Review



csl small interference  (Santa Cruz Biotechnology)


Bioz Verified Symbol Santa Cruz Biotechnology is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 90
      Buy from Supplier

    Structured Review

    Santa Cruz Biotechnology csl small interference
    (A) Representative results <t>of</t> <t>CSL-siRNA</t> inhibition on leptin upregulation of protein levels of Notch 1-3, activated NICD1 and Notch targeted genes, CSL, survivin and Hey2 in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for (B) CSL; (C) Notch1; (D) NICD1; (E) Notch 2; (F) Notch 3; (G) Hey2 and (H) survivin. Cells cotransfected with siRNA oligonucleotides (CSL-siRNA or control-siRNA) were treated with leptin (0 and 1.2 nM) for 24 h. (a) P<0.05 when comparing protein levels to cells treated with control-siRNA (basal) or CSL-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.
    Csl Small Interference, supplied by Santa Cruz Biotechnology, 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/product/csl+small+interference/pmc03121792-129-10-20?v=Santa+Cruz+Biotechnology
    Average 90 stars, based on 1 article reviews
    csl small interference - by Bioz Stars, 2026-07
    90/100 stars

    Images

    1) Product Images from "Notch, IL-1 and Leptin Crosstalk Outcome (NILCO) Is Critical for Leptin-Induced Proliferation, Migration and VEGF/VEGFR-2 Expression in Breast Cancer"

    Article Title: Notch, IL-1 and Leptin Crosstalk Outcome (NILCO) Is Critical for Leptin-Induced Proliferation, Migration and VEGF/VEGFR-2 Expression in Breast Cancer

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0021467

    (A) Representative results of CSL-siRNA inhibition on leptin upregulation of protein levels of Notch 1-3, activated NICD1 and Notch targeted genes, CSL, survivin and Hey2 in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for (B) CSL; (C) Notch1; (D) NICD1; (E) Notch 2; (F) Notch 3; (G) Hey2 and (H) survivin. Cells cotransfected with siRNA oligonucleotides (CSL-siRNA or control-siRNA) were treated with leptin (0 and 1.2 nM) for 24 h. (a) P<0.05 when comparing protein levels to cells treated with control-siRNA (basal) or CSL-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.
    Figure Legend Snippet: (A) Representative results of CSL-siRNA inhibition on leptin upregulation of protein levels of Notch 1-3, activated NICD1 and Notch targeted genes, CSL, survivin and Hey2 in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for (B) CSL; (C) Notch1; (D) NICD1; (E) Notch 2; (F) Notch 3; (G) Hey2 and (H) survivin. Cells cotransfected with siRNA oligonucleotides (CSL-siRNA or control-siRNA) were treated with leptin (0 and 1.2 nM) for 24 h. (a) P<0.05 when comparing protein levels to cells treated with control-siRNA (basal) or CSL-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Techniques Used: Inhibition, Western Blot, Software, Derivative Assay

