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non target control shrna shntc  (Addgene inc)


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    Addgene inc non target control shrna shntc
    (A) KIF7-CC inhibited AKT phosphorylation at Ser 473 , increased LKB1, LKB1 phosphorylation at Ser 428 and PTEN phosphorylation at Ser 380 /Thr 382/383 by western blot. KIF7-CC over-expression increased both nuclear and cytoplasmic LKB1 expression in PC3, C4-2B and 22Rv1 cells by western blot. As PTEN was slightly expressed in LNCaP-derived C4-2B cells, increasing protein amount and extending exposure are needed for PTEN detection in C4-2B cells. (B) correlation of KIF7 with LKB1 from cBioPortal. Downregulation of LKB1 by shRNAs restored the inhibitory effect of KIF7-CC on AKT phosphorylation at Ser 473 (C) cell proliferation (D) and colony formation (E) in PC3, C4-2B and 22Rv1 cells by western blot, cell number counting as well as colony formation assays, respectively. *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with KIF7-CC <t>shNTC,</t> mean ± SD was presented.
    Non Target Control Shrna Shntc, supplied by Addgene inc, used in various techniques. Bioz Stars score: 96/100, based on 1089 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/non+target+control+shrna+shntc/scramble+shRNA+(Plasmid+%231864)/pmc05589603-195-33-48
    Average 96 stars, based on 1089 article reviews
    non target control shrna shntc - by Bioz Stars, 2026-09
    96/100 stars

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    1) Product Images from "KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition"

    Article Title: KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition

    Journal: Oncotarget

    doi: 10.18632/oncotarget.17421

    (A) KIF7-CC inhibited AKT phosphorylation at Ser 473 , increased LKB1, LKB1 phosphorylation at Ser 428 and PTEN phosphorylation at Ser 380 /Thr 382/383 by western blot. KIF7-CC over-expression increased both nuclear and cytoplasmic LKB1 expression in PC3, C4-2B and 22Rv1 cells by western blot. As PTEN was slightly expressed in LNCaP-derived C4-2B cells, increasing protein amount and extending exposure are needed for PTEN detection in C4-2B cells. (B) correlation of KIF7 with LKB1 from cBioPortal. Downregulation of LKB1 by shRNAs restored the inhibitory effect of KIF7-CC on AKT phosphorylation at Ser 473 (C) cell proliferation (D) and colony formation (E) in PC3, C4-2B and 22Rv1 cells by western blot, cell number counting as well as colony formation assays, respectively. *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with KIF7-CC shNTC, mean ± SD was presented.
    Figure Legend Snippet: (A) KIF7-CC inhibited AKT phosphorylation at Ser 473 , increased LKB1, LKB1 phosphorylation at Ser 428 and PTEN phosphorylation at Ser 380 /Thr 382/383 by western blot. KIF7-CC over-expression increased both nuclear and cytoplasmic LKB1 expression in PC3, C4-2B and 22Rv1 cells by western blot. As PTEN was slightly expressed in LNCaP-derived C4-2B cells, increasing protein amount and extending exposure are needed for PTEN detection in C4-2B cells. (B) correlation of KIF7 with LKB1 from cBioPortal. Downregulation of LKB1 by shRNAs restored the inhibitory effect of KIF7-CC on AKT phosphorylation at Ser 473 (C) cell proliferation (D) and colony formation (E) in PC3, C4-2B and 22Rv1 cells by western blot, cell number counting as well as colony formation assays, respectively. *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with KIF7-CC shNTC, mean ± SD was presented.

    Techniques Used: Phospho-proteomics, Western Blot, Over Expression, Expressing, Derivative Assay

    Stable knockdown of LKB1 by shRNAs and the non-target control (shNTC) in PC3 and 22Rv1 KIF7-CC over-expression cells together with their parental controls were subcutaneously implanted into the nude mice. (A&D) tumor growth was monitored at various time points. (B&E) representative tumor images from PC3 and 22Rv1 cell-derived xenografts were shown. (C&F) bar-char summarizing the tumor weights from different groups; *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with the KIF7-CC shNTC group. Data represent the mean ± SD of different group, there are 6 mice in each group. (G) schematic representation depicting inhibitory effect of KIF7-CC on AKT through LKB1/PTEN signaling.
    Figure Legend Snippet: Stable knockdown of LKB1 by shRNAs and the non-target control (shNTC) in PC3 and 22Rv1 KIF7-CC over-expression cells together with their parental controls were subcutaneously implanted into the nude mice. (A&D) tumor growth was monitored at various time points. (B&E) representative tumor images from PC3 and 22Rv1 cell-derived xenografts were shown. (C&F) bar-char summarizing the tumor weights from different groups; *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with the KIF7-CC shNTC group. Data represent the mean ± SD of different group, there are 6 mice in each group. (G) schematic representation depicting inhibitory effect of KIF7-CC on AKT through LKB1/PTEN signaling.

