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mouse anti ccnd2  (Boster Bio)


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    Structured Review

    Boster Bio mouse anti ccnd2
    MiR-198 directly bound to the 3′-UTR of <t>CCND2</t> mRNA. ( A ) Bioinformatics analyses showed that 10 potential target genes of miR-198 were predicted by three different databases; ( B ) The two distinct predicted binding sites of miR-198 in the 3′-UTR of CCND2 mRNA were allocated, and the fragments containing either mutated binding site were amplified according to the mature miR-198 sequence; ( C ) In pMIR-REPORT™ vector, CCND2 mRNA 3′-UTRfragment containing either the wild type or the mutated Site 1 was fused downstream the reporter gene. When the vectors were cotransfected with miR-198 mimic or mimic control, and the relative luciferase activity, normalised by β-gal, was significantly suppressed in vector with wild type Site 1 than that with mutated Site 1 (32.80% ± 6.89%); ( D ) In the presence of wild type Site 2, not the mutated one, miR-198 was able to significantly inhibit luciferase activity although to a less extent than wild type Site 1 (55.39% ± 8.48%). (NC, negative control; WT, wide-type; MT, mutated-type. * Compared with NC, p < 0.05).
    Mouse Anti Ccnd2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti ccnd2/product/Boster Bio
    Average 90 stars, based on 1 article reviews
    mouse anti ccnd2 - by Bioz Stars, 2026-03
    90/100 stars

    Images

    1) Product Images from "miR-198 Represses the Proliferation of HaCaT Cells by Targeting Cyclin D2"

    Article Title: miR-198 Represses the Proliferation of HaCaT Cells by Targeting Cyclin D2

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms160817018

    MiR-198 directly bound to the 3′-UTR of CCND2 mRNA. ( A ) Bioinformatics analyses showed that 10 potential target genes of miR-198 were predicted by three different databases; ( B ) The two distinct predicted binding sites of miR-198 in the 3′-UTR of CCND2 mRNA were allocated, and the fragments containing either mutated binding site were amplified according to the mature miR-198 sequence; ( C ) In pMIR-REPORT™ vector, CCND2 mRNA 3′-UTRfragment containing either the wild type or the mutated Site 1 was fused downstream the reporter gene. When the vectors were cotransfected with miR-198 mimic or mimic control, and the relative luciferase activity, normalised by β-gal, was significantly suppressed in vector with wild type Site 1 than that with mutated Site 1 (32.80% ± 6.89%); ( D ) In the presence of wild type Site 2, not the mutated one, miR-198 was able to significantly inhibit luciferase activity although to a less extent than wild type Site 1 (55.39% ± 8.48%). (NC, negative control; WT, wide-type; MT, mutated-type. * Compared with NC, p < 0.05).
    Figure Legend Snippet: MiR-198 directly bound to the 3′-UTR of CCND2 mRNA. ( A ) Bioinformatics analyses showed that 10 potential target genes of miR-198 were predicted by three different databases; ( B ) The two distinct predicted binding sites of miR-198 in the 3′-UTR of CCND2 mRNA were allocated, and the fragments containing either mutated binding site were amplified according to the mature miR-198 sequence; ( C ) In pMIR-REPORT™ vector, CCND2 mRNA 3′-UTRfragment containing either the wild type or the mutated Site 1 was fused downstream the reporter gene. When the vectors were cotransfected with miR-198 mimic or mimic control, and the relative luciferase activity, normalised by β-gal, was significantly suppressed in vector with wild type Site 1 than that with mutated Site 1 (32.80% ± 6.89%); ( D ) In the presence of wild type Site 2, not the mutated one, miR-198 was able to significantly inhibit luciferase activity although to a less extent than wild type Site 1 (55.39% ± 8.48%). (NC, negative control; WT, wide-type; MT, mutated-type. * Compared with NC, p < 0.05).

