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Santa Cruz Biotechnology cdk2 shrna m lentiviral particles

A. Spontaneous colony formation in AMPKα1-KO MEFs. Wild type (WT), AMPKα1-KO, and AMPKα2-KO MEFs (1 × 10 5 cells/mL) were seeded and cultured on 6-well plates. Culture medium was changed every 2 days for 3 weeks. (Upper) Representative images showing colony formation of MEFs. (Bottom) Quantification of colony formation. n =5, * P <0.001 versus WT. B. Anchorage-independent cell growth assay (soft agar assay) of MEFs. (Upper) Representative images for colony formation. Scale bar =500 μm. (Bottom) Quantification of colony formation. n =10, * P <0.001 versus WT. C. Phosphorylated <t>CDK2</t> at The-160 (pCDK2-T160) and CDK2 are upregulated in AMPKα1-KO MEFs. pCDK2-T160 and <t>CDK2</t> <t>protein</t> in WT, AMPKα1-KO, and AMPKα2-KO MEFs were analyzed by Western blot (top). Quantification of pCDK2 and CDK2 data (bottom). n =4, * P <0.01 versus WT; † P <0.05 versus WT. D. Diminished anchorage-independent growth of AMPKα1-KO MEFs following CDK2 knockdown by <t>shRNA.</t> Representative images are shown. Scale bar =500 μm. E. Representative Western blot data indicate CDK2 knockdown by shRNA (top). Quantification of anchorage-independent MEF growth (bottom). n =4, * P <0.01 versus WT/control shRNA; † P <0.01 versus α1-KO/control shRNA.

Cdk2 Shrna M Lentiviral Particles, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "AMPKα1 deletion in fibroblasts promotes tumorigenesis in athymic nude mice by p52-mediated elevation of erythropoietin and CDK2"

Article Title: AMPKα1 deletion in fibroblasts promotes tumorigenesis in athymic nude mice by p52-mediated elevation of erythropoietin and CDK2

Journal: Oncotarget

doi: 10.18632/oncotarget.10687

Figure Legend Snippet: A. Spontaneous colony formation in AMPKα1-KO MEFs. Wild type (WT), AMPKα1-KO, and AMPKα2-KO MEFs (1 × 10 5 cells/mL) were seeded and cultured on 6-well plates. Culture medium was changed every 2 days for 3 weeks. (Upper) Representative images showing colony formation of MEFs. (Bottom) Quantification of colony formation. n =5, * P <0.001 versus WT. B. Anchorage-independent cell growth assay (soft agar assay) of MEFs. (Upper) Representative images for colony formation. Scale bar =500 μm. (Bottom) Quantification of colony formation. n =10, * P <0.001 versus WT. C. Phosphorylated CDK2 at The-160 (pCDK2-T160) and CDK2 are upregulated in AMPKα1-KO MEFs. pCDK2-T160 and CDK2 protein in WT, AMPKα1-KO, and AMPKα2-KO MEFs were analyzed by Western blot (top). Quantification of pCDK2 and CDK2 data (bottom). n =4, * P <0.01 versus WT; † P <0.05 versus WT. D. Diminished anchorage-independent growth of AMPKα1-KO MEFs following CDK2 knockdown by shRNA. Representative images are shown. Scale bar =500 μm. E. Representative Western blot data indicate CDK2 knockdown by shRNA (top). Quantification of anchorage-independent MEF growth (bottom). n =4, * P <0.01 versus WT/control shRNA; † P <0.01 versus α1-KO/control shRNA.

Techniques Used: Cell Culture, Growth Assay, Soft Agar Assay, Western Blot, Knockdown, shRNA, Control

