Review



anti bmpr1b  (R&D Systems)


Bioz Verified Symbol R&D Systems is a verified supplier
Bioz Manufacturer Symbol R&D Systems manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 92

    Structured Review

    R&D Systems anti bmpr1b
    Anti Bmpr1b, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti bmpr1b/product/R&D Systems
    Average 92 stars, based on 8 article reviews
    anti bmpr1b - by Bioz Stars, 2026-05
    92/100 stars

    Images



    Similar Products

    92
    R&D Systems anti bmpr1b
    Anti Bmpr1b, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti bmpr1b/product/R&D Systems
    Average 92 stars, based on 1 article reviews
    anti bmpr1b - by Bioz Stars, 2026-05
    92/100 stars
      Buy from Supplier

    92
    R&D Systems alk6
    Receptor expressions of ALK2, ALK4, <t>ALK6,</t> ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/− BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤ 0.05, ** p ≤ 0.01; n = 6, BMP-2 450 ng/mL).
    Alk6, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/alk6/product/R&D Systems
    Average 92 stars, based on 1 article reviews
    alk6 - by Bioz Stars, 2026-05
    92/100 stars
      Buy from Supplier

    93
    Novus Biologicals bmpr1b antibody
    Receptor expressions of ALK2, ALK4, <t>ALK6,</t> ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/− BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤ 0.05, ** p ≤ 0.01; n = 6, BMP-2 450 ng/mL).
    Bmpr1b Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bmpr1b antibody/product/Novus Biologicals
    Average 93 stars, based on 1 article reviews
    bmpr1b antibody - by Bioz Stars, 2026-05
    93/100 stars
      Buy from Supplier

    93
    R&D Systems mouse anti bmpr 1b
    Receptor expressions of ALK2, ALK4, <t>ALK6,</t> ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/− BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤ 0.05, ** p ≤ 0.01; n = 6, BMP-2 450 ng/mL).
    Mouse Anti Bmpr 1b, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti bmpr 1b/product/R&D Systems
    Average 93 stars, based on 1 article reviews
    mouse anti bmpr 1b - by Bioz Stars, 2026-05
    93/100 stars
      Buy from Supplier

    91
    R&D Systems Hematology chimeric fc
    Receptor expressions of ALK2, ALK4, <t>ALK6,</t> ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/− BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤ 0.05, ** p ≤ 0.01; n = 6, BMP-2 450 ng/mL).
    Chimeric Fc, supplied by R&D Systems Hematology, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/chimeric fc/product/R&D Systems Hematology
    Average 91 stars, based on 1 article reviews
    chimeric fc - by Bioz Stars, 2026-05
    91/100 stars
      Buy from Supplier

    91
    Boster Bio digoxigenin dig labeled bmpr1b as1 probes
    Receptor expressions of ALK2, ALK4, <t>ALK6,</t> ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/− BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤ 0.05, ** p ≤ 0.01; n = 6, BMP-2 450 ng/mL).
    Digoxigenin Dig Labeled Bmpr1b As1 Probes, supplied by Boster Bio, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/digoxigenin dig labeled bmpr1b as1 probes/product/Boster Bio
    Average 91 stars, based on 1 article reviews
    digoxigenin dig labeled bmpr1b as1 probes - by Bioz Stars, 2026-05
    91/100 stars
      Buy from Supplier

    91
    Boster Bio bmpr1b as1 probes
    Sequences used in this study.
    Bmpr1b As1 Probes, supplied by Boster Bio, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bmpr1b as1 probes/product/Boster Bio
    Average 91 stars, based on 1 article reviews
    bmpr1b as1 probes - by Bioz Stars, 2026-05
    91/100 stars
      Buy from Supplier

    Image Search Results


    Receptor expressions of ALK2, ALK4, ALK6, ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/− BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤ 0.05, ** p ≤ 0.01; n = 6, BMP-2 450 ng/mL).

