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control empty vectors nc  (Genechem)

 
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    Genechem control empty vectors nc
    Overexpression of SNHG1 or HDAC6 partially reverses the pro-angiogenic effect of EPC-EVs on MAECs. MAECs were transfected with SNHG1 overexpression <t>vectors</t> (oe-SNHG1), HDAC6 overexpression vectors (oe-HDAC6), or <t>empty</t> vectors (oe-NC, <t>control)</t> in HG (30 mM) medium. A : Transfection efficiency of oe-SNHG1 and oe-HDAC6 was verified by qRT-PCR (n = 3). Cells were then co-treated with EPC-EVs-miR in HG medium. B : SNHG1 and HDAC6 expression was detected by qRT-PCR (n = 3). C : Expression of HDAC6, CD31, and VEGFA was measured by Western blot (n = 3). D : Cell viability was assessed by CCK-8 assay (n = 3). E : Angiogenic capacity was evaluated by tube formation assay (n = 3). F : Cell migration was measured by scratch wound healing assay (n = 3). Data are presented as mean ± standard deviation. Data in panel A were analyze using student’s t-test. Data in panels B , D , E , and F were analyzed using one-way ANOVA. Data in panel C were analyzed using two-way ANOVA, followed by Tukey’s multiple comparisons test. * p < 0.05 and ** p < 0.01
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    Images

    1) Product Images from "Endothelial progenitor cell derived extracellular vesicles promotes wound healing in diabetic mice via activating mobilization and neovascularization"

    Article Title: Endothelial progenitor cell derived extracellular vesicles promotes wound healing in diabetic mice via activating mobilization and neovascularization

    Journal: Cell Biology and Toxicology

    doi: 10.1007/s10565-025-10134-3

    Overexpression of SNHG1 or HDAC6 partially reverses the pro-angiogenic effect of EPC-EVs on MAECs. MAECs were transfected with SNHG1 overexpression vectors (oe-SNHG1), HDAC6 overexpression vectors (oe-HDAC6), or empty vectors (oe-NC, control) in HG (30 mM) medium. A : Transfection efficiency of oe-SNHG1 and oe-HDAC6 was verified by qRT-PCR (n = 3). Cells were then co-treated with EPC-EVs-miR in HG medium. B : SNHG1 and HDAC6 expression was detected by qRT-PCR (n = 3). C : Expression of HDAC6, CD31, and VEGFA was measured by Western blot (n = 3). D : Cell viability was assessed by CCK-8 assay (n = 3). E : Angiogenic capacity was evaluated by tube formation assay (n = 3). F : Cell migration was measured by scratch wound healing assay (n = 3). Data are presented as mean ± standard deviation. Data in panel A were analyze using student’s t-test. Data in panels B , D , E , and F were analyzed using one-way ANOVA. Data in panel C were analyzed using two-way ANOVA, followed by Tukey’s multiple comparisons test. * p < 0.05 and ** p < 0.01
    Figure Legend Snippet: Overexpression of SNHG1 or HDAC6 partially reverses the pro-angiogenic effect of EPC-EVs on MAECs. MAECs were transfected with SNHG1 overexpression vectors (oe-SNHG1), HDAC6 overexpression vectors (oe-HDAC6), or empty vectors (oe-NC, control) in HG (30 mM) medium. A : Transfection efficiency of oe-SNHG1 and oe-HDAC6 was verified by qRT-PCR (n = 3). Cells were then co-treated with EPC-EVs-miR in HG medium. B : SNHG1 and HDAC6 expression was detected by qRT-PCR (n = 3). C : Expression of HDAC6, CD31, and VEGFA was measured by Western blot (n = 3). D : Cell viability was assessed by CCK-8 assay (n = 3). E : Angiogenic capacity was evaluated by tube formation assay (n = 3). F : Cell migration was measured by scratch wound healing assay (n = 3). Data are presented as mean ± standard deviation. Data in panel A were analyze using student’s t-test. Data in panels B , D , E , and F were analyzed using one-way ANOVA. Data in panel C were analyzed using two-way ANOVA, followed by Tukey’s multiple comparisons test. * p < 0.05 and ** p < 0.01

    Techniques Used: Over Expression, Transfection, Control, Quantitative RT-PCR, Expressing, Western Blot, CCK-8 Assay, Tube Formation Assay, Migration, Wound Healing Assay, Standard Deviation

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    Article Title: The Role of NF-κB/MIR155HG in Regulating the Stemness and Radioresistance in Breast Cancer Stem Cells
    Article Snippet: The pcDNA3.1-RelA (RelA) and control empty vector plasmids (vector) were acquired from GeneChem (Shanghai, China).

