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recombinant human bmp2 protein r d systems (R&D Systems)

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R&D Systems recombinant human bmp2 protein r d systems
Recombinant Human Bmp2 Protein R D Systems, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 224 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+bmp2/Recombinant+Human+BMP-2+GMP+Protein%2C+CF/pm41932341-856-64-68
Average 95 stars, based on 224 article reviews

recombinant human bmp2 protein r d systems - by Bioz Stars, 2026-09

95/100 stars

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Enzyme-linked Immunosorbent Assay:

Article Title: Nanotopography Influences Host-Pathogen Quorum Sensing and Facilitates Selection of Bioactive Metabolites in Mesenchymal Stromal Cells and Pseudomonas aeruginosa Co-Cultures.
Article Snippet: .. FN and BMP2 levels in the supernatants were calculated using enzyme-linked immunosorbent assay (ELISA) duo-set Human Fibronectin (DY1918, R&D systems), and Human BMP2 (DY355, R&D systems), respectively, following instructions from the manufacturer. ..

Article Title: Nanotopography Influences Host–Pathogen Quorum Sensing and Facilitates Selection of Bioactive Metabolites in Mesenchymal Stromal Cells and Pseudomonas aeruginosa Co-Cultures
Article Snippet: .. FN and BMP2 levels in the supernatants were calculated using enzyme-linked immunosorbent assay (ELISA) duo-set Human Fibronectin (DY1918, R&D systems), and Human BMP2 (DY355, R&D systems), respectively, following instructions from the manufacturer. ..

Binding Assay:

Article Title: Anti-GDF15 antibodies, compositions and methods of use
Article Snippet: .. An OctetRED 384 (ForteBio, Menlo Park, Calif.) was used to evaluate off-target binding of monomeric GDF15_001 (CH23LS-GBT-GDF15_001) to ten TGFβ family members including human GDNF (R&D, 212-GD/CF), human Inhibin A (R&D, 8506-AB/CF), human Activin B (R&D, 659-AB/CF) human TGFβ-1 (R&D, 240-B/CF) human BMP2 (R&D, 355-BM/CF), human BMP3b (R&D, 1543-BP/CF), human BMP6 (R&D, 507-BP/CF), human BMP9 (R&D, 3209-BP/CF), human BMP11 (R&D, 1958-CD/CF), human GDF8 (Pfizer, 41075-201) and control human GDF15 (Mu IgG1Fc_Fxa_Hu GDF15). .. The TGFβ family members were diluted to 10 ug/ml in 10 mM Sodium Acetate pH 4.5 and amine coupled onto AR2G biosensors (catalogue #18-5092, ForteBio) according to the manufacturer's instructions.

Control:

Recombinant:

Article Title: Signaling pathways associated with Lgr6 to regulate osteogenesis
Article Snippet: Cells were cultured at a density of 3000 cells/cm 2 using alpha-MEM supplemented with 16.5 % FBS (Atlas Biologicals, CO) in standard culture conditions for propagation and used within passage 7. .. Osteoblast differentiation was achieved using BMP stimulation by adding 200 ng/ml of recombinant human BMP2 (R&D Systems, MN) to the cell monolayer using osteopermissive media (serum-free alpha-MEM additionally supplemented with 25 μg/ml l -Ascorbic Acid Phosphate Magnesium Salt n-Hydrate (AA2P) (FUJIFILM Wako Chemicals USA Corp., VA), 5 mM β-glycerophosphate disodium salt hydrate (BGP) (Sigma, MO) and 1× Insulin-transferrin-selenous acid premix (ITS) (Corning, NY))[ 21 , 22 ]. ..

Article Title: Signaling pathways associated with Lgr6 to regulate osteogenesis.
Article Snippet: Fracture management largely relies on the bone's inherent healing capabilities and, when necessary, surgical intervention.. Currently, there are limited osteoinductive therapies to promote healing, making targeting skeletal stem/progenitor cells (SSPCs) a promising avenue for therapeutic development.. A limiting factor for this approach is our incomplete understanding of the molecular mechanisms governing SSPCs' behavior.

Article Title: GWAS-informed data integration and non-coding CRISPRi screen illuminate genetic etiology of bone mineral density
Article Snippet: .. For osteoblastic differentiation, we plated 15,000 cells/cm 2 in alpha-MEM consisting of 16.5% FBS, 25 μg/ml ascorbic acid-2-phosphate, 5 mM beta-glycerophosphate, and 1% insulin-transferrin-selenous acid (osteogenic media) and stimulated them the next day with recombinant human BMP2 (300 ng/ml) (R&D Systems, MN) in serum-free osteogenic media. ..

