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cdk5 inhibitor 20 233  (MedChemExpress)


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    Structured Review

    MedChemExpress cdk5 inhibitor 20 233
    ( A ) Phosphorylated and total ERK (pERK and ERK, respectively) were detected in 293 T cells expressing CD4-mCherry (Control), TMPRSS2-mCherry (TM2-WT), TMPRSS2-dCT-mCherry (TM2-dCT), or TMPRSS2-S441A-mCherry (TM2-S441A) at the indicated time (h) post-transfection by immunoblotting analysis. The ratio of pERK to total ERK at 0 hr was set as 1, and the ratio of pERK to total ERK at each time point to that is shown in the graph (the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). The samples were obtained from the same experiment, and the gels and blots were processed in parallel. The results of Student’s t tests for the value of Ctrl at each time point are shown above the points. ( B ) IPA analysis of differentially expressed proteins between TM2-WT- and TM2-S441A-transfected 293T cells. ( C ) Experimental scheme for ( D , E ). ( D ) Inhibition of TM2-induced Golgi disruption using ERK or CDK inhibitors was analyzed in 293T cells, transfected with Golgi-YFP (green) and TM2-WT (red), and cultured for 24 h in the presence of 200 μM nafamostat. After removing nafamostat, the cells were cultured with the indicated concentrations of ERK or <t>CDK5</t> inhibitor for 180 min before undergoing fixation. ( E ) Quantitative analysis of the images. Sixty cells were randomly selected from at least three independent images and plotted. Representative data from three independent experiments are shown. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars. .
    Cdk5 Inhibitor 20 233, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cdk5/CDK5+inhibitor+20-223/pmc13303877-204-0-4
    Average 94 stars, based on 4 article reviews
    cdk5 inhibitor 20 233 - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "TMPRSS2-induced Golgi disruption restricts the incorporation of virus envelope glycoproteins into virions"

    Article Title: TMPRSS2-induced Golgi disruption restricts the incorporation of virus envelope glycoproteins into virions

    Journal: EMBO Reports

    doi: 10.1038/s44319-026-00797-2

    ( A ) Phosphorylated and total ERK (pERK and ERK, respectively) were detected in 293 T cells expressing CD4-mCherry (Control), TMPRSS2-mCherry (TM2-WT), TMPRSS2-dCT-mCherry (TM2-dCT), or TMPRSS2-S441A-mCherry (TM2-S441A) at the indicated time (h) post-transfection by immunoblotting analysis. The ratio of pERK to total ERK at 0 hr was set as 1, and the ratio of pERK to total ERK at each time point to that is shown in the graph (the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). The samples were obtained from the same experiment, and the gels and blots were processed in parallel. The results of Student’s t tests for the value of Ctrl at each time point are shown above the points. ( B ) IPA analysis of differentially expressed proteins between TM2-WT- and TM2-S441A-transfected 293T cells. ( C ) Experimental scheme for ( D , E ). ( D ) Inhibition of TM2-induced Golgi disruption using ERK or CDK inhibitors was analyzed in 293T cells, transfected with Golgi-YFP (green) and TM2-WT (red), and cultured for 24 h in the presence of 200 μM nafamostat. After removing nafamostat, the cells were cultured with the indicated concentrations of ERK or CDK5 inhibitor for 180 min before undergoing fixation. ( E ) Quantitative analysis of the images. Sixty cells were randomly selected from at least three independent images and plotted. Representative data from three independent experiments are shown. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars. .
    Figure Legend Snippet: ( A ) Phosphorylated and total ERK (pERK and ERK, respectively) were detected in 293 T cells expressing CD4-mCherry (Control), TMPRSS2-mCherry (TM2-WT), TMPRSS2-dCT-mCherry (TM2-dCT), or TMPRSS2-S441A-mCherry (TM2-S441A) at the indicated time (h) post-transfection by immunoblotting analysis. The ratio of pERK to total ERK at 0 hr was set as 1, and the ratio of pERK to total ERK at each time point to that is shown in the graph (the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). The samples were obtained from the same experiment, and the gels and blots were processed in parallel. The results of Student’s t tests for the value of Ctrl at each time point are shown above the points. ( B ) IPA analysis of differentially expressed proteins between TM2-WT- and TM2-S441A-transfected 293T cells. ( C ) Experimental scheme for ( D , E ). ( D ) Inhibition of TM2-induced Golgi disruption using ERK or CDK inhibitors was analyzed in 293T cells, transfected with Golgi-YFP (green) and TM2-WT (red), and cultured for 24 h in the presence of 200 μM nafamostat. After removing nafamostat, the cells were cultured with the indicated concentrations of ERK or CDK5 inhibitor for 180 min before undergoing fixation. ( E ) Quantitative analysis of the images. Sixty cells were randomly selected from at least three independent images and plotted. Representative data from three independent experiments are shown. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars. .

