anterior secondary palate and for osteoblast differentiation during palatal bone formation; Bmpr1a loss reduces Msx1 and Fgf10 in palatal mesenchyme and Shh in palatal epithelium, indicating Bmp signaling regulates mesenchymal-epithelial crosstalk. Palatal mesenchyme-specific conditional knockout; proliferation analysis; in situ hybridization for Msx1, Fgf10, Shh Developmental biology High 21185278
2011 Conditional deletion of Bmpr1a in differentiated osteoclasts (Ctsk-Cre) increases osteoblastic bone formation rates in remodeling bone and increases bone volume; expression of bone-resorption markers was increased, suggesting BMPR1A signaling negatively regulates osteoclast differentiation; comparison with osteoblast-specific Bmpr1a deletion (Col1a1-Cre) showed opposite effects on bone formation rate. Osteoclast-specific and osteoblast-specific conditional knockouts; bone histomorphometry; bone marker analysis Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research High 21786321
2013 BMP15 suppresses progesterone production in human granulosa cells by downregulating StAR via ALK3-mediated SMAD1/5/8 signaling; siRNA-mediated depletion of ALK3 reverses BMP15-induced SMAD1/5/8 phosphorylation and StAR expression changes. siRNA knockdown of ALK3 in immortalized (SVOG) and tumor (KGN) human granulosa cells; pharmacological inhibition with dorsomorphin and DMH-1; SMAD1/5/8 phosphorylation assays; StAR and progesterone measurement Molecular endocrinology (Baltimore, Md.) High 24140593
2013 BMP signaling via ALK3 in SHF-derived cells at the cardiac venous pole is required for proliferative expansion of the DMP progenitor population; conditional deletion of Alk3 from venous pole SHF cells impairs DMP formation and causes ostium primum defect with decreased proliferative index of SHF cells. SHF-specific conditional knockout; proliferative index measurement; DMP volume analysis; BMP/TGFβ signaling marker analysis Circulation research High 23584254
2014 USP15 deubiquitylates ALK3 (BMPR1A): USP15 interacts with SMAD6 and ALK3, removes K48-linked polyubiquitin from ALK3, stabilizes ALK3 protein, and enhances BMP-induced SMAD1 phosphorylation and BMP target gene transcription; loss of USP15 increases ALK3 ubiquitylation and reduces BMP signaling and osteoblast differentiation. Co-immunoprecipitation; RNAi depletion; ubiquitylation assays (K48-linked); SMAD1 phosphorylation assays; reporter assays; Xenopus embryogenesis functional validation Open biology High 24850914
2014 HFE interacts with ALK3 (BMPR1A), inhibiting ALK3 ubiquitination and proteasomal degradation, thereby increasing ALK3 protein expression and cell-surface accumulation, which enhances SMAD1/5/8 phosphorylation and hepcidin expression; HH-associated HFE mutants (C282Y and H63D) fail to increase ALK3 cell-surface expression. Co-immunoprecipitation; ubiquitylation assays; cell-surface expression analysis; HFE overexpression/inhibition in Hep3B cells; Hfe knockout mouse liver analysis Blood High 24904118
2014 Alk3-mediated BMP signaling in epicardium-derived cells (EPDCs) is required for their contribution to the AV sulcus, annulus fibrosus, and parietal leaflets of AV valves; deletion of Alk3 in Wt1+ epicardial cells reduces EPDC contribution and causes myxomatous valve changes. Wt1-Cre epicardial conditional knockout; cell fate tracing; electrophysiology; histological and morphological analysis Developmental biology High 25300579
2015 BMPR1A signaling in the uterus is necessary for blastocyst attachment; conditional knockout of ALK3 in the uterus causes sterility with defects in luminal epithelium polarity, increased microvilli density, elevated estrogen response, and unopposed epithelial proliferation; SMAD4 and progesterone receptor converge on Klf15 transcription to inhibit epithelial proliferation downstream of ALK3. Pgr-Cre conditional knockout; fertility analysis; uterine epithelial morphology; KLF15 dual transcriptional regulation analysis Proceedings of the National Academy of Sciences of the United States of America High 26721398