Article Title: GWAS-informed data integration and non-coding CRISPRi screen illuminate genetic etiology of bone mineral density
Article Snippet: .. For osteoblastic differentiation, we plated 15,000 cells/cm 2 in alpha-MEM consisting of 16.5% FBS, 25 μg/ml Ascorbic acid-2-phosphate, 5 mM beta-glycerophosphate and 1% insulin-transferrin-selenous acid (osteogenic media) and stimulated them the next day with recombinant human BMP2 (300 ng/ml) (R&D Systems, MN) in serum-free osteogenic media. ..

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Comparative effects of BMP9 and BMP2 on osteogenic differentiation and osteoclastogenesis in vitro. (A) Real‐time PCR analysis of key osteogenic genes (Col1, Runx2, ALP, and OCN) in MC3T3‐E1 cells treated with 8 nM of BMP2 or BMP9 for 3, 5, and 7 days. All gene‐expression levels were normalized to GAPDH. (B) Western blot analysis of osteogenic marker proteins in cell lysates harvested after 7 days of treatment with BMP2 or BMP9. GAPDH was used as the loading control. Densitometric quantification of band intensities (integrated density) normalized to GAPDH is shown below the blots and presented as relative protein expression. (C) Western blot showing dose‐dependent p‐Smad1/5/9 in MC3T3‐E1 cells exposed to varying concentrations of BMP2 or BMP9. Phosphorylation was quantified by densitometry and expressed as fold change vs. control after normalization using [(p‐Smad1/5/9)/(total Smad1/5/9)] and further normalized to GAPDH, as shown in the graph below the blots. Asterisks indicate statistical significance for pairwise comparisons between BMP2 and BMP9 at the same concentration (****, p < 0.0001), unless otherwise indicated. (D) ALP activity and representative images of ALP staining in MC3T3‐E1 cultures after 7 days of induction with BMP2 or BMP9. (E) Alizarin Red S staining illustrating mineralized nodule formation after extended culture with BMP2 or BMP9. (F) Representative TRAP‐stained images of RAW 264.7‐derived osteoclasts following treatment with RANKL (3 nM), BMP2 (8 nM), or BMP9 (8 nM) for 5 days. TRAP‐positive multinucleated osteoclasts are indicated by arrows. Scale bar, 20 μm. (G) Quantification of TRAP‐positive multinucleated cells per well. Data are presented as the mean ± SD ( n = 3 independent experiments), and p ‐values were calculated using one‐way analysis of variance (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). BMP, bone morphogenetic protein; PCR, polymerase chain reaction; ALP, alkaline phosphatase; Col1, collagen type I; Runx2, runt‐related transcription factor 2; OCN, osteocalcin; GAPDH, glyceraldehyde‐3‐phosphate dehydrogenase.

Journal: Clinical Implant Dentistry and Related Research

Article Title: Bone Morphogenetic Protein ( BMP ) 9 Outperforms BMP2 in Osteogenesis and Osseointegration: In Vitro and In Vivo

doi: 10.1111/cid.70135

Figure Lengend Snippet: Comparative effects of BMP9 and BMP2 on osteogenic differentiation and osteoclastogenesis in vitro. (A) Real‐time PCR analysis of key osteogenic genes (Col1, Runx2, ALP, and OCN) in MC3T3‐E1 cells treated with 8 nM of BMP2 or BMP9 for 3, 5, and 7 days. All gene‐expression levels were normalized to GAPDH. (B) Western blot analysis of osteogenic marker proteins in cell lysates harvested after 7 days of treatment with BMP2 or BMP9. GAPDH was used as the loading control. Densitometric quantification of band intensities (integrated density) normalized to GAPDH is shown below the blots and presented as relative protein expression. (C) Western blot showing dose‐dependent p‐Smad1/5/9 in MC3T3‐E1 cells exposed to varying concentrations of BMP2 or BMP9. Phosphorylation was quantified by densitometry and expressed as fold change vs. control after normalization using [(p‐Smad1/5/9)/(total Smad1/5/9)] and further normalized to GAPDH, as shown in the graph below the blots. Asterisks indicate statistical significance for pairwise comparisons between BMP2 and BMP9 at the same concentration (****, p < 0.0001), unless otherwise indicated. (D) ALP activity and representative images of ALP staining in MC3T3‐E1 cultures after 7 days of induction with BMP2 or BMP9. (E) Alizarin Red S staining illustrating mineralized nodule formation after extended culture with BMP2 or BMP9. (F) Representative TRAP‐stained images of RAW 264.7‐derived osteoclasts following treatment with RANKL (3 nM), BMP2 (8 nM), or BMP9 (8 nM) for 5 days. TRAP‐positive multinucleated osteoclasts are indicated by arrows. Scale bar, 20 μm. (G) Quantification of TRAP‐positive multinucleated cells per well. Data are presented as the mean ± SD ( n = 3 independent experiments), and p ‐values were calculated using one‐way analysis of variance (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). BMP, bone morphogenetic protein; PCR, polymerase chain reaction; ALP, alkaline phosphatase; Col1, collagen type I; Runx2, runt‐related transcription factor 2; OCN, osteocalcin; GAPDH, glyceraldehyde‐3‐phosphate dehydrogenase.