    Techniques Used: Knockdown, Control, Over Expression, Derivative Assay

    Related Articles

    Knockdown:

    Article Title: KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition
    Article Snippet: GFP-positive cells were selected by fluorescence-activated cell sorting using BD Aria (BD Biosciences). .. LKB1 knockdown in the KIF7-CC over-expression clones from PC3, C4-2B and 22Rv1 cells was performed by infection with lentivirus that expressed human LKB1-specific short hairpin RNAs (shH and shM) (61231 & 61242) or non-target control shRNA (shNTC) (1864), which were packaged with psPAX2 (12260) and pMD2.G (12259) from Addgene (Cambrige, MA; http://www.addgene.org ) using lipofectamine 2000. .. Infected cells were selected by puromycin (2 μg/ml, Sigma).

    Clone Assay:

    Article Title: KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition
    Article Snippet: GFP-positive cells were selected by fluorescence-activated cell sorting using BD Aria (BD Biosciences). .. LKB1 knockdown in the KIF7-CC over-expression clones from PC3, C4-2B and 22Rv1 cells was performed by infection with lentivirus that expressed human LKB1-specific short hairpin RNAs (shH and shM) (61231 & 61242) or non-target control shRNA (shNTC) (1864), which were packaged with psPAX2 (12260) and pMD2.G (12259) from Addgene (Cambrige, MA; http://www.addgene.org ) using lipofectamine 2000. .. Infected cells were selected by puromycin (2 μg/ml, Sigma).

    Infection:

    Article Title: KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition
    Article Snippet: GFP-positive cells were selected by fluorescence-activated cell sorting using BD Aria (BD Biosciences). .. LKB1 knockdown in the KIF7-CC over-expression clones from PC3, C4-2B and 22Rv1 cells was performed by infection with lentivirus that expressed human LKB1-specific short hairpin RNAs (shH and shM) (61231 & 61242) or non-target control shRNA (shNTC) (1864), which were packaged with psPAX2 (12260) and pMD2.G (12259) from Addgene (Cambrige, MA; http://www.addgene.org ) using lipofectamine 2000. .. Infected cells were selected by puromycin (2 μg/ml, Sigma).

    Control:

    Article Title: KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition
    Article Snippet: GFP-positive cells were selected by fluorescence-activated cell sorting using BD Aria (BD Biosciences). .. LKB1 knockdown in the KIF7-CC over-expression clones from PC3, C4-2B and 22Rv1 cells was performed by infection with lentivirus that expressed human LKB1-specific short hairpin RNAs (shH and shM) (61231 & 61242) or non-target control shRNA (shNTC) (1864), which were packaged with psPAX2 (12260) and pMD2.G (12259) from Addgene (Cambrige, MA; http://www.addgene.org ) using lipofectamine 2000. .. Infected cells were selected by puromycin (2 μg/ml, Sigma).

    shRNA:

    Article Title: KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition
    Article Snippet: GFP-positive cells were selected by fluorescence-activated cell sorting using BD Aria (BD Biosciences). .. LKB1 knockdown in the KIF7-CC over-expression clones from PC3, C4-2B and 22Rv1 cells was performed by infection with lentivirus that expressed human LKB1-specific short hairpin RNAs (shH and shM) (61231 & 61242) or non-target control shRNA (shNTC) (1864), which were packaged with psPAX2 (12260) and pMD2.G (12259) from Addgene (Cambrige, MA; http://www.addgene.org ) using lipofectamine 2000. .. Infected cells were selected by puromycin (2 μg/ml, Sigma).



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    Fig. 1 Experimental study design. Fibrosis was induced in mice by carbon tetrachlo- ride (CCl4) for 8 weeks, and mice were treated with PlGF <t>siRNA</t> or non-targeting control (NTC) siRNA four cycles via tail vein injection starting 2 weeks after initiat- ing CCl4 injections.
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    (A) KIF7-CC inhibited AKT phosphorylation at Ser 473 , increased LKB1, LKB1 phosphorylation at Ser 428 and PTEN phosphorylation at Ser 380 /Thr 382/383 by western blot. KIF7-CC over-expression increased both nuclear and cytoplasmic LKB1 expression in PC3, C4-2B and 22Rv1 cells by western blot. As PTEN was slightly expressed in LNCaP-derived C4-2B cells, increasing protein amount and extending exposure are needed for PTEN detection in C4-2B cells. (B) correlation of KIF7 with LKB1 from cBioPortal. Downregulation of LKB1 by shRNAs restored the inhibitory effect of KIF7-CC on AKT phosphorylation at Ser 473 (C) cell proliferation (D) and colony formation (E) in PC3, C4-2B and 22Rv1 cells by western blot, cell number counting as well as colony formation assays, respectively. *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with KIF7-CC <t>shNTC,</t> mean ± SD was presented.
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    Image Search Results


