Review



negative control lentivirus infected hepg2 cells  (Biotium)


Bioz Verified Symbol Biotium is a verified supplier
Bioz Manufacturer Symbol Biotium manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 93
      Buy from Supplier

    Structured Review

    Biotium negative control lentivirus infected hepg2 cells
    Fig. 4 ACSL4 promotes the proliferation of hepatoblastoma cells in vitro and tumor growth in vivo. (A) The viability of <t>HepG2</t> and Huh6 cells transfected with siACSL4 or NC was detected by CCK8 assays. (B) Colony formation assays were performed in ACSL4-silenced and control cells. *p < 0.05, **p < 0.01, ***p < 0.001
    Negative Control Lentivirus Infected Hepg2 Cells, supplied by Biotium, used in various techniques. Bioz Stars score: 93/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/negative+control+lentivirus+infected+hepg2+cells/pm39901207-110-8-24?v=Biotium
    Average 93 stars, based on 21 article reviews
    negative control lentivirus infected hepg2 cells - by Bioz Stars, 2026-08
    93/100 stars

    Images

    1) Product Images from "ACSL4 promotes the formation of the proliferative subtype in hepatoblastoma."

    Article Title: ACSL4 promotes the formation of the proliferative subtype in hepatoblastoma.

    Journal: BMC cancer

    doi: 10.1186/s12885-025-13592-4

    Fig. 4 ACSL4 promotes the proliferation of hepatoblastoma cells in vitro and tumor growth in vivo. (A) The viability of HepG2 and Huh6 cells transfected with siACSL4 or NC was detected by CCK8 assays. (B) Colony formation assays were performed in ACSL4-silenced and control cells. *p < 0.05, **p < 0.01, ***p < 0.001
    Figure Legend Snippet: Fig. 4 ACSL4 promotes the proliferation of hepatoblastoma cells in vitro and tumor growth in vivo. (A) The viability of HepG2 and Huh6 cells transfected with siACSL4 or NC was detected by CCK8 assays. (B) Colony formation assays were performed in ACSL4-silenced and control cells. *p < 0.05, **p < 0.01, ***p < 0.001

    Techniques Used: In Vitro, In Vivo, Transfection, Control

    Fig. 6 ACSL4 promotes the formation of proliferative HB subtype via MAVS/IRF3/STAT1 signailing pathway. (A) GSEA enrichment analysis results of dif ferential genes between ACSL4 high-expression and ACSL4 low-expression hepatoblastoma tissues in GSE133039 dataset. (B) Enrichment results for IFNα response via GSEA of the hepatoblastoma tissues in GSE133039 dataset. (C) Enrichment results for IFNγ response via GSEA of the hepatoblastoma tissues in GSE133039 dataset. (D) The enrichment results of the interferon-γ response signaling pathway between the ACSL4-high hepatoblastoma subgroup and the ACSL4-low hepatoblastoma subgroup in GSE186975 dataset. (E) The enrichment results of the interferon-γ response signaling pathway between ACSL4 knockdown HepG2 cell line and negative control cells. (F) The MAVS/IRF3/STAT1 interferon response pathway-associated proteins were detected by Western blot in ACSL4 knockdown cells and controls. (G) Inferred intercellular communication network among ACSL4 high tumor cells and other cell clusters, shown in a circle plot. The thickness of the lines represents the strength of cell communication. (H) Circle plots showing cell-cell communications between ACSL4 low tumor cells and other cell clusters
    Figure Legend Snippet: Fig. 6 ACSL4 promotes the formation of proliferative HB subtype via MAVS/IRF3/STAT1 signailing pathway. (A) GSEA enrichment analysis results of dif ferential genes between ACSL4 high-expression and ACSL4 low-expression hepatoblastoma tissues in GSE133039 dataset. (B) Enrichment results for IFNα response via GSEA of the hepatoblastoma tissues in GSE133039 dataset. (C) Enrichment results for IFNγ response via GSEA of the hepatoblastoma tissues in GSE133039 dataset. (D) The enrichment results of the interferon-γ response signaling pathway between the ACSL4-high hepatoblastoma subgroup and the ACSL4-low hepatoblastoma subgroup in GSE186975 dataset. (E) The enrichment results of the interferon-γ response signaling pathway between ACSL4 knockdown HepG2 cell line and negative control cells. (F) The MAVS/IRF3/STAT1 interferon response pathway-associated proteins were detected by Western blot in ACSL4 knockdown cells and controls. (G) Inferred intercellular communication network among ACSL4 high tumor cells and other cell clusters, shown in a circle plot. The thickness of the lines represents the strength of cell communication. (H) Circle plots showing cell-cell communications between ACSL4 low tumor cells and other cell clusters