Article Snippet: Recombinant human BMP2 (R&D Systems, Minneapolis, MN, USA) was used as the control.

Techniques: In Vitro, Real-time Polymerase Chain Reaction, Gene Expression, Western Blot, Marker, Control, Expressing, Phospho-proteomics, Concentration Assay, Activity Assay, Staining, Derivative Assay, Polymerase Chain Reaction

Experimental timeline, surgical procedure, and implant stability in the beagle saddle‐type peri‐implant defect model. (A) Timeline of the in vivo study. On the surgery day a saddle‐type peri‐implant defect was created, a dental implant was inserted, and bone grafting was performed with group allocation as follows. Non‐graft, collagenated xenograft matrix only, collagenated xenograft matrix + BMP2, and collagenated xenograft matrix + BMP9. Calcein was injected subcutaneously on day 54. At 8 weeks implant stability was recorded, micro CT was acquired, and animals were sacrificed. (B) Surgical procedure. (C) ISQ measured immediately before sacrifice. Bars show mean ± SD. Asterisks indicate statistical significance as marked in the plot.

Journal: Clinical Implant Dentistry and Related Research

Article Title: Bone Morphogenetic Protein ( BMP ) 9 Outperforms BMP2 in Osteogenesis and Osseointegration: In Vitro and In Vivo

doi: 10.1111/cid.70135

Figure Lengend Snippet: Experimental timeline, surgical procedure, and implant stability in the beagle saddle‐type peri‐implant defect model. (A) Timeline of the in vivo study. On the surgery day a saddle‐type peri‐implant defect was created, a dental implant was inserted, and bone grafting was performed with group allocation as follows. Non‐graft, collagenated xenograft matrix only, collagenated xenograft matrix + BMP2, and collagenated xenograft matrix + BMP9. Calcein was injected subcutaneously on day 54. At 8 weeks implant stability was recorded, micro CT was acquired, and animals were sacrificed. (B) Surgical procedure. (C) ISQ measured immediately before sacrifice. Bars show mean ± SD. Asterisks indicate statistical significance as marked in the plot.

Article Snippet: Recombinant human BMP2 (R&D Systems, Minneapolis, MN, USA) was used as the control.

Techniques: In Vivo, Injection, Micro-CT

Multiplex orthogonal gene regulation and programmable editing by OREC with therapeutic application in osteoblasts (A) Experimental illustration of orthogonal activation and repression of ASCL1 and RAB7A gene expression in HEK293T cells using distinct chemical and light inductions. (B) RT-qPCR time course analysis demonstrating orthogonal and reversible control of ASCL1 activation and RAB7A repression in response to alternating Dox and light stimuli. Data represent mean ± SEM ( n = 3). vs. RAB7A baseline (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001); vs. RAB7A 36 h ( $ p < 0.05, $$$ p < 0.001); vs. ASCL1 baseline ( && p < 0.01, &&&& p < 0.0001); vs. ASCL1 48 h ( ## p < 0.01, #### p < 0.0001). (C) Schematic diagram illustrating crRNA guide-length-dependent transcriptional repression and HDR-based gene editing using OREC c system. (D) Transcriptional repression of RAB7A and FZD1 genes following 72 h doxycycline treatment using 15 bp crRNA guides. Data represent mean ± SEM ( n = 3) (∗∗∗∗ p < 0.0001). (E) Luciferase activity analysis following HDR-mediated luciferase knockin using 20 bp crRNA guides. Data represent mean ± SEM ( n = 3) (∗∗∗∗ p < 0.0001). (F) Flow cytometry analysis showing percentage of GFP-positive cells following HDR-mediated GFP knockin. Data represent mean ± SEM ( n = 3) (∗∗∗∗ p < 0.0001). (G) Schematic representation illustrating simultaneous orthogonal activation of Bmp2 and repression of Dkk1 expression in MC3T3-E1 cells. (H) RT-qPCR analysis demonstrating significantly enhanced Bmp2 activation and Dkk1 repression under simultaneous orthogonal induction compared with single-gene regulatory conditions. Data are presented as mean ± SEM ( n = 3). ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (I) Representative images of alizarin red S (ARS) and alkaline phosphatase (ALP) staining showing significantly enhanced osteogenic differentiation following orthogonal OREC induction compared to single-gene controls. Color code for experimental conditions: white: empty vector control; gray: OREC o construct only; crosshatched: OREC c construct only; red: OREC o + Light (optogenetic activation); green: OREC c + Dox (chemogenetic activation) (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). (J) RT-qPCR analysis demonstrating synergistic upregulation of osteogenic marker genes ( Alp , Bglap , and Sp7 ) upon simultaneous Bmp2 activation and Dkk1 repression. Data represent mean ± SEM ( n = 3) (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). (K) The CCK-8 assay quantifies viable cells via dehydrogenase-mediated formazan formation measured at 450 nm, showing that OREC treatments do not affect cell viability in MC3T3-E1 cells. Data shown as mean ± SEM ( n = 3). See also and .

