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flnc  (Boster Bio)


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    Structured Review

    Boster Bio flnc
    Flnc, supplied by Boster Bio, 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/flnc/pm40505291-127-13-16?v=Boster+Bio
    Average 93 stars, based on 1 article reviews
    flnc - by Bioz Stars, 2026-08
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    Low-frequency r T MS suppresses cell proliferation by downregulating the expression of FLNA and <t>FLNC</t> in the in vitro GBM model. U87MG were used as the in vitro GBM model. The model was divided into two groups: a sham group (non-treated, n ​= ​4) and a low-frequency group (treated with low-frequency rTMS, n ​= ​4). (A) Schematic figure of low-frequency rTMS treatment on an in vitro GBM model. (B) Cell counting kit-8 (CCK-8) assay of the in vitro GBM model with or without low-frequency rTMS treatment. (C) Quantification of CCK-8 assay. (D) ATP assay of in vitro GBM model with or without low-frequency rTMS treatment. (E) The relative gene expression of FLNA and FLNC in the in vitro GBM model with or without low-frequency rTMS treatment, as detected by RT-qPCR. (F) Western blot analysis of FLNA and FLNC in the in vitro glioblastoma model with or without low-frequency rTMS treatment. (G) Quantification of Western blot signals for FLNA and FLNC. Values are presented as means ​± ​standard error of the mean (SEM). Statistically significant differences are shown as ∗ P ​< ​0.05, ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.
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    Low-frequency r T MS suppresses cell proliferation by downregulating the expression of FLNA and <t>FLNC</t> in the in vitro GBM model. U87MG were used as the in vitro GBM model. The model was divided into two groups: a sham group (non-treated, n ​= ​4) and a low-frequency group (treated with low-frequency rTMS, n ​= ​4). (A) Schematic figure of low-frequency rTMS treatment on an in vitro GBM model. (B) Cell counting kit-8 (CCK-8) assay of the in vitro GBM model with or without low-frequency rTMS treatment. (C) Quantification of CCK-8 assay. (D) ATP assay of in vitro GBM model with or without low-frequency rTMS treatment. (E) The relative gene expression of FLNA and FLNC in the in vitro GBM model with or without low-frequency rTMS treatment, as detected by RT-qPCR. (F) Western blot analysis of FLNA and FLNC in the in vitro glioblastoma model with or without low-frequency rTMS treatment. (G) Quantification of Western blot signals for FLNA and FLNC. Values are presented as means ​± ​standard error of the mean (SEM). Statistically significant differences are shown as ∗ P ​< ​0.05, ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.
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    Low-frequency r T MS suppresses cell proliferation by downregulating the expression of FLNA and <t>FLNC</t> in the in vitro GBM model. U87MG were used as the in vitro GBM model. The model was divided into two groups: a sham group (non-treated, n ​= ​4) and a low-frequency group (treated with low-frequency rTMS, n ​= ​4). (A) Schematic figure of low-frequency rTMS treatment on an in vitro GBM model. (B) Cell counting kit-8 (CCK-8) assay of the in vitro GBM model with or without low-frequency rTMS treatment. (C) Quantification of CCK-8 assay. (D) ATP assay of in vitro GBM model with or without low-frequency rTMS treatment. (E) The relative gene expression of FLNA and FLNC in the in vitro GBM model with or without low-frequency rTMS treatment, as detected by RT-qPCR. (F) Western blot analysis of FLNA and FLNC in the in vitro glioblastoma model with or without low-frequency rTMS treatment. (G) Quantification of Western blot signals for FLNA and FLNC. Values are presented as means ​± ​standard error of the mean (SEM). Statistically significant differences are shown as ∗ P ​< ​0.05, ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.
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    Proteintech flnc
    Fig. 10. <t>FLNC</t> enhances glioma cell resistance to staurosporine. (A, B) CCK8 assay assessed the effect of FLNC overexpression on the resistance of U87 and U251 cell lines to staurosporine. (C, D) CCK-8 assay demonstrated the impact of FLNC knockdown on the resistance of U87 and U251 cell lines to staurosporine. (E-H) Colony formation assay evaluated the influence of FLNC overexpression on the colony-forming ability of U87 and U251 cells under staurosporine treatment (20 nM), with representative images (E, G) (Scale bar = 50 μm) and statistical results (F, H). (I, J) In U87 and U251 cells, FLNC overexpression/knockdown modulated the inhibitory effect of staurosporine (5 nM) on the Erk <t>and</t> <t>JAK2/STAT3</t> pathways. *P < 0.05; **P < 0.01; ***P < 0.001.
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    Image Search Results