    Article Title: Macrophage-Derived GSDMD Plays an Essential Role in Atherosclerosis and Cross Talk Between Macrophages via the Mitochondria-STING-IRF3/NF-κB Axis
    Article Snippet: Eightweek-old male ApoE−/− mice were microinjected with either the macrophage-specific control shRNA-AAV9 (AAV-F4/80-empty vector) or GSDMD shRNA (short hairpin RNA)-AAV9 (AAVF4/80-shGSDMD [shRNA-GSDMD]; 2E+11 vg; Genechem Co, Ltd, Shanghai, China) through tail vein.

    Article Title: System-wide identification of novel de-ubiquitination targets for USP10 in gastric cancer metastasis through multi-omics screening
    Article Snippet: When the cells reached to 70–80% confluence, GV492-USP10 (GV492 was the empty vector), psPAX2, and pMD2.G (mole ratio 1: 1:1) (Genechem, China) were transfected into cells with lipofectamineTM 2000 (11,668,019, invitrogen, Thermo Fisher Scientific, Carlsbad, CA, USA) according to the manufacturer’s instructions.

    Article Title: Sulfiredoxin 1 ameliorates doxorubicin-induced cardiotoxicity by suppressing oxidative stress and inflammation via the Sirt1/NLRP3 pathway.
    Article Snippet: Background: Doxorubicin (DOX) is limited in clinical use due to its cardiotoxic side effects.. Oxidative stress and inflammation are pivotal mechanisms underlying doxorubicin-induced cardiotoxicity (DIC).. Sulfiredoxin 1 (Srxn1) plays a central role in antioxidant effects.

    Article Title: Role of Nuclear Receptor Subfamily 1 Group D Member 1 in the Proliferation, Migration of Vascular Smooth Muscle Cell, and Vascular Intimal Hyperplasia
    Article Snippet: Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) cause neointimal hyperplasia after percutaneous vascular interventions.. Nuclear receptor subfamily 1 group D member 1 (NR1D1), a crucial member of circadian clock, is involved in the regulation of atherosclerosis and cellular proliferation.. However, whether NR1D1 affects vascular neointimal hyperplasia remains unclear.

    Transfection:

    Article Title: Creatine Promotes Endometriosis by Inducing Ferroptosis Resistance via Suppression of PrP.
    Article Snippet: .. Cells were then transfected with PRNP-overexpressing lentiviruses (LVPRNP) or negative control lentiviruses (GV492 empty vector) (both from Genechem, Shanghai, China) with an optimal multiplicity of infection (MOI) determined to be 10. .. The supernatant was replaced with a complete culture medium after 12 h. The transfection efficiency can be observed under a fluorescence microscope (Olympus Corporation) after 48 h. The transfection efficiency of PRNP was evaluated by qRT-PCR and western blotting after 72 h. The stably transfected HESCs that overexpress PRNP were selected using 10 mg L−1 puromycin. siRNA Transfection: Negative control, PRNP-724, PRNP-597, PRNP476, and PRNP-2407 siRNA oligos were specifically designed and procured from GenePharma Company (Shanghai, China).

    Negative Control:

    Article Title: Creatine Promotes Endometriosis by Inducing Ferroptosis Resistance via Suppression of PrP.
    Article Snippet: .. Cells were then transfected with PRNP-overexpressing lentiviruses (LVPRNP) or negative control lentiviruses (GV492 empty vector) (both from Genechem, Shanghai, China) with an optimal multiplicity of infection (MOI) determined to be 10. .. The supernatant was replaced with a complete culture medium after 12 h. The transfection efficiency can be observed under a fluorescence microscope (Olympus Corporation) after 48 h. The transfection efficiency of PRNP was evaluated by qRT-PCR and western blotting after 72 h. The stably transfected HESCs that overexpress PRNP were selected using 10 mg L−1 puromycin. siRNA Transfection: Negative control, PRNP-724, PRNP-597, PRNP476, and PRNP-2407 siRNA oligos were specifically designed and procured from GenePharma Company (Shanghai, China).