    Leptin transcriptional activation of CBF (or CSL) promoter is linked to several leptin-induced signaling pathways. (A) 4T1 cells were transiently transfected with a CBF-Luc reporter construct and incubated with leptin (0 and 1.2 nM) alone or plus siRNA oligonucleotides (SignalSilence control-siRNA and STAT3, MEK1, AKT1, mTOR, JNK, p38-siRNA). (B) Protein levels of kinases after siRNA treatment were determined by WB analysis using β-actin as loading control. (C) 4T1 cells transfected with CBF-Luc reporter were incubated with leptin alone or plus pharmacological inhibitors of JAK2/STAT3 (AG490, 30 µM), MEK/MAPK/ERK1/2 (PD98059, 30 µΜ), PI-3K/AKT1 (Wortmannin, 50 nM), PKC-Ca dependant (Gö6976, 30 µΜ), p38 kinase (SB203580, 2 µΜ), JNK (SP600125, 30 µM) and mTOR (Rapamycin, 20 nM) signaling pathways for 24 h. Luciferase activity was determined as described (see M &M) and expressed as a percent of basal or leptin-treated cells. (a) P<0.05 when comparing levels of luciferase activity to control (basal) or leptin-treated cells. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.
    Figure Legend Snippet: Leptin transcriptional activation of CBF (or CSL) promoter is linked to several leptin-induced signaling pathways. (A) 4T1 cells were transiently transfected with a CBF-Luc reporter construct and incubated with leptin (0 and 1.2 nM) alone or plus siRNA oligonucleotides (SignalSilence control-siRNA and STAT3, MEK1, AKT1, mTOR, JNK, p38-siRNA). (B) Protein levels of kinases after siRNA treatment were determined by WB analysis using β-actin as loading control. (C) 4T1 cells transfected with CBF-Luc reporter were incubated with leptin alone or plus pharmacological inhibitors of JAK2/STAT3 (AG490, 30 µM), MEK/MAPK/ERK1/2 (PD98059, 30 µΜ), PI-3K/AKT1 (Wortmannin, 50 nM), PKC-Ca dependant (Gö6976, 30 µΜ), p38 kinase (SB203580, 2 µΜ), JNK (SP600125, 30 µM) and mTOR (Rapamycin, 20 nM) signaling pathways for 24 h. Luciferase activity was determined as described (see M &M) and expressed as a percent of basal or leptin-treated cells. (a) P<0.05 when comparing levels of luciferase activity to control (basal) or leptin-treated cells. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Techniques Used: Activation Assay, Transfection, Construct, Incubation, Luciferase, Activity Assay, Derivative Assay

    A) Representative results from immunocytochemistry (ICC, hematoxylin staining) of leptin and DAPT effects on migration of 4T1 cells as compared to basal conditions. B) Quantitative assessment of cell migration under the effects of leptin and DAPT. C) Representative results from ICC after addition of control-siRNA (Ctr-siRNA), CLS-siRNA and leptin. D) Quantitative assessment of cell migration under the effects of leptin, CSL-siRNA and Crt-siRNA. E) Effects of leptin and DAPT on 4T1 cell proliferation. F) Effects of leptin, Ctr-siRNA and CSL-siRNA on 4T1 cell proliferation. Results from cell migration (Boyden chamber cell migration assay) and proliferation (MTT cell proliferation assay) were obtained after 24 h and normalized to basal conditions (see Material and Methods). Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.
    Figure Legend Snippet: A) Representative results from immunocytochemistry (ICC, hematoxylin staining) of leptin and DAPT effects on migration of 4T1 cells as compared to basal conditions. B) Quantitative assessment of cell migration under the effects of leptin and DAPT. C) Representative results from ICC after addition of control-siRNA (Ctr-siRNA), CLS-siRNA and leptin. D) Quantitative assessment of cell migration under the effects of leptin, CSL-siRNA and Crt-siRNA. E) Effects of leptin and DAPT on 4T1 cell proliferation. F) Effects of leptin, Ctr-siRNA and CSL-siRNA on 4T1 cell proliferation. Results from cell migration (Boyden chamber cell migration assay) and proliferation (MTT cell proliferation assay) were obtained after 24 h and normalized to basal conditions (see Material and Methods). Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Techniques Used: Immunocytochemistry, Staining, Migration, Cell Migration Assay, MTT Cell Proliferation, Derivative Assay