    Journal: Biology

    Article Title: BMP-2-Driven Osteogenesis: A Comparative Analysis of Porcine BMSCs and ASCs and the Role of TGF-β and FGF Signaling

    doi: 10.3390/biology14060610

    Figure Lengend Snippet: Receptor expressions of ALK2, ALK4, ALK6, ALK5, ALK7, BMPR-II in pASC. Grouped representation of the respective receptor expression in the course of osteogenic differentiation (OM +/− BMP-2). From day 19, there is a significant induction of ALK 2, ALK 6, and ALK 5 with the addition of BMP-2. BMPR-II expression in the OM group decreased in OM and tended to stay increased under BMP-2 supplementation from day 19, but was not considered significant (* p ≤ 0.05, ** p ≤ 0.01; n = 6, BMP-2 450 ng/mL).

    Article Snippet: The respective conjugated antibodies were used for the expressions of ALK3 (Cat. No.: AF436), ALK 5 (Cat. No.: FAB5871), ALK6 (Cat. No.: FAB5051A), TGF-β2-RII (Cat. No.: FAB532P), ALK7 (Cat. No.: FAB77491A), ALK2 (Cat. No.: AF637), ALK4 (Cat. No.: MAB2221), and BMPR-II (Cat. No.: AF811) (by R&D Systems, Minneapolis, MN, USA), and the pASCs and pBMSCs were compared for their expressions of the specific surface antigens CD45 (Cat. No.: MCA1568GA, Bio-Rad, Hercules, CA, USA), HLA-DR (human leukocyte antigen–antigen D-related surface molecule) (Cat. No.: MCA2314F, Bio-Rad, Hercules, CA, USA), CD29 (Cat. No.: 561,496, BD Pharmingen, Franklin Lakes, NJ, USA), CD79alpha (Bio-Rad, Cat. No.: MCA2538GA), CD14 (Cat. No.: MCA1568GA, Bio-Rad, Hercules, CA, USA), CD31 (Cat. No.: AF3387, R&D Systems, Minneapolis, MN, USA), CD105 (Cat. No.: NB110-58718APC, Novus Biologicals, Minneapolis, MN, USA), CD26 (, Cat. No.: NB600-552APC, Novus Biologicals, Minneapolis, MN, USA), CD73 (, Cat. No.: AF4488, R&D Systems, Minneapolis, MN, USA), CD90 (Cat. No.: 559,869, BD Pharmingen, Franklin Lakes, NJ, USA), CD34 (Cat. No.: 81289, abcam, Cambridge, UK), and CD44 (Cat. No.: 5531, BD Pharmingen, Franklin Lakes, NJ, USA).

    Techniques: Expressing

    Sequences used in this study.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: Sequences used in this study.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques:

    The expression of lncRNA BMPR1B-AS1 in endometrial cancer tissues and cell lines. A, Volcano map of dysregulated lncRNAs between EC tissues and adjacent normal tissues. The results were obtained from TCGA database. B, Expression levels of lncRNA BMPR1B-AS1 in paired EC and adjacent noncancerous tissues (n = 28). C, RT-qPCR analysis of BMPR1B-AS1 expression in human EC cell lines (Ishikawa, Hec-1a and Hec-1b cells). The data are representative of three independent experiments. Bars, ±SD. **p < 0.01, ****p < 0.0001.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: The expression of lncRNA BMPR1B-AS1 in endometrial cancer tissues and cell lines. A, Volcano map of dysregulated lncRNAs between EC tissues and adjacent normal tissues. The results were obtained from TCGA database. B, Expression levels of lncRNA BMPR1B-AS1 in paired EC and adjacent noncancerous tissues (n = 28). C, RT-qPCR analysis of BMPR1B-AS1 expression in human EC cell lines (Ishikawa, Hec-1a and Hec-1b cells). The data are representative of three independent experiments. Bars, ±SD. **p < 0.01, ****p < 0.0001.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: Expressing, Quantitative RT-PCR