A. Upregulation of CDK2 transcription in AMPKα1-KO MEFs. CDK2 mRNA levels were measured by quantitative reverse transcription polymerase chain reaction in WT and AMPKα1-KO MEFs. n =5, * P <0.01 versus WT. B. p52 is responsible for CDK2 elevation in AMPKα1-KO MEFs. MEFs were transfected with either control siRNA or p52 siRNA (100 nmol/L) for 72 hours. Representative blot from three independent experiments (top). Quantification of Western blot data (bottom). n =3, * P <0.01 versus WT/control siRNA; † P <0.05 versus α1-KO/control siRNA. C. Chromatin immunoprecipitation (ChIP) analysis of the CDK2 gene. MEF chromatin from WT and AMPKα1-KO mice was immunoprecipitated with anti-p52 or rabbit IgG as a negative control. Precipitated DNA or 10% of the chromatin input was amplified with gene-specific primers for mouse CDK2 promoter. This result is representative of four independent experiments. n =4, * P <0.05 versus WT. D. p52 knockdown by shRNA diminishes anchorage-independent growth of AMPKα1-KO MEFs. Representative images are shown. Scale bar =500 μm. E. Quantification of anchorage-independent MEF growth. Data are mean ± SD, n =5, * P <0.01 versus WT/control shRNA; † P <0.01 versus α1-KO/control shRNA.

Figure Legend Snippet: A. Upregulation of CDK2 transcription in AMPKα1-KO MEFs. CDK2 mRNA levels were measured by quantitative reverse transcription polymerase chain reaction in WT and AMPKα1-KO MEFs. n =5, * P <0.01 versus WT. B. p52 is responsible for CDK2 elevation in AMPKα1-KO MEFs. MEFs were transfected with either control siRNA or p52 siRNA (100 nmol/L) for 72 hours. Representative blot from three independent experiments (top). Quantification of Western blot data (bottom). n =3, * P <0.01 versus WT/control siRNA; † P <0.05 versus α1-KO/control siRNA. C. Chromatin immunoprecipitation (ChIP) analysis of the CDK2 gene. MEF chromatin from WT and AMPKα1-KO mice was immunoprecipitated with anti-p52 or rabbit IgG as a negative control. Precipitated DNA or 10% of the chromatin input was amplified with gene-specific primers for mouse CDK2 promoter. This result is representative of four independent experiments. n =4, * P <0.05 versus WT. D. p52 knockdown by shRNA diminishes anchorage-independent growth of AMPKα1-KO MEFs. Representative images are shown. Scale bar =500 μm. E. Quantification of anchorage-independent MEF growth. Data are mean ± SD, n =5, * P <0.01 versus WT/control shRNA; † P <0.01 versus α1-KO/control shRNA.

Techniques Used: Reverse Transcription, Polymerase Chain Reaction, Transfection, Control, Western Blot, Chromatin Immunoprecipitation, Immunoprecipitation, Negative Control, Amplification, Knockdown, shRNA

A. Plasma concentrations of Epo in nude mice inoculated with WT or AMPKα1-KO MEFs. n =10-13 per group; * P <0.01 versus WT. B. Epo upregulation in inoculated AMPKα1-KO MEFs in nude mice. Implanted MEF tissues were collected from nude mice euthanized by carbon dioxide inhalation at 6 weeks after MEFs implantation. Representative images show Epo staining (top). Quantification of anti-Epo staining (bottom). n =5 per group; * P <0.01 versus WT. C. Tumor growth rate of AMPKα1-KO MEFs in nude mice injected intraperitoneally (IP) with an antibody specific to Epo or IgG. n =8–10 per group, † P <0.01 versus WT/IgG; * P <0.01 versus α1-KO/IgG. D. Representative images showing staining with antibodies specific to CD-31 or smooth muscle (SM)-α-actin (left). Scale bar =50 μm. Quantification of anti-CD31or SM-α-actin staining (right). Implanted AMPKα1-KO MEFs were collected from nude mice euthanized by carbon dioxide inhalation at the end of experiment (8 weeks after MEFs implantation). n =5–6 per group; * P <0.01 versus IgG. E. Mechanisms of AMPKα1deletion-stimulated anchorage-independent growth, neovascularization, and consequent tumorigenesis. AMPKα1 deletion in fibroblast activates NIK, which phosphorylates and activates IκKα, then enhance p100 phosphorylation recruiting E3 ubiquitin ligase β-TrCP, which facilitates p100 processing to p52. Upregulated p52 controls CDK2 and Epo expression. Epo-mediated neovascularization cooperating with CDK2-mediated anchorage-independent growth contributes to tumorigenesis in vivo .