    Low-frequency r T MS suppresses cell proliferation by downregulating the expression of FLNA and FLNC in the in vitro GBM model. U87MG were used as the in vitro GBM model. The model was divided into two groups: a sham group (non-treated, n ​= ​4) and a low-frequency group (treated with low-frequency rTMS, n ​= ​4). (A) Schematic figure of low-frequency rTMS treatment on an in vitro GBM model. (B) Cell counting kit-8 (CCK-8) assay of the in vitro GBM model with or without low-frequency rTMS treatment. (C) Quantification of CCK-8 assay. (D) ATP assay of in vitro GBM model with or without low-frequency rTMS treatment. (E) The relative gene expression of FLNA and FLNC in the in vitro GBM model with or without low-frequency rTMS treatment, as detected by RT-qPCR. (F) Western blot analysis of FLNA and FLNC in the in vitro glioblastoma model with or without low-frequency rTMS treatment. (G) Quantification of Western blot signals for FLNA and FLNC. Values are presented as means ​± ​standard error of the mean (SEM). Statistically significant differences are shown as ∗ P ​< ​0.05, ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.

    Journal: Neurotherapeutics

    Article Title: Tumor suppressive effect of low-frequency repetitive transcranial magnetic stimulation on glioblastoma progression

    doi: 10.1016/j.neurot.2025.e00569

    Figure Lengend Snippet: Low-frequency r T MS suppresses cell proliferation by downregulating the expression of FLNA and FLNC in the in vitro GBM model. U87MG were used as the in vitro GBM model. The model was divided into two groups: a sham group (non-treated, n ​= ​4) and a low-frequency group (treated with low-frequency rTMS, n ​= ​4). (A) Schematic figure of low-frequency rTMS treatment on an in vitro GBM model. (B) Cell counting kit-8 (CCK-8) assay of the in vitro GBM model with or without low-frequency rTMS treatment. (C) Quantification of CCK-8 assay. (D) ATP assay of in vitro GBM model with or without low-frequency rTMS treatment. (E) The relative gene expression of FLNA and FLNC in the in vitro GBM model with or without low-frequency rTMS treatment, as detected by RT-qPCR. (F) Western blot analysis of FLNA and FLNC in the in vitro glioblastoma model with or without low-frequency rTMS treatment. (G) Quantification of Western blot signals for FLNA and FLNC. Values are presented as means ​± ​standard error of the mean (SEM). Statistically significant differences are shown as ∗ P ​< ​0.05, ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.

    Article Snippet: FLNA or FLNC overexpression plasmids (CAT# RC221764, CAT# RC212462) and the negative control (NC) empty pCMV6 vector (CAT# PS100001) were purchased from Origene (Rockwill, MD, USA).

    Techniques: Expressing, In Vitro, Cell Counting, CCK-8 Assay, ATP Assay, Gene Expression, Quantitative RT-PCR, Western Blot

    Low-frequency r T MS suppresses cell proliferation and sphereformation by downregulating FLNA and FLNC expression in in vitro GBM models. U87MG TS, TS15-88, and TS21-117 were used as the in vitro GBM models. Models were divided into two groups: a sham group (non-treated, n ​= ​4) and a low-frequency group (treated with low-frequency rMS, n ​= ​4). (A) In vitro GBM sphere models with or without low-frequency rTMS treatment. (B) The ratio of sphere formation in vitro with or without low-frequency rTMS treatment. (C) The sphere radius of in vitro GBM models with or without low-frequency rTMS treatment. (D) Cell counting kit-8 (CCK-8) assay of the in vitro GBM models with or without low-frequency rTMS treatment. (E) Quantification of CCK-8 assay. (F) ATP assay of in vitro GBM models with or without low-frequency rTMS treatment. (G) The relative gene expression of FLNA and FLNC in the in vitro GBM models with or without low-frequency rTMS treatment, as detected by RT-qPCR. (H) Western blot analysis of FLNA and FLNC in the in vitro GBM models with or without low-frequency rTMS treatment. (I) Quantification of Western blot signals for FLNA and FLNC. (J) Western blot analysis of FLNA and Ki-67 in the in U87MG TS transfected with FLNA or pCNV6 and with or without low-frequency rTMS treatment (K) Quantification of Western blot signals for FLNA and Ki-67. (L) Western blot analysis of FLNC and Ki-67 in U87MG TS transduced with FLNC or pCNV6 and with or without low-frequency rTMS treatment (M) Quantification of Western blot signals for FLNC and Ki-67. Values are presented as means ​± ​standard error of the mean (SEM). Statistically significant differences are shown as ∗ P ​< ​0.05, ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.