    Techniques Used: Expressing, Control, Transfection, Western Blot, Inhibition, Disruption, Cell Culture

    ( A ) Inhibition of TMPRSS2-induced Golgi disruption using ERK or CDK inhibitors, analyzed in 293T cells, transfected with Golgi-YFP (green) and TMPRSS2-WT-mCherry (TM2-WT-Cherry, red) and cultured for 24 h with 200 μM nafamostat. After removing nafamostat, cells were cultured with 20 μM ERK (20-233) or CDK1 (Ro 3306) inhibitors for 180 min before fixation. Scale bars indicate 10 μm. ( B ) Quantitative analysis of Golgi disruption in the images. Forty cells were randomly selected from at least three independent images and plotted. Representative data from two independent experiments are shown. ( C ) Immunoblotting analysis of CoV-2-S pseudotyped lentiviruses in 293T cells expressing CD4 (Ctrl), or TMPRSS2 (TM2) with or without 50 μM of ERK inhibitor. The ratio of CoV-2-S2 to p24 was calculated based on band density (right, the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). ( D ) Inhibition of TM2 function by CoV-2-E. Luciferase activity for the infectivity of CoV-2-S pseudotyped lentiviruses produced in CD4-mCherry- (CD4)-, or TMPRSS2-mCherry- (TM2)-, and CoV-2-E or CoV-2-EdN14 expressing 293 T cells (the quantified results from a representative experiment in the two experiments independently conducted are expressed as mean ± SEM, n = 6). ( E ) Immunofluorescence analysis of Golgi-YFP (green) and CoV-2-E (blue) in CD4-mCherry (CD4-Cherry)-, TMPRSS2-WT-mCherry (TM2-WT-Cherry)-, TMPRSS2-dCT-mCherry (TM2-dCT-Cherry)-, or TMPRSS2-S441A-mCherry (TM2-S441A-Cherry)-expressing 293T cells cultured with CoV-2-E inhibitory peptide (+) or control peptide (−) at 24 h post-transfection. ( F ) Immunofluorescence analysis for CoV-2-S structural changes using anti-CoV-2-S2 (1A9, green) antibodies in CoV-2-S and CoV-2-E (blue) in CD4-Cherry-, TM2-WT-Cherry, TM2-dCT-Cherry, or TM2-S441A-Cherry (red) -expressing 293 T cells cultured with CoV-2-E inhibitory peptide (+) or control peptide (−) at 24 h post-transfection. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars.
    Figure Legend Snippet: ( A ) Inhibition of TMPRSS2-induced Golgi disruption using ERK or CDK inhibitors, analyzed in 293T cells, transfected with Golgi-YFP (green) and TMPRSS2-WT-mCherry (TM2-WT-Cherry, red) and cultured for 24 h with 200 μM nafamostat. After removing nafamostat, cells were cultured with 20 μM ERK (20-233) or CDK1 (Ro 3306) inhibitors for 180 min before fixation. Scale bars indicate 10 μm. ( B ) Quantitative analysis of Golgi disruption in the images. Forty cells were randomly selected from at least three independent images and plotted. Representative data from two independent experiments are shown. ( C ) Immunoblotting analysis of CoV-2-S pseudotyped lentiviruses in 293T cells expressing CD4 (Ctrl), or TMPRSS2 (TM2) with or without 50 μM of ERK inhibitor. The ratio of CoV-2-S2 to p24 was calculated based on band density (right, the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). ( D ) Inhibition of TM2 function by CoV-2-E. Luciferase activity for the infectivity of CoV-2-S pseudotyped lentiviruses produced in CD4-mCherry- (CD4)-, or TMPRSS2-mCherry- (TM2)-, and CoV-2-E or CoV-2-EdN14 expressing 293 T cells (the quantified results from a representative experiment in the two experiments independently conducted are expressed as mean ± SEM, n = 6). ( E ) Immunofluorescence analysis of Golgi-YFP (green) and CoV-2-E (blue) in CD4-mCherry (CD4-Cherry)-, TMPRSS2-WT-mCherry (TM2-WT-Cherry)-, TMPRSS2-dCT-mCherry (TM2-dCT-Cherry)-, or TMPRSS2-S441A-mCherry (TM2-S441A-Cherry)-expressing 293T cells cultured with CoV-2-E inhibitory peptide (+) or control peptide (−) at 24 h post-transfection. ( F ) Immunofluorescence analysis for CoV-2-S structural changes using anti-CoV-2-S2 (1A9, green) antibodies in CoV-2-S and CoV-2-E (blue) in CD4-Cherry-, TM2-WT-Cherry, TM2-dCT-Cherry, or TM2-S441A-Cherry (red) -expressing 293 T cells cultured with CoV-2-E inhibitory peptide (+) or control peptide (−) at 24 h post-transfection. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars.