    Overexpression of BMPR1B-AS1 promotes the proliferation, migration and invasion of Hec-1b cells while inhibiting apoptosis. A, Overexpression of BMPR1B-AS1 was confirmed by RT-qPCR. B, Overexpression of BMPR1B-AS1 promoted the proliferation of Hec-1b cells. C, E, G, H, Transwell migration assay (magnification, 200×) and wound healing assay (magnification, 100×) showed that overexpression of BMPR1B-AS1 facilitated the migration of Hec-1b cells. D, F, Transwell invasion assay showed that overexpression of BMPR1B-AS1 facilitated the invasion of Hec-1b cells (magnification, 200×). I, K, Flow cytometry results showed that BMPR1B-AS1 overexpression inhibited Hec-1b cell apoptosis. J, L, Flow cytometry results showed that BMPR1B-AS1 overexpression increased the accumulation of cells in the S-phase and decreased the accumulation of cells in the G0/G1 phase. M, N, O, P, Q, Western blot and analysis showed that the protein level of E-cadherin was decreased, but the protein levels of N-cadherin, Cyclin D1 and CDK4 were increased in the BMPR1B-AS1 overexpression group. Lv, lentiviral vector. The data are representative of three independent experiments. Bars, ±SD. *P < .05, **P < .01, ***P < .001, ****P < 0.0001.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: Overexpression of BMPR1B-AS1 promotes the proliferation, migration and invasion of Hec-1b cells while inhibiting apoptosis. A, Overexpression of BMPR1B-AS1 was confirmed by RT-qPCR. B, Overexpression of BMPR1B-AS1 promoted the proliferation of Hec-1b cells. C, E, G, H, Transwell migration assay (magnification, 200×) and wound healing assay (magnification, 100×) showed that overexpression of BMPR1B-AS1 facilitated the migration of Hec-1b cells. D, F, Transwell invasion assay showed that overexpression of BMPR1B-AS1 facilitated the invasion of Hec-1b cells (magnification, 200×). I, K, Flow cytometry results showed that BMPR1B-AS1 overexpression inhibited Hec-1b cell apoptosis. J, L, Flow cytometry results showed that BMPR1B-AS1 overexpression increased the accumulation of cells in the S-phase and decreased the accumulation of cells in the G0/G1 phase. M, N, O, P, Q, Western blot and analysis showed that the protein level of E-cadherin was decreased, but the protein levels of N-cadherin, Cyclin D1 and CDK4 were increased in the BMPR1B-AS1 overexpression group. Lv, lentiviral vector. The data are representative of three independent experiments. Bars, ±SD. *P < .05, **P < .01, ***P < .001, ****P < 0.0001.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: Over Expression, Migration, Quantitative RT-PCR, Transwell Migration Assay, Wound Healing Assay, Transwell Invasion Assay, Flow Cytometry, Western Blot, Plasmid Preparation

    Knockdown of BMPR1B-AS1 expression inhibits the proliferation, migration and invasion of Ishikawa cells while promoting apoptosis. A, BMPR1B-AS1 knockdown efficiency was confirmed by RT-qPCR. B, Knockdown of BMPR1B-AS1 expression inhibited the proliferation of Ishikawa cells. C, E, G, H, Transwell migration assay (magnification, 200×) and wound healing assay (magnification, 100×) showed that knockdown of BMPR1B-AS1 expression decreased the migration of Ishikawa cells. D, F, Transwell invasion assay showed that knockdown of BMPR1B-AS1 expression decreased the invasion of Ishikawa cells (magnification, 200×). I, K, Flow cytometry results showed that BMPR1B-AS1 knockdown facilitated Ishikawa cell apoptosis. J, L, Flow cytometry results showed that BMPR1B-AS1 knockdown increased the accumulation of cells in the G0/G1 phase and decreased the accumulation of cells in the S-phase. M, N, O, P, Q, Western blot and analysis showed that the protein level of E-cadherin was increased, but the protein levels of N-cadherin, Cyclin D1 and CDK4 were decreased in the BMPR1B-AS1 knockdown group. Sh, short hairpin. The data are representative of three independent experiments. Bars, ±SD. **P < .01, ***P < .001, ****P < 0.0001.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: Knockdown of BMPR1B-AS1 expression inhibits the proliferation, migration and invasion of Ishikawa cells while promoting apoptosis. A, BMPR1B-AS1 knockdown efficiency was confirmed by RT-qPCR. B, Knockdown of BMPR1B-AS1 expression inhibited the proliferation of Ishikawa cells. C, E, G, H, Transwell migration assay (magnification, 200×) and wound healing assay (magnification, 100×) showed that knockdown of BMPR1B-AS1 expression decreased the migration of Ishikawa cells. D, F, Transwell invasion assay showed that knockdown of BMPR1B-AS1 expression decreased the invasion of Ishikawa cells (magnification, 200×). I, K, Flow cytometry results showed that BMPR1B-AS1 knockdown facilitated Ishikawa cell apoptosis. J, L, Flow cytometry results showed that BMPR1B-AS1 knockdown increased the accumulation of cells in the G0/G1 phase and decreased the accumulation of cells in the S-phase. M, N, O, P, Q, Western blot and analysis showed that the protein level of E-cadherin was increased, but the protein levels of N-cadherin, Cyclin D1 and CDK4 were decreased in the BMPR1B-AS1 knockdown group. Sh, short hairpin. The data are representative of three independent experiments. Bars, ±SD. **P < .01, ***P < .001, ****P < 0.0001.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: Expressing, Migration, Quantitative RT-PCR, Transwell Migration Assay, Wound Healing Assay, Transwell Invasion Assay, Flow Cytometry, Western Blot