    Techniques Used: Expressing, Knockdown, Negative Control, Western Blot



    Similar Products

    negative control lentivirus infected hepg2 cells  (Biotium)
    93
    Biotium negative control lentivirus infected hepg2 cells
    Fig. 4 ACSL4 promotes the proliferation of hepatoblastoma cells in vitro and tumor growth in vivo. (A) The viability of <t>HepG2</t> and Huh6 cells transfected with siACSL4 or NC was detected by CCK8 assays. (B) Colony formation assays were performed in ACSL4-silenced and control cells. *p < 0.05, **p < 0.01, ***p < 0.001
    Negative Control Lentivirus Infected Hepg2 Cells, supplied by Biotium, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/negative+control+lentivirus+infected+hepg2+cells/pm39901207-110-8-24?v=Biotium
    Average 93 stars, based on 1 article reviews
    negative control lentivirus infected hepg2 cells - by Bioz Stars, 2026-08
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    Fig. 4 ACSL4 promotes the proliferation of hepatoblastoma cells in vitro and tumor growth in vivo. (A) The viability of HepG2 and Huh6 cells transfected with siACSL4 or NC was detected by CCK8 assays. (B) Colony formation assays were performed in ACSL4-silenced and control cells. *p < 0.05, **p < 0.01, ***p < 0.001

    Journal: BMC cancer

    Article Title: ACSL4 promotes the formation of the proliferative subtype in hepatoblastoma.

    doi: 10.1186/s12885-025-13592-4

    Figure Lengend Snippet: Fig. 4 ACSL4 promotes the proliferation of hepatoblastoma cells in vitro and tumor growth in vivo. (A) The viability of HepG2 and Huh6 cells transfected with siACSL4 or NC was detected by CCK8 assays. (B) Colony formation assays were performed in ACSL4-silenced and control cells. *p < 0.05, **p < 0.01, ***p < 0.001

    Article Snippet: Total RNA was extracted from ACSL4 knockdown and negative control lentivirus-infected HepG2 cells using the RNAstorm Fresh Cell and Tissue RNA Isolation Kit from Cell Data Sciences (USA).

    Techniques: In Vitro, In Vivo, Transfection, Control

    Fig. 6 ACSL4 promotes the formation of proliferative HB subtype via MAVS/IRF3/STAT1 signailing pathway. (A) GSEA enrichment analysis results of dif ferential genes between ACSL4 high-expression and ACSL4 low-expression hepatoblastoma tissues in GSE133039 dataset. (B) Enrichment results for IFNα response via GSEA of the hepatoblastoma tissues in GSE133039 dataset. (C) Enrichment results for IFNγ response via GSEA of the hepatoblastoma tissues in GSE133039 dataset. (D) The enrichment results of the interferon-γ response signaling pathway between the ACSL4-high hepatoblastoma subgroup and the ACSL4-low hepatoblastoma subgroup in GSE186975 dataset. (E) The enrichment results of the interferon-γ response signaling pathway between ACSL4 knockdown HepG2 cell line and negative control cells. (F) The MAVS/IRF3/STAT1 interferon response pathway-associated proteins were detected by Western blot in ACSL4 knockdown cells and controls. (G) Inferred intercellular communication network among ACSL4 high tumor cells and other cell clusters, shown in a circle plot. The thickness of the lines represents the strength of cell communication. (H) Circle plots showing cell-cell communications between ACSL4 low tumor cells and other cell clusters

    Journal: BMC cancer

    Article Title: ACSL4 promotes the formation of the proliferative subtype in hepatoblastoma.

    doi: 10.1186/s12885-025-13592-4

    Figure Lengend Snippet: Fig. 6 ACSL4 promotes the formation of proliferative HB subtype via MAVS/IRF3/STAT1 signailing pathway. (A) GSEA enrichment analysis results of dif ferential genes between ACSL4 high-expression and ACSL4 low-expression hepatoblastoma tissues in GSE133039 dataset. (B) Enrichment results for IFNα response via GSEA of the hepatoblastoma tissues in GSE133039 dataset. (C) Enrichment results for IFNγ response via GSEA of the hepatoblastoma tissues in GSE133039 dataset. (D) The enrichment results of the interferon-γ response signaling pathway between the ACSL4-high hepatoblastoma subgroup and the ACSL4-low hepatoblastoma subgroup in GSE186975 dataset. (E) The enrichment results of the interferon-γ response signaling pathway between ACSL4 knockdown HepG2 cell line and negative control cells. (F) The MAVS/IRF3/STAT1 interferon response pathway-associated proteins were detected by Western blot in ACSL4 knockdown cells and controls. (G) Inferred intercellular communication network among ACSL4 high tumor cells and other cell clusters, shown in a circle plot. The thickness of the lines represents the strength of cell communication. (H) Circle plots showing cell-cell communications between ACSL4 low tumor cells and other cell clusters

    Article Snippet: Total RNA was extracted from ACSL4 knockdown and negative control lentivirus-infected HepG2 cells using the RNAstorm Fresh Cell and Tissue RNA Isolation Kit from Cell Data Sciences (USA).

    Techniques: Expressing, Knockdown, Negative Control, Western Blot