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anti sox2  (R&D Systems)


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    R&D Systems anti sox2
    Anti Sox2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 720 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+sox2+antibody/Human%2FMouse%2FRat+SOX2+Antibody/pm42032298-92-12-15
    Average 97 stars, based on 720 article reviews
    anti sox2 - by Bioz Stars, 2026-09
    97/100 stars

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    other:

    Article Title: A whole‐genome scan for Artemisinin cytotoxicity reveals a novel therapy for human brain tumors
    Article Snippet: The following antibodies were used: anti‐GFP antibody (Abcam, ab13970, 1:500), anti‐Ki‐67 monoclonal antibody (SolA15, eBioscience, 14‐5698‐82, 1:100), anti‐cleaved caspase‐3 antibody (Asp175, Cell Signaling Technology, 966S1, 1:300), anti‐Sox2 antibody (R&D Systems, AF2018; or Abcam, ab97959, 1:1000), anti‐Map2 antibody (Millipore, MAB3418, 1:500), and anti‐gamma‐H2A.X antibody (phospho S139, Abcam, ab11174, 1:300).

    Article Title: Treating myelin diseases with optimized cell preparations
    Article Snippet: and AQP4 (1:200, Chemicon, Bellerica, Mass.), and for neuronal markers, βIII-tubulin (clone TuJ1, 1:1000, Covance, Princeton, N.J.) and HuD (clone 16A11, 10 ng/ml, Invitrogen, La Jolla, Calif.).

    Enzyme-linked Immunosorbent Assay:

    Article Title: Coating Bioactive Microcapsules with Tannic Acid Enhances the Phenotype of the Encapsulated Pluripotent Stem Cells.
    Article Snippet: Human pluripotent stem cells (hPSCs) may be differentiated into any adult cell type and therefore hold incredible promise for cell therapeutics and disease modeling.. There is increasing interest in three-dimensional (3D) hPSC culture because of improved differentiation outcomes and potential for scale up.. Our team has recently described bioactive heparin (Hep)containing core−shell microcapsules that promote rapid aggregation of stem cells into spheroids and may also be loaded with growth factors for the local and sustained delivery to the encapsulated cells.