    Techniques Used: Inhibition, Disruption, Transfection, Cell Culture, Western Blot, Expressing, Luciferase, Activity Assay, Infection, Produced, Immunofluorescence, Control

    Related Articles

    Infection:

    Article Title: Neuronal double-stranded DNA accumulation induced by DNase II deficiency drives tau phosphorylation and neurodegeneration
    Article Snippet: .. Meanwhile, at 48 h after infection, the cells were treated with 2.5 μM roscovitine [ ] (MedChemExpress, #HY-30237) for 24 h to inhibit CDK5, or 5 μM DT061 [ ] (MedChemExpress, #HY-112929) for 24 h to activate PP2A. .. Then the cells were harvested in an ice-cold RIPA lysis solution (MedChemExpress, #HY-K1001) with 1 mM phenylmethylsulfonyl fluoride, protease inhibitor cocktail set I (Millipore, Billerica, MA, #539131), and 1% ( v / v ) phosphatase inhibitor cocktails (Solarbio Left Sciences, Beijing, China, #P1260).

    Article Title: Neuronal double-stranded DNA accumulation induced by DNase II deficiency drives tau phosphorylation and neurodegeneration.
    Article Snippet: .. Meanwhile, at 48 h after infection, the cells were treated with 2.5 μM roscovitine [28] (MedChemExpress, #HY-30237) for 24 h to inhibit CDK5, or 5 μM DT061 [29] (MedChemExpress, #HY-112929) for 24 h to activate PP2A. .. Then the cells were harvested in an ice-cold RIPA lysis solution (MedChemExpress, #HYK1001) with 1 mM phenylmethylsulfonyl fluoride, protease inhibitor cocktail set I (Millipore, Billerica, MA, #539131), and 1% (v/v) phosphatase inhibitor cocktails (Solarbio Left Sciences, Beijing, China, #P1260).

    Cell Culture:

    Article Title: Gestational dexamethasone exposure impacts hippocampal excitatory synaptic transmission and learning and memory function with transgenerational effects
    Article Snippet: .. To confirm the role of the glucocorticoid receptor (GR), miR-133a-3p and CDK5, the cells were cultured for 3 days with 500 nmol/L DEX and (or) 2.5 μmol/L RU486 (HY-13683, MedchemExpress Biotechnology Inc., USA, a GR antagonist), 500 nmol/L DEX and (or) 10 μmol/L miR -133a-3p inhibitor (RiboBio Technology, Guangzhou, China), or 500 nmol/L DEX and (or) 25 μmol/L Roscovitine (HY-B0231, Medchem Express Biotechnology Inc., a CDK5 inhibitor), respectively, and harvested for subsequent analysis. ..

    In Vitro:

    Article Title: CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling.
    Article Snippet: .. To evaluate in vitro the role of CDK5 in DP1 degradation by ubiquitination, MKN45 cells were treated with MG-132 (10 mmol/L; MedChemExpress, Shanghai, China) for 6 h. The total cell lysates were immunoprecipitated with an anti-DP1 antibody overnight and subsequently rotated and incubated with protein A/G beads for 2–4 h at 4 °C. ..