Figure Legend Snippet: A. Plasma concentrations of Epo in nude mice inoculated with WT or AMPKα1-KO MEFs. n =10-13 per group; * P <0.01 versus WT. B. Epo upregulation in inoculated AMPKα1-KO MEFs in nude mice. Implanted MEF tissues were collected from nude mice euthanized by carbon dioxide inhalation at 6 weeks after MEFs implantation. Representative images show Epo staining (top). Quantification of anti-Epo staining (bottom). n =5 per group; * P <0.01 versus WT. C. Tumor growth rate of AMPKα1-KO MEFs in nude mice injected intraperitoneally (IP) with an antibody specific to Epo or IgG. n =8–10 per group, † P <0.01 versus WT/IgG; * P <0.01 versus α1-KO/IgG. D. Representative images showing staining with antibodies specific to CD-31 or smooth muscle (SM)-α-actin (left). Scale bar =50 μm. Quantification of anti-CD31or SM-α-actin staining (right). Implanted AMPKα1-KO MEFs were collected from nude mice euthanized by carbon dioxide inhalation at the end of experiment (8 weeks after MEFs implantation). n =5–6 per group; * P <0.01 versus IgG. E. Mechanisms of AMPKα1deletion-stimulated anchorage-independent growth, neovascularization, and consequent tumorigenesis. AMPKα1 deletion in fibroblast activates NIK, which phosphorylates and activates IκKα, then enhance p100 phosphorylation recruiting E3 ubiquitin ligase β-TrCP, which facilitates p100 processing to p52. Upregulated p52 controls CDK2 and Epo expression. Epo-mediated neovascularization cooperating with CDK2-mediated anchorage-independent growth contributes to tumorigenesis in vivo .

Techniques Used: Clinical Proteomics, Staining, Injection, Phospho-proteomics, Ubiquitin Proteomics, Expressing, In Vivo

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Journal: Oncotarget

Article Title: AMPKα1 deletion in fibroblasts promotes tumorigenesis in athymic nude mice by p52-mediated elevation of erythropoietin and CDK2

doi: 10.18632/oncotarget.10687

Figure Lengend Snippet: A. Spontaneous colony formation in AMPKα1-KO MEFs. Wild type (WT), AMPKα1-KO, and AMPKα2-KO MEFs (1 × 10 5 cells/mL) were seeded and cultured on 6-well plates. Culture medium was changed every 2 days for 3 weeks. (Upper) Representative images showing colony formation of MEFs. (Bottom) Quantification of colony formation. n =5, * P <0.001 versus WT. B. Anchorage-independent cell growth assay (soft agar assay) of MEFs. (Upper) Representative images for colony formation. Scale bar =500 μm. (Bottom) Quantification of colony formation. n =10, * P <0.001 versus WT. C. Phosphorylated CDK2 at The-160 (pCDK2-T160) and CDK2 are upregulated in AMPKα1-KO MEFs. pCDK2-T160 and CDK2 protein in WT, AMPKα1-KO, and AMPKα2-KO MEFs were analyzed by Western blot (top). Quantification of pCDK2 and CDK2 data (bottom). n =4, * P <0.01 versus WT; † P <0.05 versus WT. D. Diminished anchorage-independent growth of AMPKα1-KO MEFs following CDK2 knockdown by shRNA. Representative images are shown. Scale bar =500 μm. E. Representative Western blot data indicate CDK2 knockdown by shRNA (top). Quantification of anchorage-independent MEF growth (bottom). n =4, * P <0.01 versus WT/control shRNA; † P <0.01 versus α1-KO/control shRNA.

Article Snippet: The following antibodies were obtained from Cell Signaling Technology (Beverly, MA): rabbit anti-CDK2 (2546), rabbit anti-pCDK2-T160 (2561), rabbit anti-pp100-S866/870 (4810), rabbit anti-pIĸKα/β (2078), rabbit anti-IĸKα (2682), rabbit anti-NF-ĸB2 p100/p52 (4882), rabbit anti-NIK (4994), rabbit anti-β-TrCP (D13F10) (4394), and rabbit anti-PCNA (13110). β-TrCP siRNA (sc-37179), p52 siRNA (m) (sc-36043), CDK2 shRNA (m) lentiviral particles (sc-29260-V), NFκB p52 shRNA (m) lentiviral particles (sc-36043-V), goat anti-pNIK-T559 (sc-12957), rabbit anti-Epo (sc-7956), mouse anti-GAPDH (sc-32233), mouse anti-β-actin (sc-47778), were purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