    Techniques Used: Binding Assay, Amplification, Sequencing, Plasmid Preparation, Luciferase, Activity Assay, Negative Control

    MiR-198 transfection repressed the mRNA and protein expression of CCND2. ( A ) MiR-198 mimic transfection reduced the expression of CCND2 mRNA at 24 h (68.09% ± 16.73%) and 48 h (45.68% ± 10.94%); ( B ) MiR-198 mimic or CCND2 siRNA transfection reduced the expression of CCND2 protein at 24 h (50.55% ± 24.04% or 34.45% ± 6.98%) and 48 h (17.38% ± 9.96% or 16.24% ± 9.23%). (NC, negative control. * Compared with NC, p < 0.05).
    Figure Legend Snippet: MiR-198 transfection repressed the mRNA and protein expression of CCND2. ( A ) MiR-198 mimic transfection reduced the expression of CCND2 mRNA at 24 h (68.09% ± 16.73%) and 48 h (45.68% ± 10.94%); ( B ) MiR-198 mimic or CCND2 siRNA transfection reduced the expression of CCND2 protein at 24 h (50.55% ± 24.04% or 34.45% ± 6.98%) and 48 h (17.38% ± 9.96% or 16.24% ± 9.23%). (NC, negative control. * Compared with NC, p < 0.05).

    Techniques Used: Transfection, Expressing, Negative Control

    CCND2 siRNA transfection inhibited HaCaT cell proliferation by blocking cell cycle at G1 phase. ( A ) CCND2 siRNA transfection led to a significant reduction of mRNA expression of CCND2 in HaCaT cells both at 24 h (73.79% ± 11.45%) and 48 h (51.18% ± 8.85%); ( B ) Cell viability analysis showed that CCND2 siRNA transfection inhibited HaCaT cell proliferation at 24 h (67.98% ± 7.31%) and 48 h (67.45% ± 6.70%); ( C ) FCM analysis showed the effect of CCND2 siRNA transfection on cell cycle progression, and G1 phase arrest was obvious at 24 h (55.51% ± 6.18%) and 48 h (70.19% ± 4.10%) compared with negative control (42.98% ± 2.48%). (NC, negative control. * Compared with NC, p < 0.05).
    Figure Legend Snippet: CCND2 siRNA transfection inhibited HaCaT cell proliferation by blocking cell cycle at G1 phase. ( A ) CCND2 siRNA transfection led to a significant reduction of mRNA expression of CCND2 in HaCaT cells both at 24 h (73.79% ± 11.45%) and 48 h (51.18% ± 8.85%); ( B ) Cell viability analysis showed that CCND2 siRNA transfection inhibited HaCaT cell proliferation at 24 h (67.98% ± 7.31%) and 48 h (67.45% ± 6.70%); ( C ) FCM analysis showed the effect of CCND2 siRNA transfection on cell cycle progression, and G1 phase arrest was obvious at 24 h (55.51% ± 6.18%) and 48 h (70.19% ± 4.10%) compared with negative control (42.98% ± 2.48%). (NC, negative control. * Compared with NC, p < 0.05).

    Techniques Used: Transfection, Blocking Assay, Expressing, Negative Control



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    Image Search Results


    Journal: Cell Reports

    Article Title: Local Translation in Perisynaptic Astrocytic Processes Is Specific and Changes after Fear Conditioning

    doi: 10.1016/j.celrep.2020.108076

    Figure Lengend Snippet:

    Article Snippet: Mouse monoclonal anti-CCND2 (B-6) , Santa Cruz , Cat#sc376676; RRID: AB_11151389.

    Techniques: Software, Virus, Recombinant

    Journal: Cancer Cell

    Article Title: The Oncogenic Transcription Factor RUNX1/ETO Corrupts Cell Cycle Regulation to Drive Leukemic Transformation

    doi: 10.1016/j.ccell.2018.08.015

    Figure Lengend Snippet:

    Article Snippet: Mouse anti-CCND2 , Proteintech , Cat#10934-1-AP; RRID: AB_2275319.

    Techniques: Virus, Recombinant, In Vivo, In Vitro, Plasmid Preparation, Gel Extraction, cDNA Synthesis, Bicinchoninic Acid Protein Assay, Sequencing, Software

    Figure 8. STAT3, p-STAT3, CCND2 and MMP-2 expressions detected applying western blotting. (A) STAT3, p-STAT3, CCND2 and MMP-2 levels of C666-1 cells were significantly inhibited in the miRNA-124-3p mimics group compared to those in the blank control group and the mimics NC group. *P<0.05 compared with the miRNA-124-3p mimics group. (B) STAT3, p-STAT3, CCND2 and MMP-2 levels of CNE2 cells were significantly increased in the miRNA‑124-3p inhibitor group as compared with those in the blank control group and the inhibitor NC group. *P<0.05 compared with miRNA-124-3p inhibitor group.

