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non targeting control shrna shctrl  (Addgene inc)


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    Structured Review

    Addgene inc non targeting control shrna shctrl
    Non Targeting Control Shrna Shctrl, supplied by Addgene inc, used in various techniques. Bioz Stars score: 96/100, based on 1415 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/control+shctrl/shRNA+(Plasmid+%2355783)/pmc12518352-130-13-24
    Average 96 stars, based on 1415 article reviews
    non targeting control shrna shctrl - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    shRNA:

    Article Title: Single-cell chromatin accessibility landscape of cardiac non-myocytes identifies tissue repair program during heart regeneration.
    Article Snippet: .. Complementary shRNA oligonucleotides targeting the Cebpd transcript were annealed and directionally cloned into the pLKO.1-blast (26655, Addgene) vector. .. For lentivirus production, HEK293T cells at 80% confluence were cultured in 10 cm dishes and transfected at approximately 90% confluency using LipofectamineTM 2000 (11668019, Thermo Fisher) with a plasmid mixture containing 16 μg lentiviral vector, 4 μg envelope plasmid (pMD2.G, 12259, Addgene), and 12.5 μg packaging plasmid (psPAX2, 12260, Addgene).

    Article Title: Cellular reprogramming to reverse aging and promote organ and tissue regeneration
    Article Snippet: .. Addgene AAV plasmids encoding shRNA sequences were used. .. Control shRNA comprised the sequence 5′-GTTCAGATGTGCGGCGAGT-3′ (plasmid #85741 from Addgene). mTET1 (Tet1 shRNA) comprised the sequence 5′-GCTCATGGAGACTAGGTTTGG-3′ (plasmid #85742 from Addgene). mTet2 (Tet2 shRNA) comprised the sequence 5′-GGATGTAAGTTTGCCAGAAGC-3′ (Plasmid #85743 from Addgene).

    Article Title: CASC19 stabilization by ALYREF via m5C modification and its impact on SCD in colorectal cancer cell aggressiveness and stemness.
    Article Snippet: 2.4Lentiviral shRNA production and infection ALYREF-targeting shRNA sequences (shRNA-1: 5′- GGAAACTGCTGGTGTCCAATC-3′; shRNA-2: 5′-GAATTCAAAGCAGCAGCTTTC-3′) were cloned into the pLKO.1 vector (GenePharma). .. HEK293T cells (ATCC) were co-transfected with shRNA plasmids and packaging plasmids (psPAX2/pMD2.G, Addgene) using Lipofectamine 3000 (Invitrogen, Cat. No. L3000015). .. Viral supernatants harvested 48 h post-transfection were filtered (0.45 μm) and used to infect CRC cells with 8 μg/mL polybrene (Sigma, Cat. No. TR-1003-G).

    Article Title: ZXDB Drives Macrophage Inflammatory Programming in Sepsis‐Induced Acute Kidney Injury by Recruiting EIF4A3 to Enhance ACACA Translation
    Article Snippet: .. Short hairpin RNA (shRNA) against mouse Zxdb, human ZXDB, human EIF4A3, or non‐targeting control shRNA was inserted into pLKO.1 lentiviral vector (8453; Addgene plasmid). .. Lentiviral particles were generated in HEK293T cells by using psPAX2 (12260; Addgene plasmid) and pMD2.G (12259; Addgene plasmid) as packaging plasmids.

    Article Title: ASCL1 promotes nuclear shrinkage in transdifferentiation by suppressing NUP37
    Article Snippet: .. We purchased the following plasmids from Addgene: pLKO.1/ p53 shRNA (#19119), pLKO.1/scrambled shRNA (#1864), pMD2.G (#12259), psPAX2 (#12260), pTight-9-124-Bclx (miR9/9 ∗ -124, #60857), pRL-SV40P (#27163), and pGL3 enhancer vector (#212938). .. The BAC clone containing the NUP37 genomic DNA was purchased from BACPAC resources (RP11-282A19).

    Article Title: NCBP2 drives colorectal cancer growth and metastasis through LIPG-mediated lipid droplet accumulation.
    Article Snippet: .. The shRNA plasmid was constructed using the pLKO.1-TRC vector (#10878, Addgene plasmid, China). ..

    Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models
    Article Snippet: .. Briefly, 8 g shRNA plasmid, 4 g psPAX2 plasmid (Addgene, #12260), and 2 g pMD2.G plasmid (Addgene, #12259) were transfected into 293T cells in 100-mm dishes using Lipofectamine 2000 (Invitrogen, #13778150). ..

    Clone Assay:

    Article Title: Single-cell chromatin accessibility landscape of cardiac non-myocytes identifies tissue repair program during heart regeneration.
    Article Snippet: .. Complementary shRNA oligonucleotides targeting the Cebpd transcript were annealed and directionally cloned into the pLKO.1-blast (26655, Addgene) vector. .. For lentivirus production, HEK293T cells at 80% confluence were cultured in 10 cm dishes and transfected at approximately 90% confluency using LipofectamineTM 2000 (11668019, Thermo Fisher) with a plasmid mixture containing 16 μg lentiviral vector, 4 μg envelope plasmid (pMD2.G, 12259, Addgene), and 12.5 μg packaging plasmid (psPAX2, 12260, Addgene).

    Bioprocessing:

    Article Title: Cellular reprogramming to reverse aging and promote organ and tissue regeneration
    Article Snippet: .. Addgene AAV plasmids encoding shRNA sequences were used. .. Control shRNA comprised the sequence 5′-GTTCAGATGTGCGGCGAGT-3′ (plasmid #85741 from Addgene). mTET1 (Tet1 shRNA) comprised the sequence 5′-GCTCATGGAGACTAGGTTTGG-3′ (plasmid #85742 from Addgene). mTet2 (Tet2 shRNA) comprised the sequence 5′-GGATGTAAGTTTGCCAGAAGC-3′ (Plasmid #85743 from Addgene).

    other:

    Article Title: DCPS modulates TDP-43-linked neurodegeneration through P-body-mediated RNA decay
    Article Snippet: Please refer to Table S5 for more details N/A ARTR-seq adapter-RT primer(5 ′ -AGACGTGTG CTCTTCCGATCTNNNNNNNNNN-3 ′ ) Xiao et al. 60 N/A ARTR-seq 3 ′ cDNA adapter (5 ′ Phos-8N-AGAT CGGAAGAGGTCGTGT-3 ′ SpC3) Xiao et al. 60 N/A Recombinant DNA Plasmid: pMDLg/pRRE Dull et al. 81 RRID: Addgene_12251 Plasmid: pRSV-Rev Dull et al. 81 RRID: Addgene_12253 Plasmid: pMD2.G A gift from Didier Trono RRID: Addgene_12259 Plasmid: pLG1-control sgRNA Tian et al. 41 N/A Plasmid: pLG1-TDP-43 sgRNA This paper N/A Plasmid: pLG1-DCPS sgRNA 1 This paper N/A Plasmid: pLG1-DCPS sgRNA 2 This paper N/A Plasmid: pLKO.1-control shRNA A gift from David Root 82 RRID: Addgene_10879 Plasmid: pLKO.1-TDP-43 shRNA This paper N/A Plasmid: pLKO.1-DCPS shRNA #1 This paper N/A Plasmid: pLKO.1-DCPS shRNA #2 This paper N/A Plasmid: Lenti-GFP-puro Zhang et al. 45 N/A Plasmid: Lenti-FLAG-TDP-43 dNLS This paper N/A Plasmid: Lenti- FLAG-TDP-43 WT -APEX2 This paper N/A Plasmid: Lenti- FLAG-TDP-43 dNLS -APEX2 This paper N/A Plasmid: pEGFP-N1-TDP-43 Cheng et al. 83 N/A Plasmid: pcDNA3.1-FLAG-TDP-43 dNLS This paper N/A Plasmid: pT7-EGFP-C1-HsDCP2 Tritschler et al. 84 RRID: Addgene_25031 (Continued on next page) e4 Neuron 114, 1–16.e1–e12, June 3, 2026

    Control:

    Article Title: ZXDB Drives Macrophage Inflammatory Programming in Sepsis‐Induced Acute Kidney Injury by Recruiting EIF4A3 to Enhance ACACA Translation
    Article Snippet: .. Short hairpin RNA (shRNA) against mouse Zxdb, human ZXDB, human EIF4A3, or non‐targeting control shRNA was inserted into pLKO.1 lentiviral vector (8453; Addgene plasmid). .. Lentiviral particles were generated in HEK293T cells by using psPAX2 (12260; Addgene plasmid) and pMD2.G (12259; Addgene plasmid) as packaging plasmids.