    (A) DAPT inhibition of γ-secretase abrogated leptin transcriptional induction of VEGF (A); VEGFR-2 (B) and IL-1α mRNA (C) as determined by real-time RT-PCR and normalized to the GAPDH expression. CSL-siRNA also inhibited leptin-induced effects on protein levels of VEGF (D); VEGFR-2 (E) and IL-1α (F) mRNA. Representative results of DAPT (G) and CSL-siRNA (M) inhibition of leptin upregulation of protein levels of VEGF, VEGFR-2, IL-1α, ERα and OB-R in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for VEGF (H and N); VEGFR-2 (I and O); IL-1α (J and P); ERα (K and Q) and OB-R (L and R) in cells treated with leptin (0 and 1.2 nM) and DAPT for 24 h or cotransfected with CSL-siRNA and control (Ctr)-SiRNA, respectively. (a) P<0.05 when comparing levels of antigens to basal conditions and control-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.
    Figure Legend Snippet: (A) DAPT inhibition of γ-secretase abrogated leptin transcriptional induction of VEGF (A); VEGFR-2 (B) and IL-1α mRNA (C) as determined by real-time RT-PCR and normalized to the GAPDH expression. CSL-siRNA also inhibited leptin-induced effects on protein levels of VEGF (D); VEGFR-2 (E) and IL-1α (F) mRNA. Representative results of DAPT (G) and CSL-siRNA (M) inhibition of leptin upregulation of protein levels of VEGF, VEGFR-2, IL-1α, ERα and OB-R in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for VEGF (H and N); VEGFR-2 (I and O); IL-1α (J and P); ERα (K and Q) and OB-R (L and R) in cells treated with leptin (0 and 1.2 nM) and DAPT for 24 h or cotransfected with CSL-siRNA and control (Ctr)-SiRNA, respectively. (a) P<0.05 when comparing levels of antigens to basal conditions and control-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Techniques Used: Inhibition, Quantitative RT-PCR, Expressing, Western Blot, Software, Derivative Assay



    Similar Products

    csl small interference  (Santa Cruz Biotechnology)
    90
    Santa Cruz Biotechnology csl small interference
    (A) Representative results <t>of</t> <t>CSL-siRNA</t> inhibition on leptin upregulation of protein levels of Notch 1-3, activated NICD1 and Notch targeted genes, CSL, survivin and Hey2 in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for (B) CSL; (C) Notch1; (D) NICD1; (E) Notch 2; (F) Notch 3; (G) Hey2 and (H) survivin. Cells cotransfected with siRNA oligonucleotides (CSL-siRNA or control-siRNA) were treated with leptin (0 and 1.2 nM) for 24 h. (a) P<0.05 when comparing protein levels to cells treated with control-siRNA (basal) or CSL-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.
    Csl Small Interference, supplied by Santa Cruz Biotechnology, 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/product/csl+small+interference/pmc03121792-129-10-20?v=Santa+Cruz+Biotechnology
    Average 90 stars, based on 1 article reviews
    csl small interference - by Bioz Stars, 2026-07
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    (A) Representative results of CSL-siRNA inhibition on leptin upregulation of protein levels of Notch 1-3, activated NICD1 and Notch targeted genes, CSL, survivin and Hey2 in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for (B) CSL; (C) Notch1; (D) NICD1; (E) Notch 2; (F) Notch 3; (G) Hey2 and (H) survivin. Cells cotransfected with siRNA oligonucleotides (CSL-siRNA or control-siRNA) were treated with leptin (0 and 1.2 nM) for 24 h. (a) P<0.05 when comparing protein levels to cells treated with control-siRNA (basal) or CSL-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Journal: PLoS ONE

    Article Title: Notch, IL-1 and Leptin Crosstalk Outcome (NILCO) Is Critical for Leptin-Induced Proliferation, Migration and VEGF/VEGFR-2 Expression in Breast Cancer

    doi: 10.1371/journal.pone.0021467

    Figure Lengend Snippet: (A) Representative results of CSL-siRNA inhibition on leptin upregulation of protein levels of Notch 1-3, activated NICD1 and Notch targeted genes, CSL, survivin and Hey2 in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for (B) CSL; (C) Notch1; (D) NICD1; (E) Notch 2; (F) Notch 3; (G) Hey2 and (H) survivin. Cells cotransfected with siRNA oligonucleotides (CSL-siRNA or control-siRNA) were treated with leptin (0 and 1.2 nM) for 24 h. (a) P<0.05 when comparing protein levels to cells treated with control-siRNA (basal) or CSL-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Article Snippet: Polyclonal anti-Notch4, anti-OB-R-NH2 antibodies, monoclonal anti-IL-1R tI, nonspecific goat IgG2b, CSL small interference (si)RNA and control siRNA-A were obtained from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA).