Journal: Cell Reports Methods

Article Title: An orthogonal CRISPR/Cpf1 platform for precise spatiotemporal gene regulation and osteoporotic fracture repair

doi: 10.1016/j.crmeth.2025.101299

Figure Lengend Snippet: Multiplex orthogonal gene regulation and programmable editing by OREC with therapeutic application in osteoblasts (A) Experimental illustration of orthogonal activation and repression of ASCL1 and RAB7A gene expression in HEK293T cells using distinct chemical and light inductions. (B) RT-qPCR time course analysis demonstrating orthogonal and reversible control of ASCL1 activation and RAB7A repression in response to alternating Dox and light stimuli. Data represent mean ± SEM ( n = 3). vs. RAB7A baseline (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001); vs. RAB7A 36 h ( $ p < 0.05, $$$ p < 0.001); vs. ASCL1 baseline ( && p < 0.01, &&&& p < 0.0001); vs. ASCL1 48 h ( ## p < 0.01, #### p < 0.0001). (C) Schematic diagram illustrating crRNA guide-length-dependent transcriptional repression and HDR-based gene editing using OREC c system. (D) Transcriptional repression of RAB7A and FZD1 genes following 72 h doxycycline treatment using 15 bp crRNA guides. Data represent mean ± SEM ( n = 3) (∗∗∗∗ p < 0.0001). (E) Luciferase activity analysis following HDR-mediated luciferase knockin using 20 bp crRNA guides. Data represent mean ± SEM ( n = 3) (∗∗∗∗ p < 0.0001). (F) Flow cytometry analysis showing percentage of GFP-positive cells following HDR-mediated GFP knockin. Data represent mean ± SEM ( n = 3) (∗∗∗∗ p < 0.0001). (G) Schematic representation illustrating simultaneous orthogonal activation of Bmp2 and repression of Dkk1 expression in MC3T3-E1 cells. (H) RT-qPCR analysis demonstrating significantly enhanced Bmp2 activation and Dkk1 repression under simultaneous orthogonal induction compared with single-gene regulatory conditions. Data are presented as mean ± SEM ( n = 3). ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (I) Representative images of alizarin red S (ARS) and alkaline phosphatase (ALP) staining showing significantly enhanced osteogenic differentiation following orthogonal OREC induction compared to single-gene controls. Color code for experimental conditions: white: empty vector control; gray: OREC o construct only; crosshatched: OREC c construct only; red: OREC o + Light (optogenetic activation); green: OREC c + Dox (chemogenetic activation) (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). (J) RT-qPCR analysis demonstrating synergistic upregulation of osteogenic marker genes ( Alp , Bglap , and Sp7 ) upon simultaneous Bmp2 activation and Dkk1 repression. Data represent mean ± SEM ( n = 3) (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). (K) The CCK-8 assay quantifies viable cells via dehydrogenase-mediated formazan formation measured at 450 nm, showing that OREC treatments do not affect cell viability in MC3T3-E1 cells. Data shown as mean ± SEM ( n = 3). See also and .

Article Snippet: Recombinant BMP2 protein , MedChemExpress , Cat# HY-P7006.