    Journal: Neurotherapeutics

    Article Title: Tumor suppressive effect of low-frequency repetitive transcranial magnetic stimulation on glioblastoma progression

    doi: 10.1016/j.neurot.2025.e00569

    Figure Lengend Snippet: Low-frequency r T MS suppresses cell proliferation and sphereformation by downregulating FLNA and FLNC expression in in vitro GBM models. U87MG TS, TS15-88, and TS21-117 were used as the in vitro GBM models. Models were divided into two groups: a sham group (non-treated, n ​= ​4) and a low-frequency group (treated with low-frequency rMS, n ​= ​4). (A) In vitro GBM sphere models with or without low-frequency rTMS treatment. (B) The ratio of sphere formation in vitro with or without low-frequency rTMS treatment. (C) The sphere radius of in vitro GBM models with or without low-frequency rTMS treatment. (D) Cell counting kit-8 (CCK-8) assay of the in vitro GBM models with or without low-frequency rTMS treatment. (E) Quantification of CCK-8 assay. (F) ATP assay of in vitro GBM models with or without low-frequency rTMS treatment. (G) The relative gene expression of FLNA and FLNC in the in vitro GBM models with or without low-frequency rTMS treatment, as detected by RT-qPCR. (H) Western blot analysis of FLNA and FLNC in the in vitro GBM models with or without low-frequency rTMS treatment. (I) Quantification of Western blot signals for FLNA and FLNC. (J) Western blot analysis of FLNA and Ki-67 in the in U87MG TS transfected with FLNA or pCNV6 and with or without low-frequency rTMS treatment (K) Quantification of Western blot signals for FLNA and Ki-67. (L) Western blot analysis of FLNC and Ki-67 in U87MG TS transduced with FLNC or pCNV6 and with or without low-frequency rTMS treatment (M) Quantification of Western blot signals for FLNC and Ki-67. Values are presented as means ​± ​standard error of the mean (SEM). Statistically significant differences are shown as ∗ P ​< ​0.05, ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.

    Article Snippet: FLNA or FLNC overexpression plasmids (CAT# RC221764, CAT# RC212462) and the negative control (NC) empty pCMV6 vector (CAT# PS100001) were purchased from Origene (Rockwill, MD, USA).

    Techniques: Expressing, In Vitro, Cell Counting, CCK-8 Assay, ATP Assay, Gene Expression, Quantitative RT-PCR, Western Blot, Transfection, Transduction

    Low-frequency rTMS suppressed tumor progression in an in vivo GBM model. The in vivo GBM model was divided into three groups: a sham group (non-treated), a low-frequency group (treated with low-frequency rTMS), and a TMZ group (treated with 30 ​mg/kg temozolomide). (A) Schematic figure of in vivo GBM model study. (B) MRI of brain tumor volume in sham, low-frequency, and TMZ groups ( n ​= ​6). (C) Tumor progression of the in vitro GBM model with or without low-frequency rTMS treatment or TMZ, as measured by tumor volume in the brain from MRI. (D) Final tumor size of the in vitro GBM model with or without low-frequency rTMS treatment, or TMZ. (E) Bioluminescence images of tumor volume on the brain of sham, low-frequency, and TMZ groups ( n ​= ​6). (F) Tumor progression of the in vitro GBM model with or without low-frequency rTMS treatment or TMZ, as measured by signal intensity of tumor mass in the brain. (G) Final signal intensity of tumor size in the in vitro GBM model with or without low-frequency rTMS treatment, or TMZ. (H) Survival rate for each group ( n ​= ​4) was estimated based on Kaplan-Meier curves. Log-rank test ( P ​= ​0.008). (I) Tumor mass stained by FLNA, FLNC and Ki67 antibody and H&E staining. (J) Quantification of cells stained with FLNA, FLNC and Ki67 antibody and H&E staining. (K) TUNEL assay in the in vivo GBM model with or without low-frequency rTMS treatment, or TMZ. (L) TUNEL assay quantification. (M) Tumor mass as stained by p -EphA, p -EGFR, p -ERK, p -JNK, p-p38, AKT, p -AKT, p-PI3K, p -mTOR, MMP2, and MMP9 antibody and H&E staining. (N) Quantification of cells stained with p -EphA, p -EGFR, p -ERK, p -JNK, p-p38, AKT, p -AKT, p-PI3K, p -mTOR, MMP2, and MMP9 staining. Values are presented as means ​± ​SEM. Scale bars ​= ​100 ​μm. Statistically significant differences are shown as ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.