    Journal: Oncology reports

    Article Title: MicroRNA-124-3p inhibits the growth and metastasis of nasopharyngeal carcinoma cells by targeting STAT3.

    doi: 10.3892/or.2015.4524

    Figure Lengend Snippet: Figure 8. STAT3, p-STAT3, CCND2 and MMP-2 expressions detected applying western blotting. (A) STAT3, p-STAT3, CCND2 and MMP-2 levels of C666-1 cells were significantly inhibited in the miRNA-124-3p mimics group compared to those in the blank control group and the mimics NC group. *P<0.05 compared with the miRNA-124-3p mimics group. (B) STAT3, p-STAT3, CCND2 and MMP-2 levels of CNE2 cells were significantly increased in the miRNA‑124-3p inhibitor group as compared with those in the blank control group and the inhibitor NC group. *P<0.05 compared with miRNA-124-3p inhibitor group.

    Article Snippet: Blocked PVDF membranes were incubated in solution (containing primary antibody [rabbit anti-human STAT3, phosphoSTAT3 (p-STAT3) and matrix metalloproteinase-2 (MMP-2) polyclonal antibody] and mouse anti-human cyclin D2 (CCND2) monoclonal antibody (Cell Signaling Technology, USA) for 2 h; eluted PVDF membranes were cultured in solution which was diluted using secondary antibody (Jinqiao Biotechnology Co., Ltd., Beijing, China) for 1 h, and reacted applying ECL chemiluminescence and then developed using X-ray.

    Techniques: Western Blot, Control

    MiR-198 directly bound to the 3′-UTR of CCND2 mRNA. ( A ) Bioinformatics analyses showed that 10 potential target genes of miR-198 were predicted by three different databases; ( B ) The two distinct predicted binding sites of miR-198 in the 3′-UTR of CCND2 mRNA were allocated, and the fragments containing either mutated binding site were amplified according to the mature miR-198 sequence; ( C ) In pMIR-REPORT™ vector, CCND2 mRNA 3′-UTRfragment containing either the wild type or the mutated Site 1 was fused downstream the reporter gene. When the vectors were cotransfected with miR-198 mimic or mimic control, and the relative luciferase activity, normalised by β-gal, was significantly suppressed in vector with wild type Site 1 than that with mutated Site 1 (32.80% ± 6.89%); ( D ) In the presence of wild type Site 2, not the mutated one, miR-198 was able to significantly inhibit luciferase activity although to a less extent than wild type Site 1 (55.39% ± 8.48%). (NC, negative control; WT, wide-type; MT, mutated-type. * Compared with NC, p < 0.05).

    Journal: International Journal of Molecular Sciences

    Article Title: miR-198 Represses the Proliferation of HaCaT Cells by Targeting Cyclin D2

    doi: 10.3390/ijms160817018

    Figure Lengend Snippet: MiR-198 directly bound to the 3′-UTR of CCND2 mRNA. ( A ) Bioinformatics analyses showed that 10 potential target genes of miR-198 were predicted by three different databases; ( B ) The two distinct predicted binding sites of miR-198 in the 3′-UTR of CCND2 mRNA were allocated, and the fragments containing either mutated binding site were amplified according to the mature miR-198 sequence; ( C ) In pMIR-REPORT™ vector, CCND2 mRNA 3′-UTRfragment containing either the wild type or the mutated Site 1 was fused downstream the reporter gene. When the vectors were cotransfected with miR-198 mimic or mimic control, and the relative luciferase activity, normalised by β-gal, was significantly suppressed in vector with wild type Site 1 than that with mutated Site 1 (32.80% ± 6.89%); ( D ) In the presence of wild type Site 2, not the mutated one, miR-198 was able to significantly inhibit luciferase activity although to a less extent than wild type Site 1 (55.39% ± 8.48%). (NC, negative control; WT, wide-type; MT, mutated-type. * Compared with NC, p < 0.05).

    Article Snippet: The antibodies used were as follows: mouse anti-GAPDH (AG019, Beyotime, China), mouse anti-CCND2 (BA2347-2, BOSTER, Wuhan, China), Horse Radish Peroxidase (HRP)-abeled Goat Anti-Mouse Immunoglobulin G (IgG) (H + L) (A0216, Beyotime, China).