    Article Title: CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling
    Article Snippet: .. To evaluate in vitro the role of CDK5 in DP1 degradation by ubiquitination, MKN45 cells were treated with MG-132 (10 mmol/L; MedChemExpress, Shanghai, China) for 6 h. The total cell lysates were immunoprecipitated with an anti-DP1 antibody overnight and subsequently rotated and incubated with protein A/G beads for 2–4 h at 4 °C. ..

    Ubiquitin Proteomics:

    Article Title: CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling.
    Article Snippet: .. To evaluate in vitro the role of CDK5 in DP1 degradation by ubiquitination, MKN45 cells were treated with MG-132 (10 mmol/L; MedChemExpress, Shanghai, China) for 6 h. The total cell lysates were immunoprecipitated with an anti-DP1 antibody overnight and subsequently rotated and incubated with protein A/G beads for 2–4 h at 4 °C. ..

    Article Title: CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling
    Article Snippet: .. To evaluate in vitro the role of CDK5 in DP1 degradation by ubiquitination, MKN45 cells were treated with MG-132 (10 mmol/L; MedChemExpress, Shanghai, China) for 6 h. The total cell lysates were immunoprecipitated with an anti-DP1 antibody overnight and subsequently rotated and incubated with protein A/G beads for 2–4 h at 4 °C. ..

    Immunoprecipitation:

    Article Title: CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling.
    Article Snippet: .. To evaluate in vitro the role of CDK5 in DP1 degradation by ubiquitination, MKN45 cells were treated with MG-132 (10 mmol/L; MedChemExpress, Shanghai, China) for 6 h. The total cell lysates were immunoprecipitated with an anti-DP1 antibody overnight and subsequently rotated and incubated with protein A/G beads for 2–4 h at 4 °C. ..

    Article Title: CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling
    Article Snippet: .. To evaluate in vitro the role of CDK5 in DP1 degradation by ubiquitination, MKN45 cells were treated with MG-132 (10 mmol/L; MedChemExpress, Shanghai, China) for 6 h. The total cell lysates were immunoprecipitated with an anti-DP1 antibody overnight and subsequently rotated and incubated with protein A/G beads for 2–4 h at 4 °C. ..

    Incubation:

    Article Title: CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling.
    Article Snippet: .. To evaluate in vitro the role of CDK5 in DP1 degradation by ubiquitination, MKN45 cells were treated with MG-132 (10 mmol/L; MedChemExpress, Shanghai, China) for 6 h. The total cell lysates were immunoprecipitated with an anti-DP1 antibody overnight and subsequently rotated and incubated with protein A/G beads for 2–4 h at 4 °C. ..

    Article Title: CDK5 promotes apoptosis and attenuates chemoresistance in gastric cancer via E2F1 signaling
    Article Snippet: .. To evaluate in vitro the role of CDK5 in DP1 degradation by ubiquitination, MKN45 cells were treated with MG-132 (10 mmol/L; MedChemExpress, Shanghai, China) for 6 h. The total cell lysates were immunoprecipitated with an anti-DP1 antibody overnight and subsequently rotated and incubated with protein A/G beads for 2–4 h at 4 °C. ..



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    ( A ) Phosphorylated and total ERK (pERK and ERK, respectively) were detected in 293 T cells expressing CD4-mCherry (Control), TMPRSS2-mCherry (TM2-WT), TMPRSS2-dCT-mCherry (TM2-dCT), or TMPRSS2-S441A-mCherry (TM2-S441A) at the indicated time (h) post-transfection by immunoblotting analysis. The ratio of pERK to total ERK at 0 hr was set as 1, and the ratio of pERK to total ERK at each time point to that is shown in the graph (the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). The samples were obtained from the same experiment, and the gels and blots were processed in parallel. The results of Student’s t tests for the value of Ctrl at each time point are shown above the points. ( B ) IPA analysis of differentially expressed proteins between TM2-WT- and TM2-S441A-transfected 293T cells. ( C ) Experimental scheme for ( D , E ). ( D ) Inhibition of TM2-induced Golgi disruption using ERK or CDK inhibitors was analyzed in 293T cells, transfected with Golgi-YFP (green) and TM2-WT (red), and cultured for 24 h in the presence of 200 μM nafamostat. After removing nafamostat, the cells were cultured with the indicated concentrations of ERK or CDK5 inhibitor for 180 min before undergoing fixation. ( E ) Quantitative analysis of the images. Sixty cells were randomly selected from at least three independent images and plotted. Representative data from three independent experiments are shown. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars. .