2015 Physiological BMPR1A signaling in osteoblast lineage exerts dual opposing functions: it restricts preosteoblast (Sp7+) proliferation (suppressing trabecular bone formation) and promotes osteoblast activity/mTORC1 signaling for periosteal bone growth; Smad4 deletion has only minor effects, indicating Bmpr1a uses Smad4-independent effectors to suppress preosteoblast proliferation; mTORC1 inhibition abolishes BMP2-induced protein anabolism in vitro. Dmp1-Cre and inducible Sp7-Cre conditional knockouts; Smad4 conditional KO comparison; bone histomorphometry; mTORC1 signaling assays; in vitro BMP2 treatment with rapamycin Development (Cambridge, England) High 26657771
2015 BMP4 and BMP7 suppress StAR expression and progesterone production in human granulosa-lutein cells via ALK3 (not ALK2 or ALK6) and SMAD1/5/8-SMAD4 signaling; siRNA knockdown of ALK3 specifically reverses these effects. siRNA knockdown of ALK3, ALK2, ALK6 in primary and immortalized human granulosa cells; pharmacological inhibition (dorsomorphin, DMH1, SB-431542); SMAD1/5/8 phosphorylation; SMAD4 siRNA knockdown Endocrinology High 26302112
2015 Bmpr1a in Myf5/MyoD-expressing myo-endothelial progenitors inhibits intramuscular adipogenesis; Bmpr1a ablation in these cells increases intramuscular fat and decreases myogenic activity, with severely decreased phospho-Smad 1/5/8 signaling; clonal studies show a cell-autonomous switch from myogenic to adipogenic differentiation. Myf5-Cre and MyoD-Cre conditional knockouts; VE-cadherin-Cre lineage tracing; clonal studies of myo-endothelial progenitors; pSmad1/5/8 signaling analysis Nature communications High 24898859
2016 BMP signaling through BMPR1A in osteocytes negatively regulates SOST (sclerostin) and RANKL expression; osteocyte-specific deletion of Bmpr1a (Dmp1-Cre) dramatically increases bone mass, decreases SOST and RANKL, increases OPG, increases β-catenin and Wnt target genes (Tcf1, Tcf3), and reduces osteoclast number. Osteocyte-specific Cre/lox conditional knockout (Dmp1-Cre); micro-CT; histomorphometry; molecular analysis of SOST, RANKL, OPG, β-catenin, Tcf1, Tcf3 Bone High 27402532
2016 BMP signaling through BMPR1A in osteoclasts suppresses osteoblast mineralization via regulation of connexin 43 (Cx43/Gja1); loss of Bmpr1a in osteoclasts increases Cx43 expression, and Cx43 knockdown in Bmpr1a-null osteoclasts reduces osteoblast mineralization in co-culture, identifying Cx43 as a downstream BMPR1A target mediating osteoclast-osteoblast communication. Co-culture of wild-type osteoblasts with Bmpr1a-null osteoclasts; siRNA knockdown of Cx43/Gja1; mineralization assays Journal of cellular biochemistry Medium 27649478
2017 BMPR1A is the major type I BMP receptor for Smad-dependent BMP signaling during skull development; pSmad1/5/9 levels are undetectable in Bmpr1a-null cells but not in Bmpr1b or Acvr1 null cells; heterozygous Bmpr1a (but not Bmpr1b or Acvr1) loss rescues constitutively active BMPR1A-induced craniosynostosis by reducing pSmad1/5/9 to normal levels. Conditional knockouts and heterozygous rescues of Bmpr1a, Bmpr1b, Acvr1 in neural crest cells; pSmad1/5/9 quantification in null cells; craniosynostosis phenotypic rescue analysis Developmental biology High 28641928
2017 Endothelial ALK3/BMPR1A and ALK2/ACVR1 are required for postnatal retinal angiogenesis; endothelial-specific inducible deletion of Alk3 delays radial vascular expansion, phenocopying BMPR2 deletion, indicating ALK3 is a key type I receptor partnering with BMPR2 for proangiogenic BMP signaling in retinal vessels. Inducible endothelial-specific conditional knockout; retinal angiogenesis analysis; comparison with Bmpr2, Alk1, Alk2 deletions Arteriosclerosis, thrombosis, and vascular biology High 28232325
2018 IL-6 enhances BMP-2-induced osteogenic and adipogenic differentiation by promoting cell-surface translocation of BMPR1A, thereby amplifying BMPR1A-mediated BMP/Smad and p38 MAPK pathways. In vitro differentiation assays with human BMSCs; cell-surface translocation assay for BMPR1A; Smad and p38 MAPK signaling analysis; in vivo rat ectopic bone model with IL-6 injection Cell death & disease Medium 29396550
