cdk dinaciclib (MedChemExpress)
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cdk dinaciclib
Cdk Dinaciclib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 57 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cdk+dinaciclib/Dinaciclib/pm41152886-217-0-8
Average 95 stars, based on 57 article reviews
Cdk Dinaciclib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 57 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cdk+dinaciclib/Dinaciclib/pm41152886-217-0-8
Average 95 stars, based on 57 article reviews
cdk dinaciclib - by Bioz Stars,
2026-10
95/100 stars
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In Vitro:Article Title: STAT3 S727 phosphorylation drives pathogenic Th17 differentiation and neuroinflammation in autoimmune disease Article Snippet: Skewing conditions were as follows: npTh17: 2.5 ng/ml rhTGF-β1 (Biolegend) plus 20 ng/ml rmIL-6 (BIolegend); Th1: 20 ng/ml rmIL-12 plus 20 ng/ml rmIL-2; Th2: 20 ng/ml rmIL-4, 20 ng/ml rmIL-2 plus 10 μg/ml anti-IFNγ; iTreg polarization: 3 ng/ml rhTGF-β1 (Biolegend); pTh17: 40 ng/ml rmIL-6, rmIL-23 and IL-1β (BIolegend). .. Article Title: STAT3 S727 phosphorylation drives pathogenic Th17 differentiation and neuroinflammation in autoimmune disease. Article Snippet: Skewing conditions were as follows: npTh17: 2.5 ng/ml rhTGF-β1 (Biolegend) plus 20 ng/ml rmIL-6 (BIolegend); Th1: 20 ng/ml rmIL-12 plus 20 ng/ml rmIL-2; Th2: 20 ng/ml rmIL-4, 20 ng/ml rmIL-2 plus 10 μg/ml anti-IFNγ; iTreg polarization: 3 ng/ml rhTGF-β1 (Biolegend); pTh17: 40 ng/ml rmIL-6, rmIL-23 and IL-1β (BIolegend). .. |
![Figure 7. 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 IC50 (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.](https://pub-med-unpaywalled-images-cdn.bioz.com/pub_med_ids_ending_with_8430/pm39668430/pm39668430__page10_image1.jpg)
![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.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9727/pmc11789727/pmc11789727__KCBT_A_2439057_F0004_OC.jpg)
![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.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9727/pmc11789727/pmc11789727__KCBT_A_2439057_F0007_OC.jpg)
![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.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9727/pmc11789727/pmc11789727__KCBT_A_2439057_F0008_B.jpg)