    Plasmid Preparation:

    Article Title: ZXDB Drives Macrophage Inflammatory Programming in Sepsis‐Induced Acute Kidney Injury by Recruiting EIF4A3 to Enhance ACACA Translation
    Article Snippet: .. Short hairpin RNA (shRNA) against mouse Zxdb, human ZXDB, human EIF4A3, or non‐targeting control shRNA was inserted into pLKO.1 lentiviral vector (8453; Addgene plasmid). .. Lentiviral particles were generated in HEK293T cells by using psPAX2 (12260; Addgene plasmid) and pMD2.G (12259; Addgene plasmid) as packaging plasmids.

    Article Title: ASCL1 promotes nuclear shrinkage in transdifferentiation by suppressing NUP37
    Article Snippet: .. We purchased the following plasmids from Addgene: pLKO.1/ p53 shRNA (#19119), pLKO.1/scrambled shRNA (#1864), pMD2.G (#12259), psPAX2 (#12260), pTight-9-124-Bclx (miR9/9 ∗ -124, #60857), pRL-SV40P (#27163), and pGL3 enhancer vector (#212938). .. The BAC clone containing the NUP37 genomic DNA was purchased from BACPAC resources (RP11-282A19).

    Article Title: NCBP2 drives colorectal cancer growth and metastasis through LIPG-mediated lipid droplet accumulation.
    Article Snippet: .. The shRNA plasmid was constructed using the pLKO.1-TRC vector (#10878, Addgene plasmid, China). ..

    Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models
    Article Snippet: .. Briefly, 8 g shRNA plasmid, 4 g psPAX2 plasmid (Addgene, #12260), and 2 g pMD2.G plasmid (Addgene, #12259) were transfected into 293T cells in 100-mm dishes using Lipofectamine 2000 (Invitrogen, #13778150). ..

    Construct:

    Article Title: NCBP2 drives colorectal cancer growth and metastasis through LIPG-mediated lipid droplet accumulation.
    Article Snippet: .. The shRNA plasmid was constructed using the pLKO.1-TRC vector (#10878, Addgene plasmid, China). ..

    Transfection:

    Article Title: Symbiotic exclusivity between CLOCK and TFPI2 drives stemness and immunosuppression in glioblastoma models
    Article Snippet: .. Briefly, 8 g shRNA plasmid, 4 g psPAX2 plasmid (Addgene, #12260), and 2 g pMD2.G plasmid (Addgene, #12259) were transfected into 293T cells in 100-mm dishes using Lipofectamine 2000 (Invitrogen, #13778150). ..



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    Image Search Results


    ASNS enhanced H 2 O 2 ‐induced retinal cell proliferation and attenuated senescence. ARPE‐19 cells were transfected with shASNS or ASNS‐OE. (A) The mRNA expression of ASNS was detected by RT‐qPCR. (B) The protein expression of ASNS was detected by WB. ARPE‐19 cells were divided into H 2 O 2 + shCtrl, H 2 O 2 + shASNS or H 2 O 2 + NC, H 2 O 2 + ASNS‐OE groups. (C) CCK8 assay was utilized to assess cell viability in H 2 O 2 ‐treated ARPE‐19 cells. (D) SA‐β‐gal staining experiments were conducted in the above groups. (E) Measurement of intracellular ROS in the above groups. (F) The protein expression of P53, P21, P16 was detected by WB. (G) The level of GSH and MDA detected by ELISA. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Biofactors (Oxford, England)