    Journal: EMBO Reports

    Article Title: TMPRSS2-induced Golgi disruption restricts the incorporation of virus envelope glycoproteins into virions

    doi: 10.1038/s44319-026-00797-2

    Figure Lengend Snippet: ( A ) Phosphorylated and total ERK (pERK and ERK, respectively) were detected in 293 T cells expressing CD4-mCherry (Control), TMPRSS2-mCherry (TM2-WT), TMPRSS2-dCT-mCherry (TM2-dCT), or TMPRSS2-S441A-mCherry (TM2-S441A) at the indicated time (h) post-transfection by immunoblotting analysis. The ratio of pERK to total ERK at 0 hr was set as 1, and the ratio of pERK to total ERK at each time point to that is shown in the graph (the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). The samples were obtained from the same experiment, and the gels and blots were processed in parallel. The results of Student’s t tests for the value of Ctrl at each time point are shown above the points. ( B ) IPA analysis of differentially expressed proteins between TM2-WT- and TM2-S441A-transfected 293T cells. ( C ) Experimental scheme for ( D , E ). ( D ) Inhibition of TM2-induced Golgi disruption using ERK or CDK inhibitors was analyzed in 293T cells, transfected with Golgi-YFP (green) and TM2-WT (red), and cultured for 24 h in the presence of 200 μM nafamostat. After removing nafamostat, the cells were cultured with the indicated concentrations of ERK or CDK5 inhibitor for 180 min before undergoing fixation. ( E ) Quantitative analysis of the images. Sixty cells were randomly selected from at least three independent images and plotted. Representative data from three independent experiments are shown. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars. .

    Article Snippet: CDK5 inhibitor 20-233 , MCE , HY-123772.

    Techniques: Expressing, Control, Transfection, Western Blot, Inhibition, Disruption, Cell Culture

    ( A ) Inhibition of TMPRSS2-induced Golgi disruption using ERK or CDK inhibitors, analyzed in 293T cells, transfected with Golgi-YFP (green) and TMPRSS2-WT-mCherry (TM2-WT-Cherry, red) and cultured for 24 h with 200 μM nafamostat. After removing nafamostat, cells were cultured with 20 μM ERK (20-233) or CDK1 (Ro 3306) inhibitors for 180 min before fixation. Scale bars indicate 10 μm. ( B ) Quantitative analysis of Golgi disruption in the images. Forty cells were randomly selected from at least three independent images and plotted. Representative data from two independent experiments are shown. ( C ) Immunoblotting analysis of CoV-2-S pseudotyped lentiviruses in 293T cells expressing CD4 (Ctrl), or TMPRSS2 (TM2) with or without 50 μM of ERK inhibitor. The ratio of CoV-2-S2 to p24 was calculated based on band density (right, the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). ( D ) Inhibition of TM2 function by CoV-2-E. Luciferase activity for the infectivity of CoV-2-S pseudotyped lentiviruses produced in CD4-mCherry- (CD4)-, or TMPRSS2-mCherry- (TM2)-, and CoV-2-E or CoV-2-EdN14 expressing 293 T cells (the quantified results from a representative experiment in the two experiments independently conducted are expressed as mean ± SEM, n = 6). ( E ) Immunofluorescence analysis of Golgi-YFP (green) and CoV-2-E (blue) in CD4-mCherry (CD4-Cherry)-, TMPRSS2-WT-mCherry (TM2-WT-Cherry)-, TMPRSS2-dCT-mCherry (TM2-dCT-Cherry)-, or TMPRSS2-S441A-mCherry (TM2-S441A-Cherry)-expressing 293T cells cultured with CoV-2-E inhibitory peptide (+) or control peptide (−) at 24 h post-transfection. ( F ) Immunofluorescence analysis for CoV-2-S structural changes using anti-CoV-2-S2 (1A9, green) antibodies in CoV-2-S and CoV-2-E (blue) in CD4-Cherry-, TM2-WT-Cherry, TM2-dCT-Cherry, or TM2-S441A-Cherry (red) -expressing 293 T cells cultured with CoV-2-E inhibitory peptide (+) or control peptide (−) at 24 h post-transfection. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars.