    BMPR1B-AS1 functions as an efficient miR-7-2-3p sponge in Hec-1b and Ishikawa cells. A, FISH assay showed that the intracellular localization of BMPR1B-AS1 was mainly in the cytoplasm in Ishikawa cells. 18S and U6 were used as controls. B, Putative binding sites of miR-7-2-3p and BMPR1B-AS1. C, Negative correlation was found between BMPR1B-AS1 expression and miR-7-2-3p expression among the 28 endometrial cancer tissue specimens. R = −.549, P = .002. D, E, The effect of the miR-7-2-3p mimic on the luciferase activities of 293 T cells transfected with WT or MUT BMPR1B-AS1 was detected 24 h and 48 h after transfection, respectively. F, RT-qPCR results showed that miR-7-2-3p expression was downregulated after BMPR1B-AS1 overexpression in Hec-1b cells. G, RT-qPCR results showed that miR-7-2-3p expression was upregulated after BMPR1B-AS1 knockdown in Ishikawa cells. H, miR-7-2-3p expression was upregulated after transfection with the miR-7-2-3p mimic in Hec-1b cells. I, The miR-7-2-3p mimic reversed the BMPR1B-AS1-mediated downregulation of miR-7-2-3p expression. J, miR-7-2-3p expression was downregulated after transfection of Ishikawa cells with the miR-7-2-3p inhibitor. K, The miR-7-2-3p inhibitor attenuated the BMPR1B-AS1-mediated upregulation of miR-7-2-3p expression. The data are representative of three independent experiments. Bars, ±SD. *P < .05, **P < .01, ***P < .001, ****P < 0.0001.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: BMPR1B-AS1 functions as an efficient miR-7-2-3p sponge in Hec-1b and Ishikawa cells. A, FISH assay showed that the intracellular localization of BMPR1B-AS1 was mainly in the cytoplasm in Ishikawa cells. 18S and U6 were used as controls. B, Putative binding sites of miR-7-2-3p and BMPR1B-AS1. C, Negative correlation was found between BMPR1B-AS1 expression and miR-7-2-3p expression among the 28 endometrial cancer tissue specimens. R = −.549, P = .002. D, E, The effect of the miR-7-2-3p mimic on the luciferase activities of 293 T cells transfected with WT or MUT BMPR1B-AS1 was detected 24 h and 48 h after transfection, respectively. F, RT-qPCR results showed that miR-7-2-3p expression was downregulated after BMPR1B-AS1 overexpression in Hec-1b cells. G, RT-qPCR results showed that miR-7-2-3p expression was upregulated after BMPR1B-AS1 knockdown in Ishikawa cells. H, miR-7-2-3p expression was upregulated after transfection with the miR-7-2-3p mimic in Hec-1b cells. I, The miR-7-2-3p mimic reversed the BMPR1B-AS1-mediated downregulation of miR-7-2-3p expression. J, miR-7-2-3p expression was downregulated after transfection of Ishikawa cells with the miR-7-2-3p inhibitor. K, The miR-7-2-3p inhibitor attenuated the BMPR1B-AS1-mediated upregulation of miR-7-2-3p expression. The data are representative of three independent experiments. Bars, ±SD. *P < .05, **P < .01, ***P < .001, ****P < 0.0001.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: Binding Assay, Expressing, Luciferase, Transfection, Quantitative RT-PCR, Over Expression

