antibodies against cyclin dependent kinase cdk 2  (Proteintech)

Journal: Alzheimer's & Dementia

Article Title: Human iPSC‐derived GABAergic interneuron transplantation restores circuit balance and cognitive function in an Alzheimer's disease model

doi: 10.1002/alz.71378

Figure Lengend Snippet: Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and NOTCH inhibitors starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.

Article Snippet: From week 5 to week 7, in addition to the continued treatment with the MEK inhibitor, NOTCH inhibitors (DAPT 10 μM; HY‐13027, MCE) and cyclin‐dependent kinase (CDK) inhibitors (PD0332991 2 μM; MCE, HY‐50767) were introduced to induce cell cycle exit in the cells during this stage.

Techniques: Derivative Assay, Immunocytochemistry, Binding Assay

Journal: Cancer Biology & Therapy

Article Title: The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer

doi: 10.1080/15384047.2024.2439057

Figure Lengend Snippet: Dinaciclib decreases cell viability dose-dependent in biliary tract cancer (BTC) and one non-tumorigenic cell line. (a) Cell viability of ten malignant BTC cell lines and one non-tumorigenic (MMNK-1) cell line after treatment with increasing dinaciclib concentrations for 72 h. Lines represent the overall fit of the four-parameter logistic regression. (b) IC 50 values including 95% confidence interval (C.I.) were calculated using four-parameter logistic regression. n. d. = not determined.

Article Snippet: Cyclin-dependent kinase (Cdk) inhibitor dinaciclib as well as cisplatin were purchased from Selleckchem (Houston, TX, USA).

Techniques:

Journal: Cancer Biology & Therapy

Article Title: The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer

doi: 10.1080/15384047.2024.2439057

Figure Lengend Snippet: Dinaciclib decreases viability, ATP levels, proliferation and induces caspase activity in biliary tract cancer (BTC). (a) ATP levels of KKU-100, OCUG-1 and OZ cells after treatment with dinaciclib concentrations ranging from 0.1–100 nM for 72 h are shown. ATP levels were normalized to the untreated control [% UTC = untreated control]. (b) Time-resolved analysis of KKU-100, OCUG-1 and OZ cell viability after treatment with dinaciclib. Viability was determined after 0, 6, 24, 48 and 72 h of incubation, respectively and normalized to the respective 0 h fluorescence values [% 0 h]. (c) Proliferation of KKU-100, OCUG-1 and OZ cells after treatment with 3.125 nM, corresponding IC 50 or 100 nM dinaciclib. The cellular impedance signal was recorded continuously for 72 h using the unitless parameter cell index that is proportional to the cell number. Shown are representative curves of one biological replicate. (d) Caspase 3/7 levels were measured to detect apoptosis in KKU-100, OCUG-1 and OZ cells after treatment with 3.125 nM, IC 50 and 50 nM dinaciclib for 24, 48 and 72 h. Luminescence values were normalized to UTC [x-fold]. Data are presented as mean values ± SEM, n = 3 and significances were tested using a one-way analysis of variance (ANOVA), Dunnett **** p < .05, * p < .01, ** p < .001 and *** p < .0001.

Article Snippet: Cyclin-dependent kinase (Cdk) inhibitor dinaciclib as well as cisplatin were purchased from Selleckchem (Houston, TX, USA).

Techniques: Activity Assay, Control, Incubation, Fluorescence

Journal: Cancer Biology & Therapy

Article Title: The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer

doi: 10.1080/15384047.2024.2439057

Figure Lengend Snippet: Dinaciclib affects the proliferation and size of 3D biliary tract cancer (BTC) spheroids. Viable (A) KKU-100, (B) OCUG-1 and (C) OZ spheroid cells after 96 h stimulation with the indicated dinaciclib concentrations measured with the Promega CellTiter-Glo® 3D cell viability assay. Exemplary pictures of each treatment condition of the different cells are presented (scale bar 500 µm). Values shown indicate concentrations in nM. Data are presented as mean values ± SEM, n = 4 and significances were tested using a one-way analysis of variance (ANOVA), Dunnett’s compared to the untreated control, **** p <.05, * p <.01, ** p <.001, *** p <.0001.

Article Snippet: Cyclin-dependent kinase (Cdk) inhibitor dinaciclib as well as cisplatin were purchased from Selleckchem (Houston, TX, USA).

