Last update 01 Nov 2024

BMPR1B

Last update 01 Nov 2024

Basic Info

Synonyms

ALK6, BMP type-1B receptor, BMPR-1B

+ [5]

Introduction

On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP7/OP-1 and GDF5. Positively regulates chondrocyte differentiation through GDF5 interaction.

Drugs associated with BMPR1B

DWP-431

Target

BMPR1A x BMPR1B

Mechanism

BMPR1A stimulants [+1]

Active Org.

Daewoong Pharmaceutical Co., Ltd.

Originator Org.

Daewoong Pharmaceutical Co., Ltd.

Active Indication

Alveolar Bone Loss [+1]

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date25 Jun 2014

Eptotermin alfa

Target

BMPR1A x BMPR1B x BMPR2

Mechanism

BMPR1A stimulants [+2]

Active Org.-

Originator Org.

Curis, Inc.

Active Indication-

Inactive Indication

Amyotrophic Lateral Sclerosis [+3]

Drug Highest PhaseWithdrawn

First Approval Ctry. / Loc.

EU [+3]

First Approval Date17 May 2001

UK-383367

Target

BMPR1A x BMPR1B

Mechanism

BMPR1A antagonists [+1]

Active Org.-

Originator Org.

Pfizer Inc.

Active Indication-

Inactive Indication

Cicatrix

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with BMPR1B

NCT04670965 / Not yet recruitingNot ApplicableIIT

Release Kinetics of RhBMP-2 Using E-PRF As an Autologous Carrier: an in Vitro Analysis

This study is seeking to evaluate the binding of a commercially-available, recombinant human osteoinductive growth factor, rhBMP-2, to a human blood derived product scaffold, enhanced Platelet-rich fibrin (E-PRF), and the release of such a growth factor over time in an in vitro (laboratory) environment. The investigators will compare these release kinetics to those of the FDA approved carrier for rhBMP-2, an absorbable collagen sponge (ACS), a combination of E-PRF and ACS, and E-PRF alone.

Start Date01 Dec 2024

Sponsor / Collaborator

The University of Alabama at Birmingham

CTRI/2024/05/067147 / Not yet recruitingPhase 4IIT

Evaluation of the effect of Recombinant Human Bone Morphogenic Protein-2 on crestal bone height and osseointegration around endosseous implants - nil

Start Date10 Jun 2024

Sponsor / Collaborator-

NCT05719181 / RecruitingPhase 1IIT

Effect of Recombinant Human Bone Morphogenetic Protein-2 With an Absorbable Collagen Sponge on Stability of Dental Implant: (Split Mouth Randomized Clinical Trial Study of 6\12\2021 to20\4\2023

Effect of Recombinant Human Bone Morphogenetic Protein-2 with an Absorbable Collagen Sponge on Stability of Dental Implant: (Split Mouth Randomized Clinical Trial Study.

Start Date06 Dec 2021

Sponsor / Collaborator

University of Baghdad

100 Clinical Results associated with BMPR1B

100 Translational Medicine associated with BMPR1B

0 Patents (Medical) associated with BMPR1B

583

Literatures (Medical) associated with BMPR1B

01 Nov 2024·International Journal of Biological Macromolecules

FecB mutation enhances follicle stimulating hormone sensitivity of granulosa cells by up-regulating the SMAD1/5–USF1–FSHR signaling pathway

Article

Author: Cong, Peiqing ; Jiao, Yafei ; He, Zuyong ; Chen, Yaosheng ; Guo, Jinming ; Liu, Xiaohong ; Jiang, Xintong ; Zhu, Yizhou