Techniques: Cell Culture, Growth Assay, Soft Agar Assay, Western Blot, Knockdown, shRNA, Control

Journal: Oncotarget

Article Title: AMPKα1 deletion in fibroblasts promotes tumorigenesis in athymic nude mice by p52-mediated elevation of erythropoietin and CDK2

doi: 10.18632/oncotarget.10687

Figure Lengend Snippet: A. Upregulation of CDK2 transcription in AMPKα1-KO MEFs. CDK2 mRNA levels were measured by quantitative reverse transcription polymerase chain reaction in WT and AMPKα1-KO MEFs. n =5, * P <0.01 versus WT. B. p52 is responsible for CDK2 elevation in AMPKα1-KO MEFs. MEFs were transfected with either control siRNA or p52 siRNA (100 nmol/L) for 72 hours. Representative blot from three independent experiments (top). Quantification of Western blot data (bottom). n =3, * P <0.01 versus WT/control siRNA; † P <0.05 versus α1-KO/control siRNA. C. Chromatin immunoprecipitation (ChIP) analysis of the CDK2 gene. MEF chromatin from WT and AMPKα1-KO mice was immunoprecipitated with anti-p52 or rabbit IgG as a negative control. Precipitated DNA or 10% of the chromatin input was amplified with gene-specific primers for mouse CDK2 promoter. This result is representative of four independent experiments. n =4, * P <0.05 versus WT. D. p52 knockdown by shRNA diminishes anchorage-independent growth of AMPKα1-KO MEFs. Representative images are shown. Scale bar =500 μm. E. Quantification of anchorage-independent MEF growth. Data are mean ± SD, n =5, * P <0.01 versus WT/control shRNA; † P <0.01 versus α1-KO/control shRNA.

Techniques: Reverse Transcription, Polymerase Chain Reaction, Transfection, Control, Western Blot, Chromatin Immunoprecipitation, Immunoprecipitation, Negative Control, Amplification, Knockdown, shRNA

Journal: Oncotarget

Article Title: AMPKα1 deletion in fibroblasts promotes tumorigenesis in athymic nude mice by p52-mediated elevation of erythropoietin and CDK2

doi: 10.18632/oncotarget.10687

Figure Lengend Snippet: A. Plasma concentrations of Epo in nude mice inoculated with WT or AMPKα1-KO MEFs. n =10-13 per group; * P <0.01 versus WT. B. Epo upregulation in inoculated AMPKα1-KO MEFs in nude mice. Implanted MEF tissues were collected from nude mice euthanized by carbon dioxide inhalation at 6 weeks after MEFs implantation. Representative images show Epo staining (top). Quantification of anti-Epo staining (bottom). n =5 per group; * P <0.01 versus WT. C. Tumor growth rate of AMPKα1-KO MEFs in nude mice injected intraperitoneally (IP) with an antibody specific to Epo or IgG. n =8–10 per group, † P <0.01 versus WT/IgG; * P <0.01 versus α1-KO/IgG. D. Representative images showing staining with antibodies specific to CD-31 or smooth muscle (SM)-α-actin (left). Scale bar =50 μm. Quantification of anti-CD31or SM-α-actin staining (right). Implanted AMPKα1-KO MEFs were collected from nude mice euthanized by carbon dioxide inhalation at the end of experiment (8 weeks after MEFs implantation). n =5–6 per group; * P <0.01 versus IgG. E. Mechanisms of AMPKα1deletion-stimulated anchorage-independent growth, neovascularization, and consequent tumorigenesis. AMPKα1 deletion in fibroblast activates NIK, which phosphorylates and activates IκKα, then enhance p100 phosphorylation recruiting E3 ubiquitin ligase β-TrCP, which facilitates p100 processing to p52. Upregulated p52 controls CDK2 and Epo expression. Epo-mediated neovascularization cooperating with CDK2-mediated anchorage-independent growth contributes to tumorigenesis in vivo .

Techniques: Clinical Proteomics, Staining, Injection, Phospho-proteomics, Ubiquitin Proteomics, Expressing, In Vivo

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