    Article Title: ASNS Regulates H 2 O 2 ‐Induced Senescence, Oxidative Stress, and Glucose Metabolism in ARPE ‐19 Cells by Modulating USP13 Expression

    doi: 10.1002/biof.70057

    Figure Lengend Snippet: ASNS enhanced H 2 O 2 ‐induced retinal cell proliferation and attenuated senescence. ARPE‐19 cells were transfected with shASNS or ASNS‐OE. (A) The mRNA expression of ASNS was detected by RT‐qPCR. (B) The protein expression of ASNS was detected by WB. ARPE‐19 cells were divided into H 2 O 2 + shCtrl, H 2 O 2 + shASNS or H 2 O 2 + NC, H 2 O 2 + ASNS‐OE groups. (C) CCK8 assay was utilized to assess cell viability in H 2 O 2 ‐treated ARPE‐19 cells. (D) SA‐β‐gal staining experiments were conducted in the above groups. (E) Measurement of intracellular ROS in the above groups. (F) The protein expression of P53, P21, P16 was detected by WB. (G) The level of GSH and MDA detected by ELISA. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Lentiviral vectors interfering with ASNS and USP13 expression (shASNS and shUSP13) and the negative control shCtrl were synthesized by GeneChem (Shanghai, China).

    Techniques: Transfection, Expressing, Quantitative RT-PCR, CCK-8 Assay, Staining, Enzyme-linked Immunosorbent Assay

    ASNS regulated glucose metabolism pathways in H 2 O 2 ‐induced retinal cells. ARPE‐19 cells were divided into H 2 O 2 + shCtrl, H 2 O 2 + shASNS or H 2 O 2 + NC, H 2 O 2 + ASNS‐OE groups. (A) Detection of glucose uptake using a kit in H 2 O 2 ‐treated ARPE‐19 cells. (B) Detection of lactate production using a kit in H 2 O 2 ‐treated ARPE‐19 cells. (C) Measuring ECAR in H 2 O 2 ‐treated ARPE‐19 cells using the XF‐96 extracellular flux analyzer. (D) Measuring OCR in H 2 O 2 ‐treated ARPE‐19 cells using the XF‐96 extracellular flux analyzer. (E) The mRNA expression of Glut1, Glut4, HK2, and PGK1was detected by RT‐qPCR. (F) The protein expression of Glut1, Glut4, HK2, and PGK1was detected by WB. (G) The protein expression of HIF‐1α was detected by WB. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Biofactors (Oxford, England)

    Article Title: ASNS Regulates H 2 O 2 ‐Induced Senescence, Oxidative Stress, and Glucose Metabolism in ARPE ‐19 Cells by Modulating USP13 Expression

    doi: 10.1002/biof.70057

    Figure Lengend Snippet: ASNS regulated glucose metabolism pathways in H 2 O 2 ‐induced retinal cells. ARPE‐19 cells were divided into H 2 O 2 + shCtrl, H 2 O 2 + shASNS or H 2 O 2 + NC, H 2 O 2 + ASNS‐OE groups. (A) Detection of glucose uptake using a kit in H 2 O 2 ‐treated ARPE‐19 cells. (B) Detection of lactate production using a kit in H 2 O 2 ‐treated ARPE‐19 cells. (C) Measuring ECAR in H 2 O 2 ‐treated ARPE‐19 cells using the XF‐96 extracellular flux analyzer. (D) Measuring OCR in H 2 O 2 ‐treated ARPE‐19 cells using the XF‐96 extracellular flux analyzer. (E) The mRNA expression of Glut1, Glut4, HK2, and PGK1was detected by RT‐qPCR. (F) The protein expression of Glut1, Glut4, HK2, and PGK1was detected by WB. (G) The protein expression of HIF‐1α was detected by WB. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Lentiviral vectors interfering with ASNS and USP13 expression (shASNS and shUSP13) and the negative control shCtrl were synthesized by GeneChem (Shanghai, China).