    Upregulation of miR-7-2-3p expression reverses the BMPR1B-AS1 overexpression-induced progression of Hec-1b cells. A, CCK8 assay showed that cotransfection with the miR-7-2-3p mimic suppressed the BMPR1B-AS1 overexpression-induced proliferation of Hec-1b cells. B, D, F, G, Transwell migration assay (magnification, 200×) and wound healing assay (magnification, 100×) showed that cotransfection with the miR-7-2-3p mimic suppressed the BMPR1B-AS1 overexpression-induced migration of Hec-1b cells. C, E, Transwell invasion assay (magnification, 200×) showed that cotransfection with the miR-7-2-3p mimic suppressed the BMPR1B-AS1 overexpression-induced invasion of Hec-1b cells. H-K, Flow cytometry showed that cotransfection with the miR-7-2-3p mimic accelerated apoptosis and cell cycle arrest, and these effects were inhibited by BMPR1B-AS1 overexpression in Hec-1b cells. The data are representative of three independent experiments. Bars, ±SD. *P < .05, **P < .01, ***P < .001, ****P < 0.0001.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: Upregulation of miR-7-2-3p expression reverses the BMPR1B-AS1 overexpression-induced progression of Hec-1b cells. A, CCK8 assay showed that cotransfection with the miR-7-2-3p mimic suppressed the BMPR1B-AS1 overexpression-induced proliferation of Hec-1b cells. B, D, F, G, Transwell migration assay (magnification, 200×) and wound healing assay (magnification, 100×) showed that cotransfection with the miR-7-2-3p mimic suppressed the BMPR1B-AS1 overexpression-induced migration of Hec-1b cells. C, E, Transwell invasion assay (magnification, 200×) showed that cotransfection with the miR-7-2-3p mimic suppressed the BMPR1B-AS1 overexpression-induced invasion of Hec-1b cells. H-K, Flow cytometry showed that cotransfection with the miR-7-2-3p mimic accelerated apoptosis and cell cycle arrest, and these effects were inhibited by BMPR1B-AS1 overexpression in Hec-1b cells. The data are representative of three independent experiments. Bars, ±SD. *P < .05, **P < .01, ***P < .001, ****P < 0.0001.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: Expressing, Over Expression, CCK-8 Assay, Cotransfection, Transwell Migration Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Flow Cytometry

    Downregulation of miR-7-2-3p expression reverses the BMPR1B-AS1 knockdown-mediated inhibition of Ishikawa cells. A, CCK8 assay showed that cotransfection with the miR-7-2-3p inhibitor reversed the BMPR1B-AS1 knockdown-mediated inhibition of proliferation of Ishikawa cells. B, D, F, G, Transwell migration assay (magnification, 200×) and wound healing assay (magnification, 100×) showed that cotransfection with the miR-7-2-3p inhibitor reversed the BMPR1B-AS1 knockdown-mediated inhibition of migration of Ishikawa cells. C, E, Transwell invasion assay (magnification, 200×) showed that cotransfection with the miR-7-2-3p inhibitor reversed the BMPR1B-AS1 knockdown-mediated inhibition of invasion of Ishikawa cells. H-K, Flow cytometry showed that cotransfection with the miR-7-2-3p inhibitor inhibited apoptosis and cell cycle arrest, and these effects were enhanced by BMPR1B-AS1 knockdown in Ishikawa cells. The data are representative of three independent experiments. Bars, ±SD. **P < .01, ***P < .001, ****P < 0.0001.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: Downregulation of miR-7-2-3p expression reverses the BMPR1B-AS1 knockdown-mediated inhibition of Ishikawa cells. A, CCK8 assay showed that cotransfection with the miR-7-2-3p inhibitor reversed the BMPR1B-AS1 knockdown-mediated inhibition of proliferation of Ishikawa cells. B, D, F, G, Transwell migration assay (magnification, 200×) and wound healing assay (magnification, 100×) showed that cotransfection with the miR-7-2-3p inhibitor reversed the BMPR1B-AS1 knockdown-mediated inhibition of migration of Ishikawa cells. C, E, Transwell invasion assay (magnification, 200×) showed that cotransfection with the miR-7-2-3p inhibitor reversed the BMPR1B-AS1 knockdown-mediated inhibition of invasion of Ishikawa cells. H-K, Flow cytometry showed that cotransfection with the miR-7-2-3p inhibitor inhibited apoptosis and cell cycle arrest, and these effects were enhanced by BMPR1B-AS1 knockdown in Ishikawa cells. The data are representative of three independent experiments. Bars, ±SD. **P < .01, ***P < .001, ****P < 0.0001.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: Expressing, Inhibition, CCK-8 Assay, Cotransfection, Transwell Migration Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Flow Cytometry