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    Miltenyi Biotec sox2
    Reprogramming of adult human dermal fibroblasts (HDFa) into induced pluripotent stem cell (iPSC) line BO-VC1. Reprogramming was performed using the Epi5 ™ Episomal iPSC Reprogramming Kit, enabling the generation of ( A ) transgene- and virus-free iPSC line BO-VC1. Successful generation of fibroblast-derived iPSCs was validated by immunocytochemical staining for the pluripotency markers ( B ) <t>SOX2,</t> C TRA 1–60, D OCT4, SSEA4 and E NANOG. Quantification of the generated iPSCs via flow cytometry revealed F 99.31% SSEA4/TRA1-60, G 97.43% SOX2/TRA1-60 and H 98.60% OCT3/4/TRA1-60 positive cells. I Quantification of the transcript levels of the stem cell markers NANOG , OCT4 , REX1 and SOX2 revealed significantly higher mRNA levels in iPSC line BO-VC1 compared to the HDFa control ( n = 3 different passages) Moreover, generated iPSCs were functionally validated by directed differentiation into all three germ layers. Subsequent immunocytochemical staining of the iPSCs before and after differentiation confirmed the expression of ( J–M ) meso-, N–Q endo- and R–U ectodermal lineage markers only in the respective differentiations. Scale bars: 50 μm. Data were tested for normal distribution using Shapiro-Wilk test. Means ± SEM (standard error of the mean) were statistically analyzed by a Kruskal-Wallis test with Dunn’s multiple comparisons test. n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)
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    Reprogramming of adult human dermal fibroblasts (HDFa) into induced pluripotent stem cell (iPSC) line BO-VC1. Reprogramming was performed using the Epi5 ™ Episomal iPSC Reprogramming Kit, enabling the generation of ( A ) transgene- and virus-free iPSC line BO-VC1. Successful generation of fibroblast-derived iPSCs was validated by immunocytochemical staining for the pluripotency markers ( B ) <t>SOX2,</t> C TRA 1–60, D OCT4, SSEA4 and E NANOG. Quantification of the generated iPSCs via flow cytometry revealed F 99.31% SSEA4/TRA1-60, G 97.43% SOX2/TRA1-60 and H 98.60% OCT3/4/TRA1-60 positive cells. I Quantification of the transcript levels of the stem cell markers NANOG , OCT4 , REX1 and SOX2 revealed significantly higher mRNA levels in iPSC line BO-VC1 compared to the HDFa control ( n = 3 different passages) Moreover, generated iPSCs were functionally validated by directed differentiation into all three germ layers. Subsequent immunocytochemical staining of the iPSCs before and after differentiation confirmed the expression of ( J–M ) meso-, N–Q endo- and R–U ectodermal lineage markers only in the respective differentiations. Scale bars: 50 μm. Data were tested for normal distribution using Shapiro-Wilk test. Means ± SEM (standard error of the mean) were statistically analyzed by a Kruskal-Wallis test with Dunn’s multiple comparisons test. n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)
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    Cell Signaling Technology Inc sox2
    Reprogramming of adult human dermal fibroblasts (HDFa) into induced pluripotent stem cell (iPSC) line BO-VC1. Reprogramming was performed using the Epi5 ™ Episomal iPSC Reprogramming Kit, enabling the generation of ( A ) transgene- and virus-free iPSC line BO-VC1. Successful generation of fibroblast-derived iPSCs was validated by immunocytochemical staining for the pluripotency markers ( B ) <t>SOX2,</t> C TRA 1–60, D OCT4, SSEA4 and E NANOG. Quantification of the generated iPSCs via flow cytometry revealed F 99.31% SSEA4/TRA1-60, G 97.43% SOX2/TRA1-60 and H 98.60% OCT3/4/TRA1-60 positive cells. I Quantification of the transcript levels of the stem cell markers NANOG , OCT4 , REX1 and SOX2 revealed significantly higher mRNA levels in iPSC line BO-VC1 compared to the HDFa control ( n = 3 different passages) Moreover, generated iPSCs were functionally validated by directed differentiation into all three germ layers. Subsequent immunocytochemical staining of the iPSCs before and after differentiation confirmed the expression of ( J–M ) meso-, N–Q endo- and R–U ectodermal lineage markers only in the respective differentiations. Scale bars: 50 μm. Data were tested for normal distribution using Shapiro-Wilk test. Means ± SEM (standard error of the mean) were statistically analyzed by a Kruskal-Wallis test with Dunn’s multiple comparisons test. n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)
    Sox2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology sox2
    LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers (P16, P53). (E–G) Assessment of stemness <t>(SOX2)</t> and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.
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    Proteintech sry box transcription factor 2
    Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and <t>SOX2</t> in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.
    Sry Box Transcription Factor 2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Proteintech sox2
    Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and <t>SOX2</t> in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.
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    R&D Systems anti sox2
    Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and <t>SOX2</t> in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.
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    Image Search Results


    Reprogramming of adult human dermal fibroblasts (HDFa) into induced pluripotent stem cell (iPSC) line BO-VC1. Reprogramming was performed using the Epi5 ™ Episomal iPSC Reprogramming Kit, enabling the generation of ( A ) transgene- and virus-free iPSC line BO-VC1. Successful generation of fibroblast-derived iPSCs was validated by immunocytochemical staining for the pluripotency markers ( B ) SOX2, C TRA 1–60, D OCT4, SSEA4 and E NANOG. Quantification of the generated iPSCs via flow cytometry revealed F 99.31% SSEA4/TRA1-60, G 97.43% SOX2/TRA1-60 and H 98.60% OCT3/4/TRA1-60 positive cells. I Quantification of the transcript levels of the stem cell markers NANOG , OCT4 , REX1 and SOX2 revealed significantly higher mRNA levels in iPSC line BO-VC1 compared to the HDFa control ( n = 3 different passages) Moreover, generated iPSCs were functionally validated by directed differentiation into all three germ layers. Subsequent immunocytochemical staining of the iPSCs before and after differentiation confirmed the expression of ( J–M ) meso-, N–Q endo- and R–U ectodermal lineage markers only in the respective differentiations. Scale bars: 50 μm. Data were tested for normal distribution using Shapiro-Wilk test. Means ± SEM (standard error of the mean) were statistically analyzed by a Kruskal-Wallis test with Dunn’s multiple comparisons test. n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)