    Techniques: Expressing, Quantitative RT-PCR

    Validation of ASNS's impact on the AMD disease process in vivo. Sprague–Dawley rats injected with sodium iodate (30 mg/kg body weight) and divided into MOCK group (No lentivirus injections, n = 10), shCtrl group (Injection of shCtrl lentivirus, n = 10), and shASNS (Injection of shASNS lentivirus, n = 10) group. (A) H&E staining analysis of rat retinal tissues in each group. (B) SA‐β‐gal staining of rat retinal tissues were conducted in the above groups. (C) Measuring ECAR and OCR in retinal tissues using the XF‐96 extracellular flux analyzer. (D) The mRNA expression of Glut1, Glut4, HK2, and PGK1 in retinal tissues was detected by RT‐qPCR. (E) The protein expression of Glut1, Glut4, HK2, and PGK1 in retinal tissues was detected by WB. (F) The protein expression of ASNS and USP13 in retinal tissues was detected by WB. (G) IF was used to analyze the expression of ASNS and USP1 in retinal tissues. (H) The protein expression of HIF‐1α in retinal tissues was detected by WB. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Biofactors (Oxford, England)

    Article Title: ASNS Regulates H 2 O 2 ‐Induced Senescence, Oxidative Stress, and Glucose Metabolism in ARPE ‐19 Cells by Modulating USP13 Expression

    doi: 10.1002/biof.70057

    Figure Lengend Snippet: Validation of ASNS's impact on the AMD disease process in vivo. Sprague–Dawley rats injected with sodium iodate (30 mg/kg body weight) and divided into MOCK group (No lentivirus injections, n = 10), shCtrl group (Injection of shCtrl lentivirus, n = 10), and shASNS (Injection of shASNS lentivirus, n = 10) group. (A) H&E staining analysis of rat retinal tissues in each group. (B) SA‐β‐gal staining of rat retinal tissues were conducted in the above groups. (C) Measuring ECAR and OCR in retinal tissues using the XF‐96 extracellular flux analyzer. (D) The mRNA expression of Glut1, Glut4, HK2, and PGK1 in retinal tissues was detected by RT‐qPCR. (E) The protein expression of Glut1, Glut4, HK2, and PGK1 in retinal tissues was detected by WB. (F) The protein expression of ASNS and USP13 in retinal tissues was detected by WB. (G) IF was used to analyze the expression of ASNS and USP1 in retinal tissues. (H) The protein expression of HIF‐1α in retinal tissues was detected by WB. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Lentiviral vectors interfering with ASNS and USP13 expression (shASNS and shUSP13) and the negative control shCtrl were synthesized by GeneChem (Shanghai, China).

    Techniques: Biomarker Discovery, In Vivo, Injection, Staining, Expressing, Quantitative RT-PCR

    Validation of USP13's impact on the AMD disease process in vivo. Sprague–Dawley rats injected with sodium iodate (30 mg/kg body weigh) and divided into MOCK group (No lentivirus injections, n = 10), shCtrl group (Injection of shCtrl lentivirus, n = 10), and shUSP13 (Injection of shUSP13 lentivirus, n = 10) group. (A) H&E staining analysis of rat retinal tissues in each group. (B) SA‐β‐gal staining of rat retinal tissues were conducted in the above groups. (C) Measuring ECAR and OCR in retinal tissues using the XF‐96 extracellular flux analyzer. (D) The mRNA expression of Glut1, Glut4, HK2, and PGK1 in retinal tissues was detected by RT‐qPCR. (E) The protein expression of Glut1, Glut4, HK2, and PGK1 in retinal tissues was detected by WB. (F) The protein expression of USP13 in retinal tissues was detected by WB. (G) The protein expression of HIF‐1α in retinal tissues was detected by WB. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Biofactors (Oxford, England)

    Article Title: ASNS Regulates H 2 O 2 ‐Induced Senescence, Oxidative Stress, and Glucose Metabolism in ARPE ‐19 Cells by Modulating USP13 Expression

    doi: 10.1002/biof.70057

    Figure Lengend Snippet: Validation of USP13's impact on the AMD disease process in vivo. Sprague–Dawley rats injected with sodium iodate (30 mg/kg body weigh) and divided into MOCK group (No lentivirus injections, n = 10), shCtrl group (Injection of shCtrl lentivirus, n = 10), and shUSP13 (Injection of shUSP13 lentivirus, n = 10) group. (A) H&E staining analysis of rat retinal tissues in each group. (B) SA‐β‐gal staining of rat retinal tissues were conducted in the above groups. (C) Measuring ECAR and OCR in retinal tissues using the XF‐96 extracellular flux analyzer. (D) The mRNA expression of Glut1, Glut4, HK2, and PGK1 in retinal tissues was detected by RT‐qPCR. (E) The protein expression of Glut1, Glut4, HK2, and PGK1 in retinal tissues was detected by WB. (F) The protein expression of USP13 in retinal tissues was detected by WB. (G) The protein expression of HIF‐1α in retinal tissues was detected by WB. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Lentiviral vectors interfering with ASNS and USP13 expression (shASNS and shUSP13) and the negative control shCtrl were synthesized by GeneChem (Shanghai, China).