    DCLK1 is a target gene of miR-7-2-3p, and BMPR1B-AS1 regulates DCLK1 expression by competitively binding to miR-7-2-3p in EC cell lines. A, Putative binding sites of miR-7-2-3p and DCLK1 mRNA. B, C, The effect of the miR-7-2-3p mimic on the luciferase activities of cells transfected with WT or MUT DCLK1 was detected after 24 h and 48 h, respectively. D, Negative correlation was found between miR-7-2-3p expression and DCLK1 mRNA expression among the 28 endometrial cancer tissue specimens. R = −.531, P = .004. E, Positive correlation was found between BMPR1B-AS1 expression and DCLK1 mRNA expression among the 28 endometrial cancer tissue specimens. R = .690, P = .000. F, J, N, RT-qPCR and western blotting results showed that DCLK1 mRNA and protein expression was upregulated after BMPR1B-AS1 overexpression. G, K, O, RT-qPCR and western blotting results showed that DCLK1 mRNA and protein expression was downregulated after BMPR1B-AS1 knockdown. H, L, P, RT-qPCR and western blotting results showed that the miR-7-2-3p mimic attenuated the BMPR1B-AS1-mediated upregulation of DCLK1 mRNA and protein expression. I, M, Q, RT-qPCR and western blotting results showed that the miR-7-2-3p inhibitor reversed the effects of BMPR1B-AS1 knockdown on DCLK1 mRNA and protein expression. The data are representative of three independent experiments. Bars, ±SD. *P < .05, **P < .01, ***P < .001, ****P < 0.0001.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: DCLK1 is a target gene of miR-7-2-3p, and BMPR1B-AS1 regulates DCLK1 expression by competitively binding to miR-7-2-3p in EC cell lines. A, Putative binding sites of miR-7-2-3p and DCLK1 mRNA. B, C, The effect of the miR-7-2-3p mimic on the luciferase activities of cells transfected with WT or MUT DCLK1 was detected after 24 h and 48 h, respectively. D, Negative correlation was found between miR-7-2-3p expression and DCLK1 mRNA expression among the 28 endometrial cancer tissue specimens. R = −.531, P = .004. E, Positive correlation was found between BMPR1B-AS1 expression and DCLK1 mRNA expression among the 28 endometrial cancer tissue specimens. R = .690, P = .000. F, J, N, RT-qPCR and western blotting results showed that DCLK1 mRNA and protein expression was upregulated after BMPR1B-AS1 overexpression. G, K, O, RT-qPCR and western blotting results showed that DCLK1 mRNA and protein expression was downregulated after BMPR1B-AS1 knockdown. H, L, P, RT-qPCR and western blotting results showed that the miR-7-2-3p mimic attenuated the BMPR1B-AS1-mediated upregulation of DCLK1 mRNA and protein expression. I, M, Q, RT-qPCR and western blotting results showed that the miR-7-2-3p inhibitor reversed the effects of BMPR1B-AS1 knockdown on DCLK1 mRNA and protein expression. The data are representative of three independent experiments. Bars, ±SD. *P < .05, **P < .01, ***P < .001, ****P < 0.0001.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: Expressing, Binding Assay, Luciferase, Transfection, Quantitative RT-PCR, Western Blot, Over Expression