    Article Title: <em>Lycii Radicis Cortex</em> suppresses the growth of non-small cell lung cancer via enhancing the anti-tumor immunity
    Article Snippet: .. A549 cells were lentivirally (Shanghai Genechem Co., Ltd., China) transduced to stably express human programmed cell death ligand 1 (PD-L1) (hereafter named A549-PD-L1-OE cells), and an empty lentiviral vector was used as a negative control (resulting in A549-NC cells). .. The efficiency of PD-L1 overexpression was assessed by Western blot following puromycin (Beyotime, ST551) selection.

    Infection:

    Article Title: Creatine Promotes Endometriosis by Inducing Ferroptosis Resistance via Suppression of PrP.
    Article Snippet: .. Cells were then transfected with PRNP-overexpressing lentiviruses (LVPRNP) or negative control lentiviruses (GV492 empty vector) (both from Genechem, Shanghai, China) with an optimal multiplicity of infection (MOI) determined to be 10. .. The supernatant was replaced with a complete culture medium after 12 h. The transfection efficiency can be observed under a fluorescence microscope (Olympus Corporation) after 48 h. The transfection efficiency of PRNP was evaluated by qRT-PCR and western blotting after 72 h. The stably transfected HESCs that overexpress PRNP were selected using 10 mg L−1 puromycin. siRNA Transfection: Negative control, PRNP-724, PRNP-597, PRNP476, and PRNP-2407 siRNA oligos were specifically designed and procured from GenePharma Company (Shanghai, China).

    Plasmid Preparation:

    Article Title: MitoQ upregulates CYP19A1 to protect dermal papilla cells from DHT-induced mitochondrial dysfunction and apoptosis in androgenetic alopecia.
    Article Snippet: Androgenetic alopecia (AGA) is a progressive hair loss disorder characterized by follicular miniaturization primarily driven by dihydrotestosterone (DHT).. Mitochondrial dysfunction in dermal papilla cells (DPCs) has emerged as a key pathological feature, yet the upstream regulatory mechanisms remain unclear.. Our previous work revealed that the mitochondria-targeted antioxidant MitoQ upregulates CYP19A1 (aromatase) and alleviates AGA-like pathology.

    Over Expression:

    Article Title: MitoQ upregulates CYP19A1 to protect dermal papilla cells from DHT-induced mitochondrial dysfunction and apoptosis in androgenetic alopecia.
    Article Snippet: Androgenetic alopecia (AGA) is a progressive hair loss disorder characterized by follicular miniaturization primarily driven by dihydrotestosterone (DHT).. Mitochondrial dysfunction in dermal papilla cells (DPCs) has emerged as a key pathological feature, yet the upstream regulatory mechanisms remain unclear.. Our previous work revealed that the mitochondria-targeted antioxidant MitoQ upregulates CYP19A1 (aromatase) and alleviates AGA-like pathology.

    Control:

    Article Title: MitoQ upregulates CYP19A1 to protect dermal papilla cells from DHT-induced mitochondrial dysfunction and apoptosis in androgenetic alopecia.
    Article Snippet: Androgenetic alopecia (AGA) is a progressive hair loss disorder characterized by follicular miniaturization primarily driven by dihydrotestosterone (DHT).. Mitochondrial dysfunction in dermal papilla cells (DPCs) has emerged as a key pathological feature, yet the upstream regulatory mechanisms remain unclear.. Our previous work revealed that the mitochondria-targeted antioxidant MitoQ upregulates CYP19A1 (aromatase) and alleviates AGA-like pathology.

    shRNA:

    Article Title: MitoQ upregulates CYP19A1 to protect dermal papilla cells from DHT-induced mitochondrial dysfunction and apoptosis in androgenetic alopecia.
    Article Snippet: Androgenetic alopecia (AGA) is a progressive hair loss disorder characterized by follicular miniaturization primarily driven by dihydrotestosterone (DHT).. Mitochondrial dysfunction in dermal papilla cells (DPCs) has emerged as a key pathological feature, yet the upstream regulatory mechanisms remain unclear.. Our previous work revealed that the mitochondria-targeted antioxidant MitoQ upregulates CYP19A1 (aromatase) and alleviates AGA-like pathology.