    Techniques: Biomarker Discovery, In Vivo, Injection, Staining, Expressing, Quantitative RT-PCR

    Exploration of potential downstream mechanism and upstream regulators of CCDC137. A Heatmap shows DEGs identified by RNA sequencing in T24-shCtrl and T24-shCCDC137-1 cells. B Bar plot displays GO and KEGG functional enrichment results of downregulated DEGs from RNA sequencing. C GSVA-Hallmark pathway enrichment analysis displayed differences between CCDC137 positive (CCDC137 +) and CCDC137 negative (CCDC137 −) cells based on single-cell sequencing data. D mRNA and protein expression of stearoyl-CoA desaturase (SCD) were detected by qRT-PCR and Western blot. E DecoupleR was used to analyze differences in transcription factor activity between CCDC137 + and CCDC137 − epithelial cells in single-cell sequencing data. F TF-Target Finder was employed to identify potential upstream transcription factors of CCDC137. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, no statistical significance

    Journal: Journal of Translational Medicine

    Article Title: CCDC137 knockdown suppresses bladder cancer progression by downregulating SCD

    doi: 10.1186/s12967-025-07033-w

    Figure Lengend Snippet: Exploration of potential downstream mechanism and upstream regulators of CCDC137. A Heatmap shows DEGs identified by RNA sequencing in T24-shCtrl and T24-shCCDC137-1 cells. B Bar plot displays GO and KEGG functional enrichment results of downregulated DEGs from RNA sequencing. C GSVA-Hallmark pathway enrichment analysis displayed differences between CCDC137 positive (CCDC137 +) and CCDC137 negative (CCDC137 −) cells based on single-cell sequencing data. D mRNA and protein expression of stearoyl-CoA desaturase (SCD) were detected by qRT-PCR and Western blot. E DecoupleR was used to analyze differences in transcription factor activity between CCDC137 + and CCDC137 − epithelial cells in single-cell sequencing data. F TF-Target Finder was employed to identify potential upstream transcription factors of CCDC137. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, no statistical significance

    Article Snippet: The shCCDC137 lentiviral particles and corresponding control lentiviral particles (shCtrl) were purchased from Genechem Co., Ltd (Shanghai, China).

    Techniques: RNA Sequencing, Functional Assay, Sequencing, Expressing, Quantitative RT-PCR, Western Blot, Activity Assay

    In vivo validation of CCDC137 regulating tumor growth. A Subcutaneous xenograft models were established in nude mice to validate the regulatory role of CCDC137 in tumor growth. B Tumor volume growth curves were plotted over 28 days after tumor cell inoculation. C Tumor weights of T24-shCtrl and T24-shCCDC137-1 groups were measured on day 28. D The Graphical Abstract described the key results in this study. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, no statistical significance

    Journal: Journal of Translational Medicine

    Article Title: CCDC137 knockdown suppresses bladder cancer progression by downregulating SCD

    doi: 10.1186/s12967-025-07033-w

    Figure Lengend Snippet: In vivo validation of CCDC137 regulating tumor growth. A Subcutaneous xenograft models were established in nude mice to validate the regulatory role of CCDC137 in tumor growth. B Tumor volume growth curves were plotted over 28 days after tumor cell inoculation. C Tumor weights of T24-shCtrl and T24-shCCDC137-1 groups were measured on day 28. D The Graphical Abstract described the key results in this study. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001; ns, no statistical significance

    Article Snippet: The shCCDC137 lentiviral particles and corresponding control lentiviral particles (shCtrl) were purchased from Genechem Co., Ltd (Shanghai, China).

    Techniques: In Vivo, Biomarker Discovery