    Fig. 1 Experimental study design. Fibrosis was induced in mice by carbon tetrachlo- ride (CCl4) for 8 weeks, and mice were treated with PlGF siRNA or non-targeting control (NTC) siRNA four cycles via tail vein injection starting 2 weeks after initiat- ing CCl4 injections.

    Journal: Journal of cellular and molecular medicine

    Article Title: Placental growth factor silencing ameliorates liver fibrosis and angiogenesis and inhibits activation of hepatic stellate cells in a murine model of chronic liver disease.

    doi: 10.1111/jcmm.13158

    Figure Lengend Snippet: Fig. 1 Experimental study design. Fibrosis was induced in mice by carbon tetrachlo- ride (CCl4) for 8 weeks, and mice were treated with PlGF siRNA or non-targeting control (NTC) siRNA four cycles via tail vein injection starting 2 weeks after initiat- ing CCl4 injections.

    Article Snippet: Retroviral HIF-1a shRNA (shHIF-1a) and non-targeting control shRNA (shNTC) were purchased from OriGene (Rockville, MD, USA).

    Techniques: Control, Injection

    Fig. 8 PlGF knockdown by siRNA inhibits the proliferation and activation of hepatic stellate cells (HSCs) via the PI3K/Akt signalling pathway. (A) Measurement of cell proliferation of rat HSCs using CCK-8 assay. Cells were transfected with PlGF siRNA or NTC siRNA; cells were treated with rPlGF administration (50 ng/ml) or co-incubation with PI3K inhibitor LY294002 for 5 days. aP < 0.001 compared with mimics control (PBS), bP < 0.001 compared with PlGF+LY294002. (B) The mRNA levels of a-SMA in rat HSCs with stimulation PlGF (50 ng/ml) for 6 or 24 hrs. (C) Rep- resentative Western blot of a-SMA expression in rat HSC treated with rPlGF (50 ng/ml) or PBS for 6–24 hrs and quantification compared to b-actin content. (D) Western blot for PI3K, phospho-Akt (p-Akt), Akt and a-SMA in rat HSCs, and b-tubulin or b-actin as loading controls. Cells were trea- ted with rPlGF administration (50 ng/mL) or co-incubation with PI3K inhibitor LY294002 for 8 hrs. (E) The Western blot results of part (D) were quantified by densitometry.

    Journal: Journal of cellular and molecular medicine

    Article Title: Placental growth factor silencing ameliorates liver fibrosis and angiogenesis and inhibits activation of hepatic stellate cells in a murine model of chronic liver disease.

    doi: 10.1111/jcmm.13158

    Figure Lengend Snippet: Fig. 8 PlGF knockdown by siRNA inhibits the proliferation and activation of hepatic stellate cells (HSCs) via the PI3K/Akt signalling pathway. (A) Measurement of cell proliferation of rat HSCs using CCK-8 assay. Cells were transfected with PlGF siRNA or NTC siRNA; cells were treated with rPlGF administration (50 ng/ml) or co-incubation with PI3K inhibitor LY294002 for 5 days. aP < 0.001 compared with mimics control (PBS), bP < 0.001 compared with PlGF+LY294002. (B) The mRNA levels of a-SMA in rat HSCs with stimulation PlGF (50 ng/ml) for 6 or 24 hrs. (C) Rep- resentative Western blot of a-SMA expression in rat HSC treated with rPlGF (50 ng/ml) or PBS for 6–24 hrs and quantification compared to b-actin content. (D) Western blot for PI3K, phospho-Akt (p-Akt), Akt and a-SMA in rat HSCs, and b-tubulin or b-actin as loading controls. Cells were trea- ted with rPlGF administration (50 ng/mL) or co-incubation with PI3K inhibitor LY294002 for 8 hrs. (E) The Western blot results of part (D) were quantified by densitometry.

    Article Snippet: Retroviral HIF-1a shRNA (shHIF-1a) and non-targeting control shRNA (shNTC) were purchased from OriGene (Rockville, MD, USA).