2018 ALK3 undergoes ligand-independent homodimerization; ALK3 forms heterodimers with ALK2 in a ligand-dependent manner (BMP2 or BMP6 required); both ALK3-ALK3 and ALK2-ALK3 complexes induce hepcidin expression in Huh7 cells; Alk2/Alk3 double hepatocyte-specific deficiency causes greater iron overload than Alk3 deficiency alone. Co-immunoprecipitation in Huh7 cells with and without BMP ligands; hepatocyte-specific double knockout mice; iron overload phenotyping; hepcidin expression assays Free radical biology & medicine High 30227271
2018 In AML, BMP4 controls expression of the survival factor ΔNp73 through binding to BMPR1A, which in turn directly induces NANOG expression and increases stem-like features in leukemic cells (increased ALDH activity); BMPR1A transcript and membrane receptor are upregulated in AML cells and further increased by BMP4 exposure. Downstream signaling analysis in AML patient cells and cell lines; functional ALDH assay; correlation of ΔNp73, BMPR1A, NANOG expression with patient outcome Cell death & disease Medium 30262802
2018 ALK2/ALK3 mediate BMP2-induced downregulation of pentraxin 3 (PTX3) in human granulosa-lutein cells via SMAD1/5/8-SMAD4; siRNA knockdown of ALK2/3 or BMPR2/ACVR2A receptors reverses BMP2-induced SMAD1/5/8 phosphorylation and PTX3 downregulation. siRNA knockdown of individual receptors and SMADs; SMAD1/5/8 phosphorylation assays; PTX3 mRNA/protein measurement; BMP receptor inhibitors Endocrinology Medium 28977600
2019 BMP signaling through ALK3/BMPR1A and SMAD1/SMAD5 controls venous endothelial identity by driving Ephb4 expression; a venous endothelium-specific Ephb4 enhancer shows enriched SMAD1/5 binding and requires SMAD binding motifs; Ephb4 expression is lost upon perturbation of BMP/ALK3 signaling in mice and zebrafish without affecting arterial identity. Genetic perturbations in mice and zebrafish; ChIP/enhancer analysis of SMAD1/5 binding to Ephb4 venous enhancer; SMAD binding motif mutagenesis; in situ hybridization for venous/arterial markers Nature communications High 30692543
2019 S-palmitoylation of BMPR1A regulates its subcellular localization and trafficking, and consequently BMP signaling levels; genetic manipulation of palmitoylation sites on BMPR1A alters its membrane localization and signaling, leading to enhanced oligodendrogenesis from neural stem cells in the mouse brain. Unbiased palmitoylation screen of NSC proteome; site-directed mutagenesis of palmitoylation sites; subcellular localization imaging; BMP signaling assays; in vivo neural lineage analysis Proceedings of the National Academy of Sciences of the United States of America High 31772009
2021 BMPR1A is essential for suture stem cell (SuSC) self-renewal; SuSC-specific disruption of Bmpr1a causes precocious differentiation and craniosynostosis initiated at the suture midline (the stem cell niche); BMPR1A serves as a cell-surface marker of human SuSCs. SuSC-specific conditional knockout; ex vivo stem cell culture; lineage analysis; craniosynostosis phenotyping; human SuSC surface marker characterization Science translational medicine High 33658353
2022 LAPTM5 recruits WWP2, which binds BMPR1A and mediates its lysosomal sorting, ubiquitination, and degradation; chloroquine (lysosomal inhibitor) restores BMPR1A expression; LAPTM5-driven BMPR1A degradation blocks lung-derived BMP signaling, sustaining cancer stem cell traits and promoting lung-specific metastasis in renal cancer. Co-immunoprecipitation of LAPTM5-WWP2-BMPR1A complex; ubiquitylation assays; chloroquine rescue of BMPR1A expression; conditional KO and overexpression in cancer cells; in vivo metastasis models Nature communications High 35842443
2023 Upon BMPR1A activation in endothelial cells, ID2 physically interacts with and sequesters ZEB1, attenuating ZEB1-driven transcription of Tgfbr2, which reduces EC responses to TGFβ and prevents excessive EndoMT; endothelial-specific deletion of Bmpr1a in adult mice causes PAH-like symptoms via excessive EndoMT; siRNA against Tgfbr2 delivered to endothelium ameliorates PAH in Bmpr1a iECKO mice. Endothelial-specific inducible conditional knockout (Bmpr1a iECKO); co-IP of ID2-ZEB1 interaction; lineage tracing of endothelial-derived smooth muscle cells; siRNA lipid nanoparticle rescue; TGFβ response assays Cardiovascular research High 36166408