    Journal: Stem Cell Research & Therapy

    Article Title: Activation of the G-protein coupled estrogen receptor 1 (GPER1) reduces transient receptor potential vanilloid 1 (TRPV1) activity and human iPSC-derived nociceptive neuron firing

    doi: 10.1186/s13287-026-05174-3

    Figure Lengend Snippet: Reprogramming of adult human dermal fibroblasts (HDFa) into induced pluripotent stem cell (iPSC) line BO-VC1. Reprogramming was performed using the Epi5 ™ Episomal iPSC Reprogramming Kit, enabling the generation of ( A ) transgene- and virus-free iPSC line BO-VC1. Successful generation of fibroblast-derived iPSCs was validated by immunocytochemical staining for the pluripotency markers ( B ) SOX2, C TRA 1–60, D OCT4, SSEA4 and E NANOG. Quantification of the generated iPSCs via flow cytometry revealed F 99.31% SSEA4/TRA1-60, G 97.43% SOX2/TRA1-60 and H 98.60% OCT3/4/TRA1-60 positive cells. I Quantification of the transcript levels of the stem cell markers NANOG , OCT4 , REX1 and SOX2 revealed significantly higher mRNA levels in iPSC line BO-VC1 compared to the HDFa control ( n = 3 different passages) Moreover, generated iPSCs were functionally validated by directed differentiation into all three germ layers. Subsequent immunocytochemical staining of the iPSCs before and after differentiation confirmed the expression of ( J–M ) meso-, N–Q endo- and R–U ectodermal lineage markers only in the respective differentiations. Scale bars: 50 μm. Data were tested for normal distribution using Shapiro-Wilk test. Means ± SEM (standard error of the mean) were statistically analyzed by a Kruskal-Wallis test with Dunn’s multiple comparisons test. n = 3 (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001)

    Article Snippet: Subsequently, cells were incubated in inside fix solution of the Inside Stain Kit (#130-090-477, Miltenyi Biotec, Bergisch Gladbach, Germany) for 20 min at RT and centrifuged at 200xg for 5 min. After washing in 500 μl PEB buffer and centrifugation at 200xg cells were stained with the nuclear stem cell markers OCT3/4 (1:50, #130-117-821, Miltenyi Biotec, Bergisch Gladbach, Germany) and SOX2 (1:50, #130-120-790, Miltenyi Biotec, Bergisch Gladbach, Germany) in inside perm solution for 10 min at RT.

    Techniques: Virus, Derivative Assay, Staining, Generated, Flow Cytometry, Control, Expressing

    LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers (P16, P53). (E–G) Assessment of stemness (SOX2) and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.

    Journal: Bioactive Materials

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    doi: 10.1016/j.bioactmat.2026.01.004

    Figure Lengend Snippet: LT-NPs-NIR protects TSPCs against oxidative stress-induced senescence and preserves tenogenic phenotype. (A–D) Immunofluorescence staining for DNA damage (γ-H2AX), proliferation (Ki67), and senescence markers (P16, P53). (E–G) Assessment of stemness (SOX2) and tenogenic differentiation markers (SCX, COL1). (H) Quantitative analysis of the indicated markers. (I) qRT-PCR analysis of SASP-related inflammatory mediators (IL-1β, CXCL10) and matrix-degrading enzymes (MMP3, MMP13). (J) Schematic illustrating the mechanism of ROS scavenging and SASP inhibition. Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. Snt: senescent cells; Yng: young cells.

    Article Snippet: After washing, cells were incubated with primary antibodies against Ki67 (ab15580, Abcam), Phosphorylated Histone H2AX (γ-H2AX) (ab81299, Abcam), SOX2 (sc-365964, Santa Cruz), Type I Collagen (COL1) (ab138492, Abcam), tenomodulin (TNMD) (ab203676, Abcam; sc-51813, Santa Cruz), Scleraxis (SCX) (sc-518082, Santa Cruz), IRF3 (ab68481, Abcam), Transcription Factor p65/RELA (P65) (A22331, Abclonal), Cyclin-Dependent Kinase Inhibitor 2A (p16INK4a) (P16) (sc-1661, Santa Cruz), P53 (10442-1-AP, Proteintech), Inducible Nitric Oxide Synthase (iNOS) (ab178945, Abcam), Arginase-1(Arg-1) (ab96183, Abcam), HSP70 (sc-32239, Santa Cruz), IL-6 (ab233706, Abcam), Matrix Metalloproteinase 13 (MMP13) (ab39012, Abcam), Double-stranded DNA (dsDNA) Marker (sc-58749, Santa Cruz), and Translocase of Outer Mitochondrial Membrane 20 (TOMM20) (11802-1-AP, Proteintech).