    Techniques: Inhibition, Western Blot, Software, Derivative Assay

    Leptin transcriptional activation of CBF (or CSL) promoter is linked to several leptin-induced signaling pathways. (A) 4T1 cells were transiently transfected with a CBF-Luc reporter construct and incubated with leptin (0 and 1.2 nM) alone or plus siRNA oligonucleotides (SignalSilence control-siRNA and STAT3, MEK1, AKT1, mTOR, JNK, p38-siRNA). (B) Protein levels of kinases after siRNA treatment were determined by WB analysis using β-actin as loading control. (C) 4T1 cells transfected with CBF-Luc reporter were incubated with leptin alone or plus pharmacological inhibitors of JAK2/STAT3 (AG490, 30 µM), MEK/MAPK/ERK1/2 (PD98059, 30 µΜ), PI-3K/AKT1 (Wortmannin, 50 nM), PKC-Ca dependant (Gö6976, 30 µΜ), p38 kinase (SB203580, 2 µΜ), JNK (SP600125, 30 µM) and mTOR (Rapamycin, 20 nM) signaling pathways for 24 h. Luciferase activity was determined as described (see M &M) and expressed as a percent of basal or leptin-treated cells. (a) P<0.05 when comparing levels of luciferase activity to control (basal) or leptin-treated cells. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Journal: PLoS ONE

    Article Title: Notch, IL-1 and Leptin Crosstalk Outcome (NILCO) Is Critical for Leptin-Induced Proliferation, Migration and VEGF/VEGFR-2 Expression in Breast Cancer

    doi: 10.1371/journal.pone.0021467

    Figure Lengend Snippet: Leptin transcriptional activation of CBF (or CSL) promoter is linked to several leptin-induced signaling pathways. (A) 4T1 cells were transiently transfected with a CBF-Luc reporter construct and incubated with leptin (0 and 1.2 nM) alone or plus siRNA oligonucleotides (SignalSilence control-siRNA and STAT3, MEK1, AKT1, mTOR, JNK, p38-siRNA). (B) Protein levels of kinases after siRNA treatment were determined by WB analysis using β-actin as loading control. (C) 4T1 cells transfected with CBF-Luc reporter were incubated with leptin alone or plus pharmacological inhibitors of JAK2/STAT3 (AG490, 30 µM), MEK/MAPK/ERK1/2 (PD98059, 30 µΜ), PI-3K/AKT1 (Wortmannin, 50 nM), PKC-Ca dependant (Gö6976, 30 µΜ), p38 kinase (SB203580, 2 µΜ), JNK (SP600125, 30 µM) and mTOR (Rapamycin, 20 nM) signaling pathways for 24 h. Luciferase activity was determined as described (see M &M) and expressed as a percent of basal or leptin-treated cells. (a) P<0.05 when comparing levels of luciferase activity to control (basal) or leptin-treated cells. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Article Snippet: Polyclonal anti-Notch4, anti-OB-R-NH2 antibodies, monoclonal anti-IL-1R tI, nonspecific goat IgG2b, CSL small interference (si)RNA and control siRNA-A were obtained from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA).

    Techniques: Activation Assay, Transfection, Construct, Incubation, Luciferase, Activity Assay, Derivative Assay

    A) Representative results from immunocytochemistry (ICC, hematoxylin staining) of leptin and DAPT effects on migration of 4T1 cells as compared to basal conditions. B) Quantitative assessment of cell migration under the effects of leptin and DAPT. C) Representative results from ICC after addition of control-siRNA (Ctr-siRNA), CLS-siRNA and leptin. D) Quantitative assessment of cell migration under the effects of leptin, CSL-siRNA and Crt-siRNA. E) Effects of leptin and DAPT on 4T1 cell proliferation. F) Effects of leptin, Ctr-siRNA and CSL-siRNA on 4T1 cell proliferation. Results from cell migration (Boyden chamber cell migration assay) and proliferation (MTT cell proliferation assay) were obtained after 24 h and normalized to basal conditions (see Material and Methods). Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Journal: PLoS ONE