    Stable Transfection:

    Article Title: <em>Lycii Radicis Cortex</em> suppresses the growth of non-small cell lung cancer via enhancing the anti-tumor immunity
    Article Snippet: .. A549 cells were lentivirally (Shanghai Genechem Co., Ltd., China) transduced to stably express human programmed cell death ligand 1 (PD-L1) (hereafter named A549-PD-L1-OE cells), and an empty lentiviral vector was used as a negative control (resulting in A549-NC cells). .. The efficiency of PD-L1 overexpression was assessed by Western blot following puromycin (Beyotime, ST551) selection.



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    a, HCT116 cells stably expressing BRIP1 R162Q were transiently transfected using PEI with empty vector (EV-EGFP) or RNaseH1-WT-eGFP. Transfection efficiency was assessed via EGFP fluorescence. b, immunoblot analysis confirming expression of GFP-tagged constructs in transfected cells. c, Immunofluorescence detection of R-loops using the S9.6 antibody in cells transfected with EGFP or EGFP-RNaseH1. d, Quantification of S9.6 mean fluorescence intensity (MFI) per nucleus. Data represent mean ± SEM of three independent experiments. e, Immunofluorescence detection of G-quadruplex (G4) structures using the BG4 antibody in cells transfected with EGFP or EGFP-RNaseH1. f, Quantification of BG4 fluorescence intensity per nucleus. Data represent mean ± SEM of three independent experiments. g, Representative DNA fiber assay images from HCT116 cells harboring BRIP1 R162Q transfected with empty vector (EV-eGFP) or RNaseH1-WT. DNA replication tracts were sequentially labeled with CldU (red) and IdU (green). h, Quantification of DNA fiber types. RNaseH1-WT expression reduced the proportion of stalled replication forks in cells harboring BRIP1 R162Q. i, While the overall fork speed was not significantly increased upon RNaseH1-WT expression, tracts displayed a more balanced distribution of CldU and IdU incorporation. j, Fork asymmetry analysis. RNaseH1-WT expression reduced fork asymmetry, indicating that left- and right-moving sister forks progressed at more similar speeds. Labeled tracks were visualized by confocal microscopy, and tract lengths were measured on raw LSM images. Lengths (µm) were converted to replication speed (kb/min) using a factor of 2.59 kb/µm. All data represent mean ± SEM from three independent experiments. At least 150 fibers per condition were analyzed in each replicate. Statistical significance was determined using paired two-tailed Student’s t-test (*p < 0.05, **p < 0.01, ***p < 0.001, ns = not significant). c, e, Representative confocal images are shown.

    Journal: bioRxiv

    Article Title: Role of a childhood cancer-linked BRIP1/FANCJ germline variant in genomic instability and cancer cell vulnerability

    doi: 10.64898/2026.03.24.714005

    Figure Lengend Snippet: a, HCT116 cells stably expressing BRIP1 R162Q were transiently transfected using PEI with empty vector (EV-EGFP) or RNaseH1-WT-eGFP. Transfection efficiency was assessed via EGFP fluorescence. b, immunoblot analysis confirming expression of GFP-tagged constructs in transfected cells. c, Immunofluorescence detection of R-loops using the S9.6 antibody in cells transfected with EGFP or EGFP-RNaseH1. d, Quantification of S9.6 mean fluorescence intensity (MFI) per nucleus. Data represent mean ± SEM of three independent experiments. e, Immunofluorescence detection of G-quadruplex (G4) structures using the BG4 antibody in cells transfected with EGFP or EGFP-RNaseH1. f, Quantification of BG4 fluorescence intensity per nucleus. Data represent mean ± SEM of three independent experiments. g, Representative DNA fiber assay images from HCT116 cells harboring BRIP1 R162Q transfected with empty vector (EV-eGFP) or RNaseH1-WT. DNA replication tracts were sequentially labeled with CldU (red) and IdU (green). h, Quantification of DNA fiber types. RNaseH1-WT expression reduced the proportion of stalled replication forks in cells harboring BRIP1 R162Q. i, While the overall fork speed was not significantly increased upon RNaseH1-WT expression, tracts displayed a more balanced distribution of CldU and IdU incorporation. j, Fork asymmetry analysis. RNaseH1-WT expression reduced fork asymmetry, indicating that left- and right-moving sister forks progressed at more similar speeds. Labeled tracks were visualized by confocal microscopy, and tract lengths were measured on raw LSM images. Lengths (µm) were converted to replication speed (kb/min) using a factor of 2.59 kb/µm. All data represent mean ± SEM from three independent experiments. At least 150 fibers per condition were analyzed in each replicate. Statistical significance was determined using paired two-tailed Student’s t-test (*p < 0.05, **p < 0.01, ***p < 0.001, ns = not significant). c, e, Representative confocal images are shown.