    Techniques: Immunofluorescence, Staining, Quantitative RT-PCR, Inhibition

    LT-NPs-NIR modulate macrophage polarization and enhance TSPC-mediated tenogenic repair in a Transwell co-culture system. (A) Schematic of the Transwell co-culture setup. (B) SA-β-gal staining of macrophages. (C–F) Immunofluorescence of TSPCs for (C) P16, (D) SOX2, (E) SCX, and (F) Tenomodulin (TNMD) with F-actin. (G) Quantification of P16, SOX2, SCX, and TNMD levels. (H) Proposed mechanism: LT-NPs-NIR promote an M1-to-M2 macrophage shift and regulate TSPC senescence/stemness balance to favor tenogenic repair, potentially via STING/NF-κB signaling. Scale bars: 100 μm (B); 50 μm (C–E); 100 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Journal: Bioactive Materials

    Article Title: On-demand mild photothermal cascade platform reprogramming mitochondrial immunity for tendon rejuvenation

    doi: 10.1016/j.bioactmat.2026.01.004

    Figure Lengend Snippet: LT-NPs-NIR modulate macrophage polarization and enhance TSPC-mediated tenogenic repair in a Transwell co-culture system. (A) Schematic of the Transwell co-culture setup. (B) SA-β-gal staining of macrophages. (C–F) Immunofluorescence of TSPCs for (C) P16, (D) SOX2, (E) SCX, and (F) Tenomodulin (TNMD) with F-actin. (G) Quantification of P16, SOX2, SCX, and TNMD levels. (H) Proposed mechanism: LT-NPs-NIR promote an M1-to-M2 macrophage shift and regulate TSPC senescence/stemness balance to favor tenogenic repair, potentially via STING/NF-κB signaling. Scale bars: 100 μm (B); 50 μm (C–E); 100 μm (F). Significance: ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

    Article Snippet: After washing, cells were incubated with primary antibodies against Ki67 (ab15580, Abcam), Phosphorylated Histone H2AX (γ-H2AX) (ab81299, Abcam), SOX2 (sc-365964, Santa Cruz), Type I Collagen (COL1) (ab138492, Abcam), tenomodulin (TNMD) (ab203676, Abcam; sc-51813, Santa Cruz), Scleraxis (SCX) (sc-518082, Santa Cruz), IRF3 (ab68481, Abcam), Transcription Factor p65/RELA (P65) (A22331, Abclonal), Cyclin-Dependent Kinase Inhibitor 2A (p16INK4a) (P16) (sc-1661, Santa Cruz), P53 (10442-1-AP, Proteintech), Inducible Nitric Oxide Synthase (iNOS) (ab178945, Abcam), Arginase-1(Arg-1) (ab96183, Abcam), HSP70 (sc-32239, Santa Cruz), IL-6 (ab233706, Abcam), Matrix Metalloproteinase 13 (MMP13) (ab39012, Abcam), Double-stranded DNA (dsDNA) Marker (sc-58749, Santa Cruz), and Translocase of Outer Mitochondrial Membrane 20 (TOMM20) (11802-1-AP, Proteintech).

    Techniques: Co-Culture Assay, Staining, Immunofluorescence

    Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

    Journal: Oncology Reports

    Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation

    doi: 10.3892/or.2026.9086

    Figure Lengend Snippet: Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

    Article Snippet: The primary antibodies were as follows: CCT2 (cat. no. 24896-1-AP), β-actin (cat. no. 66009-1-Ig), MMP2 (cat. no. 10373-2-AP), myeloid cell leukemia sequence 1 (MCL1; cat. no. 16225-1-AP) and SRY-box transcription factor 2 (SOX2; cat. no. 11064-1-AP; all Proteintech Group, Inc.) and STAT3 (cat. no. 4904) and phosphorylated (p-)STAT3 (Tyr705; cat. no. 4113; both Cell Signaling Technology, Inc.) The membranes were washed three times in TBST (0.1% Tween-20) for 5 min each at room temperature.

    Techniques: Knockdown, Activation Assay, Western Blot, Immunohistochemical staining, Staining, Negative Control, Sequencing

    Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

    Journal: Oncology Reports

    Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation

    doi: 10.3892/or.2026.9086

    Figure Lengend Snippet: Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

    Article Snippet: The primary antibodies, including p-STAT3 (cat. no. 4113, Cell Signaling Technology), MCL1 (cat. no. 16225-1-AP), MMP2 (cat. no. 10373-2-AP) and SOX2 (cat. no. 11064-1-AP; all Proteintech Group, Inc.), were diluted 1:100 in antibody diluent (cat. no. PR30016; Proteintech Group, Inc.) and applied at 4°C overnight.

    Techniques: Knockdown, Activation Assay, Western Blot, Immunohistochemical staining, Staining, Negative Control, Sequencing