    Techniques: Binding Assay, Amplification, Sequencing, Plasmid Preparation, Luciferase, Activity Assay, Negative Control

    MiR-198 transfection repressed the mRNA and protein expression of CCND2. ( A ) MiR-198 mimic transfection reduced the expression of CCND2 mRNA at 24 h (68.09% ± 16.73%) and 48 h (45.68% ± 10.94%); ( B ) MiR-198 mimic or CCND2 siRNA transfection reduced the expression of CCND2 protein at 24 h (50.55% ± 24.04% or 34.45% ± 6.98%) and 48 h (17.38% ± 9.96% or 16.24% ± 9.23%). (NC, negative control. * Compared with NC, p < 0.05).

    Journal: International Journal of Molecular Sciences

    Article Title: miR-198 Represses the Proliferation of HaCaT Cells by Targeting Cyclin D2

    doi: 10.3390/ijms160817018

    Figure Lengend Snippet: MiR-198 transfection repressed the mRNA and protein expression of CCND2. ( A ) MiR-198 mimic transfection reduced the expression of CCND2 mRNA at 24 h (68.09% ± 16.73%) and 48 h (45.68% ± 10.94%); ( B ) MiR-198 mimic or CCND2 siRNA transfection reduced the expression of CCND2 protein at 24 h (50.55% ± 24.04% or 34.45% ± 6.98%) and 48 h (17.38% ± 9.96% or 16.24% ± 9.23%). (NC, negative control. * Compared with NC, p < 0.05).

    Article Snippet: The antibodies used were as follows: mouse anti-GAPDH (AG019, Beyotime, China), mouse anti-CCND2 (BA2347-2, BOSTER, Wuhan, China), Horse Radish Peroxidase (HRP)-abeled Goat Anti-Mouse Immunoglobulin G (IgG) (H + L) (A0216, Beyotime, China).

    Techniques: Transfection, Expressing, Negative Control

    CCND2 siRNA transfection inhibited HaCaT cell proliferation by blocking cell cycle at G1 phase. ( A ) CCND2 siRNA transfection led to a significant reduction of mRNA expression of CCND2 in HaCaT cells both at 24 h (73.79% ± 11.45%) and 48 h (51.18% ± 8.85%); ( B ) Cell viability analysis showed that CCND2 siRNA transfection inhibited HaCaT cell proliferation at 24 h (67.98% ± 7.31%) and 48 h (67.45% ± 6.70%); ( C ) FCM analysis showed the effect of CCND2 siRNA transfection on cell cycle progression, and G1 phase arrest was obvious at 24 h (55.51% ± 6.18%) and 48 h (70.19% ± 4.10%) compared with negative control (42.98% ± 2.48%). (NC, negative control. * Compared with NC, p < 0.05).

    Journal: International Journal of Molecular Sciences

    Article Title: miR-198 Represses the Proliferation of HaCaT Cells by Targeting Cyclin D2

    doi: 10.3390/ijms160817018

    Figure Lengend Snippet: CCND2 siRNA transfection inhibited HaCaT cell proliferation by blocking cell cycle at G1 phase. ( A ) CCND2 siRNA transfection led to a significant reduction of mRNA expression of CCND2 in HaCaT cells both at 24 h (73.79% ± 11.45%) and 48 h (51.18% ± 8.85%); ( B ) Cell viability analysis showed that CCND2 siRNA transfection inhibited HaCaT cell proliferation at 24 h (67.98% ± 7.31%) and 48 h (67.45% ± 6.70%); ( C ) FCM analysis showed the effect of CCND2 siRNA transfection on cell cycle progression, and G1 phase arrest was obvious at 24 h (55.51% ± 6.18%) and 48 h (70.19% ± 4.10%) compared with negative control (42.98% ± 2.48%). (NC, negative control. * Compared with NC, p < 0.05).

    Article Snippet: The antibodies used were as follows: mouse anti-GAPDH (AG019, Beyotime, China), mouse anti-CCND2 (BA2347-2, BOSTER, Wuhan, China), Horse Radish Peroxidase (HRP)-abeled Goat Anti-Mouse Immunoglobulin G (IgG) (H + L) (A0216, Beyotime, China).

    Techniques: Transfection, Blocking Assay, Expressing, Negative Control