2000 BMP-2 and the constitutively active form of ALK3 inhibit renal collecting duct morphogenesis via Smad1 phosphorylation, Smad1/Smad4 complex formation, and Smad1 nuclear translocation; HGF overcomes BMP-2/ALK3 inhibition without interrupting any of these known Smad1 signaling events, indicating parallel pathways downstream of their receptors. Stable expression of constitutively active ALK3 in mIMCD-3 cells; Smad1 phosphorylation and nuclear translocation assays; BMP-responsive promoter (Tlx2) reporter; rescue with HGF and other RTK ligands Journal of cell science Medium 10633078
2018 HFE signals predominantly via ALK3 to induce hepcidin in vivo; HFE overexpression in control mice increases hepcidin and pSmad1/5 levels, but overexpression of HFE in hepatocyte-specific Alk3-deficient mice produces no change in hepcidin or pSmad1/5, establishing ALK3 as the required in vivo mediator of HFE-driven hepcidin regulation. AAV2/8-Hfe-Flag injection in hepatocyte-specific Alk3 knockout vs control mice; hepcidin expression; pSmad1/5 measurement; iron and blood parameter analysis Communications biology High 30271947
2009 BMPR1A is the preferred BMP2 type I receptor in LβT2 gonadotroph cells for regulating Fshb transcription; siRNA knockdown of endogenous BMPR1A (but not ACVR1 or BMPR1B) significantly impairs BMP2 synergism with activin A on FSHβ reporter activity; constitutively active BMPR1A with BMPR2 stimulates SMAD1/5 phosphorylation and Fshb transcription. siRNA knockdown of BMPR1A, ACVR1, BMPR1B; constitutively active receptor co-expression; Fshb promoter-reporter assay; SMAD1/5 phosphorylation assays Biology of reproduction Medium 19211807
2011 Alk3 controls nephron number and testosterone production via lineage-specific mechanisms in intermediate mesoderm progenitors; in kidney, Alk3 deficiency reduces metanephric blastema contribution and expression of nephron progenitor markers Osr1 and SIX2 via phospho-p38 MAPK pathway; in testis, Alk3 regulates Leydig cell formation via pSMAD1/5/8 signaling. Intermediate mesoderm progenitor-specific conditional knockout; lineage contribution analysis; marker expression; phospho-p38 MAPK and pSMAD1/5/8 analysis in respective tissues Development (Cambridge, England) High 21613322
2023 BMPR1A mediates BMP signaling-induced deep quiescence in pallial neural stem cells postnatally; Bmpr1a manipulation demonstrates its key role in synchronizing quiescence induction and blockade of glutamatergic neuron differentiation to silence pallial germinal activity after birth. Single-cell RNA sequencing of postnatal dorsal V-SVZ; Bmpr1a genetic manipulation; analysis of NSC quiescence states and neurogenic output Science advances Medium 37146152

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 341 15781876
2002 Requirement of Bmpr1a for Müllerian duct regression during male sexual development. Nature genetics 338 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 168 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 117 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
2006 Essential functions of Alk3 during AV cushion morphogenesis in mouse embryonic hearts. Developmental biology 76 16959237
2017 Unintended targeting of Dmp1-Cre reveals a critical role for Bmpr1a signaling in the gastrointestinal mesenchyme of adult mice. Bone research 75 28163952
2013 BMP15 suppresses progesterone production by down-regulating StAR via ALK3 in human granulosa cells. Molecular endocrinology (Baltimore, Md.) 75 24140593
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 63 33658353
2015 Dual function of Bmpr1a signaling in restricting preosteoblast proliferation and stimulating osteoblast activity in mouse. Development (Cambridge, England) 61 26657771
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