Techniques: Viability Assay, Control

Journal: Cancer Biology & Therapy

Article Title: The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer

doi: 10.1080/15384047.2024.2439057

Figure Lengend Snippet: Dinaciclib affects the expression of genes involved in cell proliferation and tumor progression. The expression of (a) AKT, (b) PTK2, (c) STAT3, (d) ERK and (e) EGFR from treated biliary tract cancer (BTC) cells KKU-100, OCUG-1 and OZ cells is shown each relative to untreated samples. mRNA levels were analyzed following dinaciclib treatment with the respective ½ IC 50 (KKU-100: 4 nM, OCUG-1: 16.5 nM, OZ: 3.5 nM), IC 50 (KKU-100: 8 nM, OCUG-1: 33 nM, OZ: 7 nM) and 50 nM (KKU-100) or 100 nM (OCUG-1 and OZ) for 24 h. Transcript levels were quantified using the delta delta CT method, whereas mRNA levels were first referred to the housekeeping gene GAPDH and treated samples were further normalized to controls. The fold-regulation is the negative inverse of the fold-change, and the respective thresholds for up- and downregulation are depicted as dotted lines. Data are presented as mean values ± SEM, n = 3 and significances were tested for each dinaciclib concentration against controls using a one-way analysis of variance (ANOVA), Dunnett **** p < .05, * p < .01, ** p < .001 and *** p < .0001.

Article Snippet: Cyclin-dependent kinase (Cdk) inhibitor dinaciclib as well as cisplatin were purchased from Selleckchem (Houston, TX, USA).

Techniques: Expressing, Concentration Assay

Journal: Cancer Biology & Therapy

Article Title: The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer

doi: 10.1080/15384047.2024.2439057

Figure Lengend Snippet: Dinaciclib affects the expression of proteins involved in cell proliferation and tumor progression. (A) Effect of dinaciclib on EGFR and STAT3 protein expression in KKU-100, OCUG-1 and OZ cells. Biliary tract cancer (BTC) cells were either treated with the corresponding IC 50 (KKU-100: 8 nM, OCUG-1: 33 nM, OZ: 7 nM), 50 nM (KKU-100) or 100 nM (OCUG-1 and OZ) dinaciclib for 24, 48 and 72 h, respectively. Protein expression was quantified via normalization to corresponding loading controls (figure S7), which were further referred to untreated control cells [x-fold to untreated control = UTC]. Data are presented as mean values ± SEM, n = at least 3 and significances were tested for each dinaciclib concentration against controls using a one-way analysis of variance (ANOVA), Dunnett **** p < .05, * p < .01, ** p < .001 and *** p < .0001. (B) Representative immunohistochemical staining of EGFR and STAT3 in the three naïve (untreated) BTC cell lines KKU-100, OCUG-1 and OZ (magnification 400×) showing heterogeneous but overall medium to high expression levels of EGFR and STAT3 in the three BTC cell lines. Data are presented as mean ± SEM of three different areas of the cell blocks.

Article Snippet: Cyclin-dependent kinase (Cdk) inhibitor dinaciclib as well as cisplatin were purchased from Selleckchem (Houston, TX, USA).

Techniques: Expressing, Control, Concentration Assay, Immunohistochemical staining, Staining

Journal: Cancer Biology & Therapy

Article Title: The Cdk inhibitor dinaciclib as a promising anti-tumorigenic agent in biliary tract cancer

doi: 10.1080/15384047.2024.2439057

Figure Lengend Snippet: Dinaciclib reduces the expression of the anti-apoptotic protein Mcl-1 and the phosphorylation at Ser64. Effect of dinaciclib on (A) Mcl-1 and (B) phospho-Mcl-1 (Ser64) protein expression in KKU-100, OCUG-1 and OZ cells. Biliary tract cancer (BTC) cells were either treated with the corresponding IC 50 (KKU-100: 8 nM, OCUG-1: 33 nM, OZ: 7 nM), 50 nM (KKU-100) or 100 nM (OCUG-1 and OZ) dinaciclib for 24, 48 and 72 h, respectively. Protein expression was quantified via normalization to corresponding loading controls (figure S7), which were further referred to untreated control cells [x-fold to untreated control = UTC]. Data are presented as mean values ± SEM, n = at least 3 and significances were tested for each dinaciclib concentration against controls using a one-way analysis of variance (ANOVA), Dunnett **** p < .05, * p < .01, ** p < .001 and *** p < .0001.

Article Snippet: Cyclin-dependent kinase (Cdk) inhibitor dinaciclib as well as cisplatin were purchased from Selleckchem (Houston, TX, USA).

Techniques: Expressing, Phospho-proteomics, Control, Concentration Assay