    Techniques: Knockdown, Activation Assay, CCK-8 Assay, Transfection, Incubation, Control, Western Blot, Expressing

    (A) KIF7-CC inhibited AKT phosphorylation at Ser 473 , increased LKB1, LKB1 phosphorylation at Ser 428 and PTEN phosphorylation at Ser 380 /Thr 382/383 by western blot. KIF7-CC over-expression increased both nuclear and cytoplasmic LKB1 expression in PC3, C4-2B and 22Rv1 cells by western blot. As PTEN was slightly expressed in LNCaP-derived C4-2B cells, increasing protein amount and extending exposure are needed for PTEN detection in C4-2B cells. (B) correlation of KIF7 with LKB1 from cBioPortal. Downregulation of LKB1 by shRNAs restored the inhibitory effect of KIF7-CC on AKT phosphorylation at Ser 473 (C) cell proliferation (D) and colony formation (E) in PC3, C4-2B and 22Rv1 cells by western blot, cell number counting as well as colony formation assays, respectively. *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with KIF7-CC shNTC, mean ± SD was presented.

    Journal: Oncotarget

    Article Title: KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition

    doi: 10.18632/oncotarget.17421

    Figure Lengend Snippet: (A) KIF7-CC inhibited AKT phosphorylation at Ser 473 , increased LKB1, LKB1 phosphorylation at Ser 428 and PTEN phosphorylation at Ser 380 /Thr 382/383 by western blot. KIF7-CC over-expression increased both nuclear and cytoplasmic LKB1 expression in PC3, C4-2B and 22Rv1 cells by western blot. As PTEN was slightly expressed in LNCaP-derived C4-2B cells, increasing protein amount and extending exposure are needed for PTEN detection in C4-2B cells. (B) correlation of KIF7 with LKB1 from cBioPortal. Downregulation of LKB1 by shRNAs restored the inhibitory effect of KIF7-CC on AKT phosphorylation at Ser 473 (C) cell proliferation (D) and colony formation (E) in PC3, C4-2B and 22Rv1 cells by western blot, cell number counting as well as colony formation assays, respectively. *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with KIF7-CC shNTC, mean ± SD was presented.

    Article Snippet: LKB1 knockdown in the KIF7-CC over-expression clones from PC3, C4-2B and 22Rv1 cells was performed by infection with lentivirus that expressed human LKB1-specific short hairpin RNAs (shH and shM) (61231 & 61242) or non-target control shRNA (shNTC) (1864), which were packaged with psPAX2 (12260) and pMD2.G (12259) from Addgene (Cambrige, MA; http://www.addgene.org ) using lipofectamine 2000.

    Techniques: Phospho-proteomics, Western Blot, Over Expression, Expressing, Derivative Assay

    Stable knockdown of LKB1 by shRNAs and the non-target control (shNTC) in PC3 and 22Rv1 KIF7-CC over-expression cells together with their parental controls were subcutaneously implanted into the nude mice. (A&D) tumor growth was monitored at various time points. (B&E) representative tumor images from PC3 and 22Rv1 cell-derived xenografts were shown. (C&F) bar-char summarizing the tumor weights from different groups; *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with the KIF7-CC shNTC group. Data represent the mean ± SD of different group, there are 6 mice in each group. (G) schematic representation depicting inhibitory effect of KIF7-CC on AKT through LKB1/PTEN signaling.

    Journal: Oncotarget

    Article Title: KIF7 attenuates prostate tumor growth through LKB1-mediated AKT inhibition

    doi: 10.18632/oncotarget.17421

    Figure Lengend Snippet: Stable knockdown of LKB1 by shRNAs and the non-target control (shNTC) in PC3 and 22Rv1 KIF7-CC over-expression cells together with their parental controls were subcutaneously implanted into the nude mice. (A&D) tumor growth was monitored at various time points. (B&E) representative tumor images from PC3 and 22Rv1 cell-derived xenografts were shown. (C&F) bar-char summarizing the tumor weights from different groups; *, p < 0.05; **, p < 0.01; ***, p < 0.001, compared with the KIF7-CC shNTC group. Data represent the mean ± SD of different group, there are 6 mice in each group. (G) schematic representation depicting inhibitory effect of KIF7-CC on AKT through LKB1/PTEN signaling.

    Article Snippet: LKB1 knockdown in the KIF7-CC over-expression clones from PC3, C4-2B and 22Rv1 cells was performed by infection with lentivirus that expressed human LKB1-specific short hairpin RNAs (shH and shM) (61231 & 61242) or non-target control shRNA (shNTC) (1864), which were packaged with psPAX2 (12260) and pMD2.G (12259) from Addgene (Cambrige, MA; http://www.addgene.org ) using lipofectamine 2000.

    Techniques: Knockdown, Control, Over Expression, Derivative Assay