    Article Title: Notch, IL-1 and Leptin Crosstalk Outcome (NILCO) Is Critical for Leptin-Induced Proliferation, Migration and VEGF/VEGFR-2 Expression in Breast Cancer

    doi: 10.1371/journal.pone.0021467

    Figure Lengend Snippet: A) Representative results from immunocytochemistry (ICC, hematoxylin staining) of leptin and DAPT effects on migration of 4T1 cells as compared to basal conditions. B) Quantitative assessment of cell migration under the effects of leptin and DAPT. C) Representative results from ICC after addition of control-siRNA (Ctr-siRNA), CLS-siRNA and leptin. D) Quantitative assessment of cell migration under the effects of leptin, CSL-siRNA and Crt-siRNA. E) Effects of leptin and DAPT on 4T1 cell proliferation. F) Effects of leptin, Ctr-siRNA and CSL-siRNA on 4T1 cell proliferation. Results from cell migration (Boyden chamber cell migration assay) and proliferation (MTT cell proliferation assay) were obtained after 24 h and normalized to basal conditions (see Material and Methods). Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Article Snippet: Polyclonal anti-Notch4, anti-OB-R-NH2 antibodies, monoclonal anti-IL-1R tI, nonspecific goat IgG2b, CSL small interference (si)RNA and control siRNA-A were obtained from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA).

    Techniques: Immunocytochemistry, Staining, Migration, Cell Migration Assay, MTT Cell Proliferation, Derivative Assay

    (A) DAPT inhibition of γ-secretase abrogated leptin transcriptional induction of VEGF (A); VEGFR-2 (B) and IL-1α mRNA (C) as determined by real-time RT-PCR and normalized to the GAPDH expression. CSL-siRNA also inhibited leptin-induced effects on protein levels of VEGF (D); VEGFR-2 (E) and IL-1α (F) mRNA. Representative results of DAPT (G) and CSL-siRNA (M) inhibition of leptin upregulation of protein levels of VEGF, VEGFR-2, IL-1α, ERα and OB-R in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for VEGF (H and N); VEGFR-2 (I and O); IL-1α (J and P); ERα (K and Q) and OB-R (L and R) in cells treated with leptin (0 and 1.2 nM) and DAPT for 24 h or cotransfected with CSL-siRNA and control (Ctr)-SiRNA, respectively. (a) P<0.05 when comparing levels of antigens to basal conditions and control-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Journal: PLoS ONE

    Article Title: Notch, IL-1 and Leptin Crosstalk Outcome (NILCO) Is Critical for Leptin-Induced Proliferation, Migration and VEGF/VEGFR-2 Expression in Breast Cancer

    doi: 10.1371/journal.pone.0021467

    Figure Lengend Snippet: (A) DAPT inhibition of γ-secretase abrogated leptin transcriptional induction of VEGF (A); VEGFR-2 (B) and IL-1α mRNA (C) as determined by real-time RT-PCR and normalized to the GAPDH expression. CSL-siRNA also inhibited leptin-induced effects on protein levels of VEGF (D); VEGFR-2 (E) and IL-1α (F) mRNA. Representative results of DAPT (G) and CSL-siRNA (M) inhibition of leptin upregulation of protein levels of VEGF, VEGFR-2, IL-1α, ERα and OB-R in 4T1 cells as determined by western blot (WB). The WB results were normalized to β-actin as loading control and densitometric analysis of bands was carried-out with the imageJ software for VEGF (H and N); VEGFR-2 (I and O); IL-1α (J and P); ERα (K and Q) and OB-R (L and R) in cells treated with leptin (0 and 1.2 nM) and DAPT for 24 h or cotransfected with CSL-siRNA and control (Ctr)-SiRNA, respectively. (a) P<0.05 when comparing levels of antigens to basal conditions and control-siRNA. Data (mean ± standard error) representative results derived from a minimum of 3 independent experiments.

    Article Snippet: Polyclonal anti-Notch4, anti-OB-R-NH2 antibodies, monoclonal anti-IL-1R tI, nonspecific goat IgG2b, CSL small interference (si)RNA and control siRNA-A were obtained from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA).

    Techniques: Inhibition, Quantitative RT-PCR, Expressing, Western Blot, Software, Derivative Assay