The FecB^B mutation, a single-point mutation (c.A746G; p.Q249R) in bone morphogenetic protein receptor type 1 B (BMPR1B), is associated with increased ovulation quotas and litter size in sheep. However, the regulatory mechanism of the FecB^B mutation in increased fecundity remains to be elucidated. Therefore, creating an immortal cell model harboring the FecB^B mutation would elucidate the regulatory mechanism of this mutation. Here, we report the creation of a human granulosa cell, COV434, model containing a homozygous FecB^B mutation through homology-directed repair (HDR) induced by clustered, regularly-interspaced, short palindromic repeats-CRISPR-associated protein 9 along with a single-stranded oligodeoxynucleotide (ssODN) template. We found that the FecB^B mutation enhanced the basal SMAD1/5 signaling activity in COV434 cells, leading to increased expression of FSHR, probably through increased formation of the SMAD1/5-SMAD4 complex to bind to the SBE element, which in turn promotes the binding of USF1 to the regulatory element E-box in the promoter of FSHR. Furthermore, the FecB^B mutation substantially enhanced estradiol (E2) synthesis in granulosa cells under follicle stimulating hormone (FSH) stimulation, indicating an enhanced sensitivity to FSH, which may promote the growth of more small follicles into mature follicles, leading to increased fecundity. Our study provides novel insights into the possible regulatory mechanisms of FecB^B mutations in increased fecundity.

01 Oct 2024·Molecular Genetics & Genomic Medicine

Acromesomelic Dysplasia With Homozygosity for a Likely Pathogenic BMPR1B Variant: Postaxial Polydactyly as a Novel Clinical Finding

Article

Author: Knaus, Alexej ; Abdelrazek, Ibrahim M. ; Krawitz, Peter M. ; Abdalla, Ebtesam M. ; Kumar, Sheetal ; Horn, Denise ; Javanmardi, Behnam

ABSTRACTBackgroundAcromesomelic chondrodysplasias are a rare subgroup of the clinically and genetically heterogeneous osteochondrodysplasias that are characterised by abnormalities in the limb development and short stature. Here, we report a 2‐year‐old boy, offspring of consanguineous parents, with acromesomelic dysplasia and postaxial polydactyly in which exome sequencing identified a novel homozygous missense variant in BMPR1B. The patient showed skeletal malformation of both hands and feet that included complex brachydactyly with the thumbs most severely affected, postaxial polydactyly of both hands, shortened toes as well as a bilateral hypoplasia of the fibula.MethodsWhole trio exome sequencing was conducted to identify potential genetic variants in the patient.ResultsThe analysis identified the biallelic variant NM_001203.3:c.821A > G;p.(Gln274Arg) in BMPR1B, a gene encoding bone morphogenetic protein receptor 1B.ConclusionThe skeletal phenotype can be brought in line with the phenotypes of previously reported cases of BMPR1B‐associated chondrodysplasias. However, the postaxial polydactyly described here is a novel clinical finding in a BMPR1B‐related case; notably, it has previously been reported in other acromesomelic dysplasia cases caused by homozygous pathogenic variants in GDF5—a gene which encodes for growth differentiation factor 5, a high‐affinity ligand to BMPR1B.

01 Jun 2024·Neoplasia

Cell communication pathway prognostic model identified detrimental neurodevelopmental pathways in neuroblastoma

Article

Author: Li, Huimin ; Zhang, Yixuan ; Xue, Yao ; Fang, Yongjun ; Zhou, Chunlei ; Ma, Xiaopeng ; Wang, Yaping ; Zhang, Yidan ; Wang, Jiali ; Rong, Liucheng

Neurodevelopmental cell communication plays a crucial role in neuroblastoma prognosis. However, determining the impact of these communication pathways on prognosis is challenging due to limited sample sizes and patchy clinical survival information of single cell RNA-seq data. To address this, we have developed the cell communication pathway prognostic model (CCPPM) in this study. CCPPM involves the identification of communication pathways through single-cell RNA-seq data, screening of prognosis-significant pathways using bulk RNA-seq data, conducting functional and attribute analysis of these pathways, and analyzing the post-effects of communication within these pathways. By employing the CCPPM, we have identified ten communication pathways significantly influencing neuroblastoma, all related to axongenesis and neural projection development, especially the BMP7-(BMPR1B-ACVR2B) communication pathway was found to promote tumor cell migration by activating the transcription factor SMAD1 and regulating UNK and MYCBP2. Notably, BMP7 expression was higher in neuroblastoma samples with distant metastases. In summary, CCPPM offers a novel approach to studying the influence of cell communication pathways on disease prognosis and identified detrimental communication pathways related to neurodevelopment.

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BMPR1B

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