Techniques: Multiplex Assay, Activation Assay, Gene Expression, Quantitative RT-PCR, Control, Luciferase, Activity Assay, Knock-In, Flow Cytometry, Expressing, Staining, Plasmid Preparation, Construct, Marker, CCK-8 Assay

$AAV-delivered OREC system design and in vivo orthogonal gene regulation in fracture healing (A) OREC o system comprises two vectors encoding dAsCpf1-Activer (upper) and TetR-CIBN-P2A-CRY2-VP16 3 with Bmp2 -targeting crRNA (lower). (B) OREC c system consists of vectors encoding dLbCpf1-Repr (upper) and another vector expressing rtTA-Advanced with Dkk1 -targeting crRNA (lower). See also . All constructs designed within AAV packaging constraints. (C) Experimental setup showing AAV intratibial injection procedure with custom LED patch device and power supply system for localized light delivery. (D) Experimental timeline: AAV intratibial injection 14 days before fracture (day 14), tibial fracture induction (day 0), and blue light treatment (470 nm, twice daily for 30 min) beginning one day post-fracture (day 1) through endpoint (day 42). (E and F) AAV2/9 vector constructs for bioluminescence analysis of OREC activity in vivo . (G) Experimental timeline showing AAV intratibial injection (day 0) followed by 14-day treatment with light stimulation (470 nm, 30 min twice daily) or oral doxycycline (30 mg/kg daily) prior to bioluminescence imaging. (H) Representative bioluminescence images demonstrating inducible luciferase expression at tibial sites by OREC with no detectable signal in distant tissues. (I) RT-qPCR analyses of Bmp2 and Dkk1 expression levels in orthogonally treated fracture sites at days 7 and 21 post-fracture. Data represent mean ± SEM ( n = 6 mice/group) (∗∗ p < 0.01, ∗∗∗∗ p < 0.0001). (J) Analysis of Bmp2 and Dkk1 expression relative to Gapdh using the 2 −ΔCt method in fracture callus tissue 7 days after light or doxycycline induction in OREC-transduced mice. Data represent mean ± SEM ( n = 6 mice per group). (K and L) RT-qPCR analysis of Bmp2 (K) and Dkk1 (L) expression in fracture callus tissue from mice exposed to inducers without OREC constructs. Data represent mean ± SEM ( n = 3 mice per group). See also and .$

Journal: Cell Reports Methods

Article Title: An orthogonal CRISPR/Cpf1 platform for precise spatiotemporal gene regulation and osteoporotic fracture repair

doi: 10.1016/j.crmeth.2025.101299

Figure Lengend Snippet: AAV-delivered OREC system design and in vivo orthogonal gene regulation in fracture healing (A) OREC o system comprises two vectors encoding dAsCpf1-Activer (upper) and TetR-CIBN-P2A-CRY2-VP16 3 with Bmp2 -targeting crRNA (lower). (B) OREC c system consists of vectors encoding dLbCpf1-Repr (upper) and another vector expressing rtTA-Advanced with Dkk1 -targeting crRNA (lower). See also . All constructs designed within AAV packaging constraints. (C) Experimental setup showing AAV intratibial injection procedure with custom LED patch device and power supply system for localized light delivery. (D) Experimental timeline: AAV intratibial injection 14 days before fracture (day 14), tibial fracture induction (day 0), and blue light treatment (470 nm, twice daily for 30 min) beginning one day post-fracture (day 1) through endpoint (day 42). (E and F) AAV2/9 vector constructs for bioluminescence analysis of OREC activity in vivo . (G) Experimental timeline showing AAV intratibial injection (day 0) followed by 14-day treatment with light stimulation (470 nm, 30 min twice daily) or oral doxycycline (30 mg/kg daily) prior to bioluminescence imaging. (H) Representative bioluminescence images demonstrating inducible luciferase expression at tibial sites by OREC with no detectable signal in distant tissues. (I) RT-qPCR analyses of Bmp2 and Dkk1 expression levels in orthogonally treated fracture sites at days 7 and 21 post-fracture. Data represent mean ± SEM ( n = 6 mice/group) (∗∗ p < 0.01, ∗∗∗∗ p < 0.0001). (J) Analysis of Bmp2 and Dkk1 expression relative to Gapdh using the 2 −ΔCt method in fracture callus tissue 7 days after light or doxycycline induction in OREC-transduced mice. Data represent mean ± SEM ( n = 6 mice per group). (K and L) RT-qPCR analysis of Bmp2 (K) and Dkk1 (L) expression in fracture callus tissue from mice exposed to inducers without OREC constructs. Data represent mean ± SEM ( n = 3 mice per group). See also and .

Article Snippet: Recombinant BMP2 protein , MedChemExpress , Cat# HY-P7006.

Techniques: In Vivo, Plasmid Preparation, Expressing, Construct, Injection, Activity Assay, Imaging, Luciferase, Quantitative RT-PCR

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recombinant human bmp2 protein r d systems (R&D Systems)

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