    Journal: Neurotherapeutics

    Article Title: Tumor suppressive effect of low-frequency repetitive transcranial magnetic stimulation on glioblastoma progression

    doi: 10.1016/j.neurot.2025.e00569

    Figure Lengend Snippet: Low-frequency rTMS suppressed tumor progression in an in vivo GBM model. The in vivo GBM model was divided into three groups: a sham group (non-treated), a low-frequency group (treated with low-frequency rTMS), and a TMZ group (treated with 30 ​mg/kg temozolomide). (A) Schematic figure of in vivo GBM model study. (B) MRI of brain tumor volume in sham, low-frequency, and TMZ groups ( n ​= ​6). (C) Tumor progression of the in vitro GBM model with or without low-frequency rTMS treatment or TMZ, as measured by tumor volume in the brain from MRI. (D) Final tumor size of the in vitro GBM model with or without low-frequency rTMS treatment, or TMZ. (E) Bioluminescence images of tumor volume on the brain of sham, low-frequency, and TMZ groups ( n ​= ​6). (F) Tumor progression of the in vitro GBM model with or without low-frequency rTMS treatment or TMZ, as measured by signal intensity of tumor mass in the brain. (G) Final signal intensity of tumor size in the in vitro GBM model with or without low-frequency rTMS treatment, or TMZ. (H) Survival rate for each group ( n ​= ​4) was estimated based on Kaplan-Meier curves. Log-rank test ( P ​= ​0.008). (I) Tumor mass stained by FLNA, FLNC and Ki67 antibody and H&E staining. (J) Quantification of cells stained with FLNA, FLNC and Ki67 antibody and H&E staining. (K) TUNEL assay in the in vivo GBM model with or without low-frequency rTMS treatment, or TMZ. (L) TUNEL assay quantification. (M) Tumor mass as stained by p -EphA, p -EGFR, p -ERK, p -JNK, p-p38, AKT, p -AKT, p-PI3K, p -mTOR, MMP2, and MMP9 antibody and H&E staining. (N) Quantification of cells stained with p -EphA, p -EGFR, p -ERK, p -JNK, p-p38, AKT, p -AKT, p-PI3K, p -mTOR, MMP2, and MMP9 staining. Values are presented as means ​± ​SEM. Scale bars ​= ​100 ​μm. Statistically significant differences are shown as ∗∗ P ​< ​0.01, ∗∗∗ P ​< ​0.001.

    Article Snippet: FLNA or FLNC overexpression plasmids (CAT# RC221764, CAT# RC212462) and the negative control (NC) empty pCMV6 vector (CAT# PS100001) were purchased from Origene (Rockwill, MD, USA).

    Techniques: In Vivo, In Vitro, Staining, TUNEL Assay

    Fig. 10. FLNC enhances glioma cell resistance to staurosporine. (A, B) CCK8 assay assessed the effect of FLNC overexpression on the resistance of U87 and U251 cell lines to staurosporine. (C, D) CCK-8 assay demonstrated the impact of FLNC knockdown on the resistance of U87 and U251 cell lines to staurosporine. (E-H) Colony formation assay evaluated the influence of FLNC overexpression on the colony-forming ability of U87 and U251 cells under staurosporine treatment (20 nM), with representative images (E, G) (Scale bar = 50 μm) and statistical results (F, H). (I, J) In U87 and U251 cells, FLNC overexpression/knockdown modulated the inhibitory effect of staurosporine (5 nM) on the Erk and JAK2/STAT3 pathways. *P < 0.05; **P < 0.01; ***P < 0.001.

    Journal: International immunopharmacology

    Article Title: Identification of therapeutic targets and immune landscape in glioblastoma through crosstalk with glioma-associated mesenchymal stem cells.

    doi: 10.1016/j.intimp.2025.114228

    Figure Lengend Snippet: Fig. 10. FLNC enhances glioma cell resistance to staurosporine. (A, B) CCK8 assay assessed the effect of FLNC overexpression on the resistance of U87 and U251 cell lines to staurosporine. (C, D) CCK-8 assay demonstrated the impact of FLNC knockdown on the resistance of U87 and U251 cell lines to staurosporine. (E-H) Colony formation assay evaluated the influence of FLNC overexpression on the colony-forming ability of U87 and U251 cells under staurosporine treatment (20 nM), with representative images (E, G) (Scale bar = 50 μm) and statistical results (F, H). (I, J) In U87 and U251 cells, FLNC overexpression/knockdown modulated the inhibitory effect of staurosporine (5 nM) on the Erk and JAK2/STAT3 pathways. *P < 0.05; **P < 0.01; ***P < 0.001.

    Article Snippet: The membranes were blocked with 5 % non-fat milk at room temperature for 2 h and then incubated overnight at 4 ◦C with primary antibodies, including FLNC (28492–1- AP, Proteintech), Erk1/2 (11257–1-AP, Proteintech), Phospho-ERK1/2 (28733–1-AP, Proteintech), JAK2 (#3230, CST), Phospho-JAK2 (#3774, CST), STAT3 (#12640, CST), Phospho-STAT3 (#9145, CST), and GAPDH (60004–1-Ig, Proteintech).

    Techniques: CCK-8 Assay, Over Expression, Knockdown, Colony Assay