    Article Snippet: For R-loop removal, cells were transiently transfected with an EGFP empty vector control (pEGFP-C1, Takara Bio, #632470), EGFP-tagged RNaseH1 wild-type (WT), or the catalytically inactive RNaseH1 D145N mutant as indicated.

    Techniques: Stable Transfection, Expressing, Transfection, Plasmid Preparation, Fluorescence, Western Blot, Construct, Immunofluorescence, Labeling, Confocal Microscopy, Two Tailed Test

    Overexpression of SNHG1 or HDAC6 partially reverses the pro-angiogenic effect of EPC-EVs on MAECs. MAECs were transfected with SNHG1 overexpression vectors (oe-SNHG1), HDAC6 overexpression vectors (oe-HDAC6), or empty vectors (oe-NC, control) in HG (30 mM) medium. A : Transfection efficiency of oe-SNHG1 and oe-HDAC6 was verified by qRT-PCR (n = 3). Cells were then co-treated with EPC-EVs-miR in HG medium. B : SNHG1 and HDAC6 expression was detected by qRT-PCR (n = 3). C : Expression of HDAC6, CD31, and VEGFA was measured by Western blot (n = 3). D : Cell viability was assessed by CCK-8 assay (n = 3). E : Angiogenic capacity was evaluated by tube formation assay (n = 3). F : Cell migration was measured by scratch wound healing assay (n = 3). Data are presented as mean ± standard deviation. Data in panel A were analyze using student’s t-test. Data in panels B , D , E , and F were analyzed using one-way ANOVA. Data in panel C were analyzed using two-way ANOVA, followed by Tukey’s multiple comparisons test. * p < 0.05 and ** p < 0.01

    Journal: Cell Biology and Toxicology

    Article Title: Endothelial progenitor cell derived extracellular vesicles promotes wound healing in diabetic mice via activating mobilization and neovascularization

    doi: 10.1007/s10565-025-10134-3

    Figure Lengend Snippet: Overexpression of SNHG1 or HDAC6 partially reverses the pro-angiogenic effect of EPC-EVs on MAECs. MAECs were transfected with SNHG1 overexpression vectors (oe-SNHG1), HDAC6 overexpression vectors (oe-HDAC6), or empty vectors (oe-NC, control) in HG (30 mM) medium. A : Transfection efficiency of oe-SNHG1 and oe-HDAC6 was verified by qRT-PCR (n = 3). Cells were then co-treated with EPC-EVs-miR in HG medium. B : SNHG1 and HDAC6 expression was detected by qRT-PCR (n = 3). C : Expression of HDAC6, CD31, and VEGFA was measured by Western blot (n = 3). D : Cell viability was assessed by CCK-8 assay (n = 3). E : Angiogenic capacity was evaluated by tube formation assay (n = 3). F : Cell migration was measured by scratch wound healing assay (n = 3). Data are presented as mean ± standard deviation. Data in panel A were analyze using student’s t-test. Data in panels B , D , E , and F were analyzed using one-way ANOVA. Data in panel C were analyzed using two-way ANOVA, followed by Tukey’s multiple comparisons test. * p < 0.05 and ** p < 0.01

    Article Snippet: For lentiviral infection, GFP-labeled miR-204-5p lentiviral overexpression vectors, SNHG1 lentiviral overexpression vectors, or control empty vectors (NC) (Genechem, Shanghai, China) were applied to transfection with 293 T cells (CRL-1573; ATCC, Manassas, VA, USA).

    Techniques: Over Expression, Transfection, Control, Quantitative RT-PCR, Expressing, Western Blot, CCK-8 Assay, Tube Formation Assay, Migration, Wound Healing Assay, Standard Deviation