2019 Venous identity requires BMP signalling through ALK3. Nature communications 58 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
2022 Exosomal miR-143-3p derived from follicular fluid promotes granulosa cell apoptosis by targeting BMPR1A in polycystic ovary syndrome. Scientific reports 48 35288625
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
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
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 44 18258849
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
2018 IL-6 potentiates BMP-2-induced osteogenesis and adipogenesis via two different BMPR1A-mediated pathways. Cell death & disease 43 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 41 26274893
2014 miR-656 inhibits glioma tumorigenesis through repression of BMPR1A. Carcinogenesis 40 24480809
2022 Lysosomal protein transmembrane 5 promotes lung-specific metastasis by regulating BMPR1A lysosomal degradation. Nature communications 39 35842443
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
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
2015 BMP4 and BMP7 Suppress StAR and Progesterone Production via ALK3 and SMAD1/5/8-SMAD4 in Human Granulosa-Lutein Cells. Endocrinology 35 26302112
2014 Intramuscular adipogenesis is inhibited by myo-endothelial progenitors with functioning Bmpr1a signalling. Nature communications 35 24898859
2018 A new signaling cascade linking BMP4, BMPR1A, ΔNp73 and NANOG impacts on stem-like human cell properties and patient outcome. Cell death & disease 34 30262802
2020 BMPR1A is necessary for chondrogenesis and osteogenesis, whereas BMPR1B prevents hypertrophic differentiation. Journal of cell science 32 32764110
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
2021 Targeting local lymphatics to ameliorate heterotopic ossification via FGFR3-BMPR1a pathway. Nature communications 29 34282140
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
2020 BMP Ligand Trap ALK3-Fc Attenuates Osteogenesis and Heterotopic Ossification in Blast-Related Lower Extremity Trauma. Stem cells and development 27 33256557
2017 BmpR1A is a major type 1 BMP receptor for BMP-Smad signaling during skull development. Developmental biology 27 28641928
2009 Myoblast sensitivity and fibroblast insensitivity to osteogenic conversion by BMP-2 correlates with the expression of Bmpr-1a. BMC musculoskeletal disorders 27 19442313
2019 MiR-15b-5p is Involved in Doxorubicin-Induced Cardiotoxicity via Inhibiting Bmpr1a Signal in H9c2 Cardiomyocyte. Cardiovascular toxicology 26 30535663
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
2014 Alk3 mediated Bmp signaling controls the contribution of epicardially derived cells to the tissues of the atrioventricular junction. Developmental biology 26 25300579
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
2016 BMP Signaling Mediated by BMPR1A in Osteoclasts Negatively Regulates Osteoblast Mineralization Through Suppression of Cx43. Journal of cellular biochemistry 25 27649478
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
2019 Palmitoylation of BMPR1a regulates neural stem cell fate. Proceedings of the National Academy of Sciences of the United States of America 23 31772009
2016 Enrichment of Adipose-Derived Stromal Cells for BMPR1A Facilitates Enhanced Adipogenesis. Tissue engineering. Part A 23 26585335
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
2023 Single-cell analysis of the postnatal dorsal V-SVZ reveals a role for Bmpr1a signaling in silencing pallial germinal activity. Science advances 22 37146152
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
2004 Loss of heterozygosity on 10q and mutational status of PTEN and BMPR1A in colorectal primary tumours and metastases. British journal of cancer 22 15026806
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
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
2014 Alk3/Alk3b and Smad5 mediate BMP signaling during lymphatic development in zebrafish. Molecules and cells 15 24608800

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