    Journal: EMBO Reports

    Article Title: TMPRSS2-induced Golgi disruption restricts the incorporation of virus envelope glycoproteins into virions

    doi: 10.1038/s44319-026-00797-2

    Figure Lengend Snippet: ( A ) Inhibition of TMPRSS2-induced Golgi disruption using ERK or CDK inhibitors, analyzed in 293T cells, transfected with Golgi-YFP (green) and TMPRSS2-WT-mCherry (TM2-WT-Cherry, red) and cultured for 24 h with 200 μM nafamostat. After removing nafamostat, cells were cultured with 20 μM ERK (20-233) or CDK1 (Ro 3306) inhibitors for 180 min before fixation. Scale bars indicate 10 μm. ( B ) Quantitative analysis of Golgi disruption in the images. Forty cells were randomly selected from at least three independent images and plotted. Representative data from two independent experiments are shown. ( C ) Immunoblotting analysis of CoV-2-S pseudotyped lentiviruses in 293T cells expressing CD4 (Ctrl), or TMPRSS2 (TM2) with or without 50 μM of ERK inhibitor. The ratio of CoV-2-S2 to p24 was calculated based on band density (right, the quantified results are expressed as mean ± SEM of three separate experiments, n = 3). ( D ) Inhibition of TM2 function by CoV-2-E. Luciferase activity for the infectivity of CoV-2-S pseudotyped lentiviruses produced in CD4-mCherry- (CD4)-, or TMPRSS2-mCherry- (TM2)-, and CoV-2-E or CoV-2-EdN14 expressing 293 T cells (the quantified results from a representative experiment in the two experiments independently conducted are expressed as mean ± SEM, n = 6). ( E ) Immunofluorescence analysis of Golgi-YFP (green) and CoV-2-E (blue) in CD4-mCherry (CD4-Cherry)-, TMPRSS2-WT-mCherry (TM2-WT-Cherry)-, TMPRSS2-dCT-mCherry (TM2-dCT-Cherry)-, or TMPRSS2-S441A-mCherry (TM2-S441A-Cherry)-expressing 293T cells cultured with CoV-2-E inhibitory peptide (+) or control peptide (−) at 24 h post-transfection. ( F ) Immunofluorescence analysis for CoV-2-S structural changes using anti-CoV-2-S2 (1A9, green) antibodies in CoV-2-S and CoV-2-E (blue) in CD4-Cherry-, TM2-WT-Cherry, TM2-dCT-Cherry, or TM2-S441A-Cherry (red) -expressing 293 T cells cultured with CoV-2-E inhibitory peptide (+) or control peptide (−) at 24 h post-transfection. Scale bars indicate 50 μm. The results of Student’s t tests are shown above the bars.

    Article Snippet: CDK5 inhibitor 20-233 , MCE , HY-123772.

    Techniques: Inhibition, Disruption, Transfection, Cell Culture, Western Blot, Expressing, Luciferase, Activity Assay, Infection, Produced, Immunofluorescence, Control

    Mechanism of integrin receptor activation induced by membrane receptor switch. A) Schematic representation of Calpain protein activity verified using fluorophores. B) The effectiveness of the fluorescence method was verified based on different groups. C) Calpain protein activity in MSCs subjected to different treatments. D) The expression of CDK5 and p-Talin head detected by Western blot analysis. E) Quantitative analysis of the Western blot results for the CDK5 and p-Talin head protein. F) The expression of p-Talin head and p-Talin detected by Western blot analysis. G) Quantitative analysis of the Western blot results for the p-Talin head protein. H) Quantitative analysis of the Western blot results for the p-Talin protein. I) Schematic diagram of Talin head and integrin β interaction verified by SPR technique. J) The association-dissociation curves of Talin head and integrin β1. K) Integrin β1 activation was verified by flow cytometry. L) Quantitative analysis of fluorescence intensity by flow cytometry. M) The expression of FAK and p-FAK detected by Western blot analysis. N) The quantification of FAK phosphorylation levels. O) Mechanism of integrin receptor activation induced by membrane receptor switch. (∗ symbol represents comparison with HAMA group, # symbol represents comparison with OBNC group). (ns: non-significant, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ## P < 0.01, ### P < 0.001).

    Journal: Bioactive Materials

    Article Title: Mechanically sensitized hydrogel microspheres trigger membrane receptor switch for cartilage repair

    doi: 10.1016/j.bioactmat.2026.03.017

    Figure Lengend Snippet: Mechanism of integrin receptor activation induced by membrane receptor switch. A) Schematic representation of Calpain protein activity verified using fluorophores. B) The effectiveness of the fluorescence method was verified based on different groups. C) Calpain protein activity in MSCs subjected to different treatments. D) The expression of CDK5 and p-Talin head detected by Western blot analysis. E) Quantitative analysis of the Western blot results for the CDK5 and p-Talin head protein. F) The expression of p-Talin head and p-Talin detected by Western blot analysis. G) Quantitative analysis of the Western blot results for the p-Talin head protein. H) Quantitative analysis of the Western blot results for the p-Talin protein. I) Schematic diagram of Talin head and integrin β interaction verified by SPR technique. J) The association-dissociation curves of Talin head and integrin β1. K) Integrin β1 activation was verified by flow cytometry. L) Quantitative analysis of fluorescence intensity by flow cytometry. M) The expression of FAK and p-FAK detected by Western blot analysis. N) The quantification of FAK phosphorylation levels. O) Mechanism of integrin receptor activation induced by membrane receptor switch. (∗ symbol represents comparison with HAMA group, # symbol represents comparison with OBNC group). (ns: non-significant, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ## P < 0.01, ### P < 0.001).

    Article Snippet: TRPC1 inhibitor (0.3 nM, Pico145, CAS No. 1628287-16-0), TRPM7 inhibitor (1.0 μM, VPC4, CAS No. 945604-76-2), TRPV2 inhibitor (5.0 μM, compound IV2-1, CAS No. 2242724-49-6), TRPM4 inhibitor (1.5 μM, CBA, CAS No. 351424-20-9), PIEZO1 inhibitor (2.5 μM, GsMTx4, CAS No. 1209500-46-8), integrin αvβ5 inhibitor (8.0 nM, Compound 12, CAS No.: 2615912-33-7), integrin αvβ1 inhibitor (0.3 nM, Compound C8, CAS No. 1689540-62-2), integrin α5β1 inhibitor (10 μM, ATN-161, 904763-27-5), and CDK5 inhibitor (5 nM, CDK5-IN-1, 2,639,540-19-3) were purchased from MCE Biotechnology Co., LTD. After the MSCs were treated, the cRGD solution was added at a concentration of 1:200 and incubated in the dark for 15 min, and the results were observed by fluorescence microscopy.

    Techniques: Activation Assay, Membrane, Activity Assay, Fluorescence, Expressing, Western Blot, Flow Cytometry, Phospho-proteomics, Comparison

    CDK5 as a target of miR-142-5p and its positive correlation with FGD5-AS1 expression. A qRT-PCR analysis of CDK5 expression levels in ESCC tissues and Adjacent tissue samples. ** p < 0.01; B Pearson correlation analysis of CDK5 and miR-142-5p expression levels. C - D qRT-PCR and Western blot analysis of CDK5 mRNA and protein expression levels in cells overexpressing or knocking down miR-142-5p. ** p < 0.01 vs. NC mimics; # p < 0.05, ## p < 0.01; E Predicted target sequences of CDK5 and miR-142-5p. F Dual-luciferase reporter assay validating the interaction between CDK5 and miR-142-5p. ** p < 0.01; G Pearson correlation analysis of FGD5-AS1 and CDK5 expression levels. H - I qRT-PCR and Western blot analysis of CDK5 expression levels in cells overexpressing or knocking down FGD5-AS1. * p < 0.05, ** p < 0.01

    Journal: World Journal of Surgical Oncology

    Article Title: The FGD5-AS1/miR-142-5p/CDK5 axis promotes ESCC progression by regulating mitochondrial fission and mitophagy: insights from integrative bioinformatics and experimental analyses

    doi: 10.1186/s12957-026-04338-y

    Figure Lengend Snippet: CDK5 as a target of miR-142-5p and its positive correlation with FGD5-AS1 expression. A qRT-PCR analysis of CDK5 expression levels in ESCC tissues and Adjacent tissue samples. ** p < 0.01; B Pearson correlation analysis of CDK5 and miR-142-5p expression levels. C - D qRT-PCR and Western blot analysis of CDK5 mRNA and protein expression levels in cells overexpressing or knocking down miR-142-5p. ** p < 0.01 vs. NC mimics; # p < 0.05, ## p < 0.01; E Predicted target sequences of CDK5 and miR-142-5p. F Dual-luciferase reporter assay validating the interaction between CDK5 and miR-142-5p. ** p < 0.01; G Pearson correlation analysis of FGD5-AS1 and CDK5 expression levels. H - I qRT-PCR and Western blot analysis of CDK5 expression levels in cells overexpressing or knocking down FGD5-AS1. * p < 0.05, ** p < 0.01

    Article Snippet: After transfer, 5% non-fat milk was used to block the membranes at room temperature for 1 h. Overnight incubation at 4 °C was performed with primary antibodies against MFN1 (A21293), MFN2 (A19678), Drp1 (A2705), BECN1 (A21191), P62 (A19700), PINK1 (A25301), Parkin (A0968), CDK5 (A2689) (all 1:1000; ABclonal, China), p-Drp1 (3455), LC3-II (3868), LC3-I (4599) (all 1:1000; CST, USA), and β-actin (1:50000, AC026, ABclonal, China).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Luciferase, Reporter Assay

    The FGD5-AS1/miR-142-5p/CDK5 axis influences ESCC progression. A Western blot analysis of CDK5 protein levels in shNC, sh-FGD5-AS1, sh-FGD5-AS1 + miR-142-5p inhibitor, and sh-FGD5-AS1 + OE-CDK5 groups of KYSE150 cells. B MTT assay of cell viability in the four groups. C TUNEL assay of apoptosis levels in the four groups. D Transwell assay of invasion capabilities in the four groups. E Scratch assay of migration capabilities in the four groups. F JC-1 assay of mitochondrial membrane potential in the four groups. G ATP assay of ATP levels in the four groups. H Western blot analysis of MFN1, MFN2, Drp1, and p-Drp1 protein levels in the four groups. I Western blot analysis of LC3-II, LC3-I, BECN1, P62, PINK1, and Parkin protein levels in the four groups. ** p < 0.01 vs. Control, ; ## p < 0.01 vs. sh-FGD5-AS1

    Journal: World Journal of Surgical Oncology

    Article Title: The FGD5-AS1/miR-142-5p/CDK5 axis promotes ESCC progression by regulating mitochondrial fission and mitophagy: insights from integrative bioinformatics and experimental analyses

    doi: 10.1186/s12957-026-04338-y

    Figure Lengend Snippet: The FGD5-AS1/miR-142-5p/CDK5 axis influences ESCC progression. A Western blot analysis of CDK5 protein levels in shNC, sh-FGD5-AS1, sh-FGD5-AS1 + miR-142-5p inhibitor, and sh-FGD5-AS1 + OE-CDK5 groups of KYSE150 cells. B MTT assay of cell viability in the four groups. C TUNEL assay of apoptosis levels in the four groups. D Transwell assay of invasion capabilities in the four groups. E Scratch assay of migration capabilities in the four groups. F JC-1 assay of mitochondrial membrane potential in the four groups. G ATP assay of ATP levels in the four groups. H Western blot analysis of MFN1, MFN2, Drp1, and p-Drp1 protein levels in the four groups. I Western blot analysis of LC3-II, LC3-I, BECN1, P62, PINK1, and Parkin protein levels in the four groups. ** p < 0.01 vs. Control, ; ## p < 0.01 vs. sh-FGD5-AS1

    Article Snippet: After transfer, 5% non-fat milk was used to block the membranes at room temperature for 1 h. Overnight incubation at 4 °C was performed with primary antibodies against MFN1 (A21293), MFN2 (A19678), Drp1 (A2705), BECN1 (A21191), P62 (A19700), PINK1 (A25301), Parkin (A0968), CDK5 (A2689) (all 1:1000; ABclonal, China), p-Drp1 (3455), LC3-II (3868), LC3-I (4599) (all 1:1000; CST, USA), and β-actin (1:50000, AC026, ABclonal, China).

    Techniques: Western Blot, MTT Assay, TUNEL Assay, Transwell Assay, Wound Healing Assay, Migration, Membrane, ATP Assay, Control