    BMPR1B-AS1 promotes endometrial cancer cell growth in vivo by targeting miR-7-2-3p. A, Images of tumor xenografts. B, The growth curves of tumor xenografts demonstrated that BMPR1B-AS1 significantly promote tumor growth in vivo , which was reversed by treatment with agomir-7-2-3p. **P < 0.01 vs. Lv-BMPR1B-AS1, ***P < 0.001 vs. Lv-BMPR1B-AS1, ****P < 0.0001 vs. Lv-BMPR1B-AS1, # P < 0.05 vs. Lv-BMPR1B-AS1+ agomiR-7-2-3p. C, The weights of tumor xenografts derived from five groups. D, The expression levels of BMPR1B-AS1 in five groups were examined by RT-qPCR. E, The expression levels of miR-7-2-3p in five groups were examined by RT-qPCR. F, G, The expression levels of DCLK1 in five groups were examined by RT-qPCR and IHC. H, Negative correlation was found between BMPR1B-AS1 and miR-7-2-3p expression in xenografts tissues. R = −.506, P = .000. I, Negative correlation was found between miR-7-2-3p and DCLK1 mRNA expression in xenografts tissues. R = −.452, P = .001. J. Positive correlation was found between BMPR1B-AS1 and DCLK1 mRNA expression in xenografts tissues. R = .387, P = .006. *P < .05, **P < .01, ***P < .001.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: BMPR1B-AS1 promotes endometrial cancer cell growth in vivo by targeting miR-7-2-3p. A, Images of tumor xenografts. B, The growth curves of tumor xenografts demonstrated that BMPR1B-AS1 significantly promote tumor growth in vivo , which was reversed by treatment with agomir-7-2-3p. **P < 0.01 vs. Lv-BMPR1B-AS1, ***P < 0.001 vs. Lv-BMPR1B-AS1, ****P < 0.0001 vs. Lv-BMPR1B-AS1, # P < 0.05 vs. Lv-BMPR1B-AS1+ agomiR-7-2-3p. C, The weights of tumor xenografts derived from five groups. D, The expression levels of BMPR1B-AS1 in five groups were examined by RT-qPCR. E, The expression levels of miR-7-2-3p in five groups were examined by RT-qPCR. F, G, The expression levels of DCLK1 in five groups were examined by RT-qPCR and IHC. H, Negative correlation was found between BMPR1B-AS1 and miR-7-2-3p expression in xenografts tissues. R = −.506, P = .000. I, Negative correlation was found between miR-7-2-3p and DCLK1 mRNA expression in xenografts tissues. R = −.452, P = .001. J. Positive correlation was found between BMPR1B-AS1 and DCLK1 mRNA expression in xenografts tissues. R = .387, P = .006. *P < .05, **P < .01, ***P < .001.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: In Vivo, Derivative Assay, Expressing, Quantitative RT-PCR

    A schematic model of the mechanism by which lncRNA BMPR1B-AS1 regulates endometrial cancer cell malignant behaviors. The BMPR1B-AS1/miR-7-2-3p/DCLK1 axis promotes the progression of endometrial cancer cells via the PI3K/Akt/NF-κB signaling pathway.

    Journal: Cell Cycle

    Article Title: Long noncoding RNA BMPR1B-AS1 facilitates endometrial cancer cell proliferation and metastasis by sponging miR-7-2-3p to modulate the DCLK1/Akt/NF-κB pathway

    doi: 10.1080/15384101.2022.2060003

    Figure Lengend Snippet: A schematic model of the mechanism by which lncRNA BMPR1B-AS1 regulates endometrial cancer cell malignant behaviors. The BMPR1B-AS1/miR-7-2-3p/DCLK1 axis promotes the progression of endometrial cancer cells via the PI3K/Akt/NF-κB signaling pathway.

    Article Snippet: Digoxigenin (DIG)-labeled BMPR1B-AS1 probes were designed and synthesized by BOSTER (Wuhan, China).

    Techniques: