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cdk1 inhibitor ro 3306  (MedChemExpress)


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    MedChemExpress cdk1 inhibitor ro 3306
    Cdk1 Inhibitor Ro 3306, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 113 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cdk1+inhibitor+ro+3306/Ro-3306/pm42156913-273-40-49
    Average 97 stars, based on 113 article reviews
    cdk1 inhibitor ro 3306 - by Bioz Stars, 2026-10
    97/100 stars

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    Related Articles

    Western Blot:

    Article Title: Functional Profiling of p53 and RB Cell Cycle Regulatory Proficiency Suggests Mechanism-Driven Molecular Stratification in Endometrial Carcinoma
    Article Snippet: .. Cell lines and organoids underwent various treatments for western blot analysis including 1) no treatment to study baseline protein levels; 2) transfection of cell lines with siRNAs as described above with harvest approximately 48 hours after the first transfection; 3) treatment for 24 hours with media containing either 0.25μM Abemaciclib or an equivalent volume of DMSO; 4) treatment for 24 hours with a dose curve of Abemaciclib including DMSO at a volume equivalent to the highest dose or 0.02μM, 0.1μM, 0.25μM, 0.5uM, or 1.0μM Abemaciclib; 5) treatment for 24 hours with media containing either 0.25μM Palbociclib (MedChemExpress Cat. #HY-50767) or an equivalent volume of DMSO; or 6) first treated with 9μM of the CDK1 inhibitor Ro-3306 (MedChemExpress Cat. #HY-12529) or media containing an equivalent volume of DMSO for 16 hours, washed five times with pre-warmed media, and then treated with either 0.1μM of the Aurora kinase B inhibitor Barasertib, 10ng/mL nocodazole (Sigma-Aldrich Cat. #SML-1665), 20ng/mL nocodazole, or an equivalent amount of DMSO for 24 hours. ..

    Transfection:

    Article Title: Functional Profiling of p53 and RB Cell Cycle Regulatory Proficiency Suggests Mechanism-Driven Molecular Stratification in Endometrial Carcinoma
    Article Snippet: .. Cell lines and organoids underwent various treatments for western blot analysis including 1) no treatment to study baseline protein levels; 2) transfection of cell lines with siRNAs as described above with harvest approximately 48 hours after the first transfection; 3) treatment for 24 hours with media containing either 0.25μM Abemaciclib or an equivalent volume of DMSO; 4) treatment for 24 hours with a dose curve of Abemaciclib including DMSO at a volume equivalent to the highest dose or 0.02μM, 0.1μM, 0.25μM, 0.5uM, or 1.0μM Abemaciclib; 5) treatment for 24 hours with media containing either 0.25μM Palbociclib (MedChemExpress Cat. #HY-50767) or an equivalent volume of DMSO; or 6) first treated with 9μM of the CDK1 inhibitor Ro-3306 (MedChemExpress Cat. #HY-12529) or media containing an equivalent volume of DMSO for 16 hours, washed five times with pre-warmed media, and then treated with either 0.1μM of the Aurora kinase B inhibitor Barasertib, 10ng/mL nocodazole (Sigma-Aldrich Cat. #SML-1665), 20ng/mL nocodazole, or an equivalent amount of DMSO for 24 hours. ..

    Cell Culture:

    Article Title: TMPRSS2-induced Golgi disruption restricts the incorporation of virus envelope glycoproteins into virions.
    Article Snippet: Ingenuity Pathway Analysis (Qiagen IPA, Qiagen, Venlo, Netherlands) was performed for 704 proteins that were statistically different (P < 0.05) in three independent analyses of TM2-WT- and TM2-S441A-transfected cells, respectively. .. At 24 h post-transfection, the medium was replaced with fresh DMEM containing 10% FBS with or without kinase inhibitors (ERK inhibitor, 15944, Cayman Chemical, Ann © The Author(s) EMBO reports 19 20 EMBO reports © The Author(s) Arbor, MI, USA; CDK1 inhibitor Ro 3306, ab141491, CDK5 inhibitor 20-233, HY-123772, MCE, Monmouth Junction, NJ, USA) and cultured for 30–180 min before fixation with 2% formaldehyde. .. At 24 h post-transfection, the medium was replaced with fresh DMEM containing 10% FBS with or without kinase inhibitors (ERK inhibitor, 15944, Cayman Chemical, Ann © The Author(s) EMBO reports 19 20 EMBO reports © The Author(s) Arbor, MI, USA; CDK1 inhibitor Ro 3306, ab141491, CDK5 inhibitor 20-233, HY-123772, MCE, Monmouth Junction, NJ, USA) and cultured for 30–180 min before fixation with 2% formaldehyde.

    Article Title: Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma
    Article Snippet: The stained tissue was photographed by microscopy (Nikon, ECLIPSE Ni-U) or a digital slide scanner (3DHISTECN, pannoramic MIDI). .. Apoptosis A total of 5×105 SKNSH and SKNBE cells were cultured in 6-well plates and incubated with DMSO, 10 μM, 15 μM, 20 μM, or 25 μM of the CDK1 inhibitor Ro-3306 (MedChemExpress, HY-12529) for 24 h. Then, the cells were collected, resuspended in binding buffer and stained with Annexin V-FITC/PI (KeyGEN BioTECH, KGA1102) for 15 min at RT in the dark. .. The apoptotic status was detected by a flow cytometer (BD Bioscience, FACSCanto) and measured by FlowJo.

    Article Title: Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma
    Article Snippet: The stained tissue was photographed by microscopy (Nikon, ECLIPSE Ni-U) or a digital slide scanner (3DHISTECN, pannoramic MIDI). .. A total of 5×10 5 SKNSH and SKNBE cells were cultured in 6-well plates and incubated with DMSO, 10 μM, 15 μM, 20 μM, or 25 μM of the CDK1 inhibitor Ro-3306 (MedChemExpress, HY-12529) for 24 h. Then, the cells were collected, resuspended in binding buffer and stained with Annexin V-FITC/PI (KeyGEN BioTECH, KGA1102) for 15 min at RT in the dark. .. The apoptotic status was detected by a flow cytometer (BD Bioscience, FACSCanto) and measured by FlowJo.

    Incubation:

    Article Title: Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma
    Article Snippet: The stained tissue was photographed by microscopy (Nikon, ECLIPSE Ni-U) or a digital slide scanner (3DHISTECN, pannoramic MIDI). .. Apoptosis A total of 5×105 SKNSH and SKNBE cells were cultured in 6-well plates and incubated with DMSO, 10 μM, 15 μM, 20 μM, or 25 μM of the CDK1 inhibitor Ro-3306 (MedChemExpress, HY-12529) for 24 h. Then, the cells were collected, resuspended in binding buffer and stained with Annexin V-FITC/PI (KeyGEN BioTECH, KGA1102) for 15 min at RT in the dark. .. The apoptotic status was detected by a flow cytometer (BD Bioscience, FACSCanto) and measured by FlowJo.

    Article Title: Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma
    Article Snippet: The stained tissue was photographed by microscopy (Nikon, ECLIPSE Ni-U) or a digital slide scanner (3DHISTECN, pannoramic MIDI). .. A total of 5×10 5 SKNSH and SKNBE cells were cultured in 6-well plates and incubated with DMSO, 10 μM, 15 μM, 20 μM, or 25 μM of the CDK1 inhibitor Ro-3306 (MedChemExpress, HY-12529) for 24 h. Then, the cells were collected, resuspended in binding buffer and stained with Annexin V-FITC/PI (KeyGEN BioTECH, KGA1102) for 15 min at RT in the dark. .. The apoptotic status was detected by a flow cytometer (BD Bioscience, FACSCanto) and measured by FlowJo.

    Binding Assay:

    Article Title: Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma
    Article Snippet: The stained tissue was photographed by microscopy (Nikon, ECLIPSE Ni-U) or a digital slide scanner (3DHISTECN, pannoramic MIDI). .. Apoptosis A total of 5×105 SKNSH and SKNBE cells were cultured in 6-well plates and incubated with DMSO, 10 μM, 15 μM, 20 μM, or 25 μM of the CDK1 inhibitor Ro-3306 (MedChemExpress, HY-12529) for 24 h. Then, the cells were collected, resuspended in binding buffer and stained with Annexin V-FITC/PI (KeyGEN BioTECH, KGA1102) for 15 min at RT in the dark. .. The apoptotic status was detected by a flow cytometer (BD Bioscience, FACSCanto) and measured by FlowJo.

    Article Title: Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma
    Article Snippet: The stained tissue was photographed by microscopy (Nikon, ECLIPSE Ni-U) or a digital slide scanner (3DHISTECN, pannoramic MIDI). .. A total of 5×10 5 SKNSH and SKNBE cells were cultured in 6-well plates and incubated with DMSO, 10 μM, 15 μM, 20 μM, or 25 μM of the CDK1 inhibitor Ro-3306 (MedChemExpress, HY-12529) for 24 h. Then, the cells were collected, resuspended in binding buffer and stained with Annexin V-FITC/PI (KeyGEN BioTECH, KGA1102) for 15 min at RT in the dark. .. The apoptotic status was detected by a flow cytometer (BD Bioscience, FACSCanto) and measured by FlowJo.

    Staining:

    Article Title: Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma
    Article Snippet: The stained tissue was photographed by microscopy (Nikon, ECLIPSE Ni-U) or a digital slide scanner (3DHISTECN, pannoramic MIDI). .. Apoptosis A total of 5×105 SKNSH and SKNBE cells were cultured in 6-well plates and incubated with DMSO, 10 μM, 15 μM, 20 μM, or 25 μM of the CDK1 inhibitor Ro-3306 (MedChemExpress, HY-12529) for 24 h. Then, the cells were collected, resuspended in binding buffer and stained with Annexin V-FITC/PI (KeyGEN BioTECH, KGA1102) for 15 min at RT in the dark. .. The apoptotic status was detected by a flow cytometer (BD Bioscience, FACSCanto) and measured by FlowJo.

    Article Title: Inhibition of CDK1 Promotes Immunogenic Cell Death in Neuroblastoma
    Article Snippet: The stained tissue was photographed by microscopy (Nikon, ECLIPSE Ni-U) or a digital slide scanner (3DHISTECN, pannoramic MIDI). .. A total of 5×10 5 SKNSH and SKNBE cells were cultured in 6-well plates and incubated with DMSO, 10 μM, 15 μM, 20 μM, or 25 μM of the CDK1 inhibitor Ro-3306 (MedChemExpress, HY-12529) for 24 h. Then, the cells were collected, resuspended in binding buffer and stained with Annexin V-FITC/PI (KeyGEN BioTECH, KGA1102) for 15 min at RT in the dark. .. The apoptotic status was detected by a flow cytometer (BD Bioscience, FACSCanto) and measured by FlowJo.

    Control:

    Article Title: Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation
    Article Snippet: .. Male SD rats (200–220 g) were kept on a 12-h light/dark cycle at 18–22 °C and 40%-60% humidity in the SPF animal laboratory and divided into 11 groups, with 6 rats in each group: Control group: administered intraperitoneal vehicle solution (60 mg/kg) on day 1, intraperitoneal injection of saline for 28 days; MCT group: administered intraperitoneal monocrotaline (MCT) (60 mg/kg, Must Bio-Technology, China) on day 1; MCT + DMSO group: administered 28 days of DMSO intraperitoneal injection after MCT administration on day 1; MCT + MCP group: received 28 days of Gal-3 inhibitor PectaSol modified citrus pectin (MCP) (100 mg/kg/d, orally, Econugenics, Santa Rosa, CA, USA) after MCT administration [ ]; MCT + TAK-242 group: received TLR4 receptor inhibitor TAK-242 (3 mg/kg/d, intraperitoneal injection, Aladdin, T125887) for 28 days after MCT administration [ ]; MCT + VP group: received YAP1 inhibitor verteporfin (VP) (4.5 mg/kg, every 2 days, intraperitoneal injection, Aladdin, V129759) for 28 days after MCT administration [ ]; MCT + NC siRNA group: received NC siRNA (0.2 mg/kg/w tail-vein injection, GenePharma, China) for 28 days after MCT administration; MCT + PLK1 siRNA-targeted group: received PLK1 siRNA molecule for 28 days after the injection of MCT; MCT + RO-3306 group: received CDK1 inhibitor RO-3306 (4 mg/kg, every 2 days, orally, MedChemExpress, USA, HY-12529) for 28 days after the injection of MCT [ ]; MCT + PBK-targeted siRNA group: received PBK siRNA molecule for 28 days after the injection of MCT; MCT + PRC1-targeted siRNA group: received PRC1 siRNA molecule for 28 days after the injection of MCT. ..

    Article Title: Resveratrol combats Salmonella infection via liberating vacuole-enclosed bacteria for enhanced autophagic clearance and blocking HMGA2-mediated G2/M arrest.
    Article Snippet: The escalating crisis of antimicrobial resistance necessitates a paradigm shift toward host-directed therapies (HDTs) that circumvent pathogen evasion strategies.. Here we show that the natural polyphenol resveratrol clears intracellular Salmonella typhimurium (S. typhimurium) by orchestrating a multipronged strategy involving Salmonella-containing vacuole (SCV) disruption via ERK1/2 inhibition to liberate bacteria for enhanced autophagic clearance, concurrently reversing pathogen-induced G2/M cell cycle arrest.. We identify High Mobility Group ATHook 2 (HMGA2) as a critical, previously unrecognized host dependency factor essential for Salmonella-driven cell cycle manipulation, which resveratrol targets to restrict bacterial replication.

    Article Title: Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation.
    Article Snippet: .. AR TIC LE IN PR ES S ARTICLE IN PRESS Control group: administered intraperitoneal vehicle solution (60 mg/kg) on day 1, intraperitoneal injection of saline for 28 days; MCT group: administered intraperitoneal monocrotaline (MCT) (60 mg/kg, Must Bio-Technology, China) on day 1; MCT + DMSO group: administered 28 days of DMSO intraperitoneal injection after MCT administration on day 1; MCT + MCP group: received 28 days of Gal3 inhibitor PectaSol modified citrus pectin (MCP) (100 mg/kg/d, orally, Econugenics, Santa Rosa, CA, USA) after MCT administration (36); MCT + TAK-242 group: received TLR4 receptor inhibitor TAK242 (3 mg/kg/d, intraperitoneal injection, Aladdin, T125887) for 28 days after MCT administration (37); MCT + VP group: received YAP1 inhibitor verteporfin (VP) (4.5 mg/kg, every 2 days, intraperitoneal injection, Aladdin, V129759) for 28 days after MCT administration (38); MCT + NC siRNA group: received NC siRNA (0.2 mg/kg/w tailvein injection, GenePharma, China) for 28 days after MCT administration; MCT + PLK1 siRNA-targeted group: received PLK1 siRNA molecule for 28 days after the injection of MCT; MCT + RO3306 group: received CDK1 inhibitor RO-3306 (4 mg/kg, every 2 days, orally, MedChemExpress, USA, HY-12529) for 28 days after the injection of MCT (39); MCT + PBK-targeted siRNA group: received PBK siRNA molecule for 28 days after the injection of MCT; MCT + PRC1-targeted siRNA group: received PRC1 siRNA molecule ..

    Injection:

    Article Title: Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation
    Article Snippet: .. Male SD rats (200–220 g) were kept on a 12-h light/dark cycle at 18–22 °C and 40%-60% humidity in the SPF animal laboratory and divided into 11 groups, with 6 rats in each group: Control group: administered intraperitoneal vehicle solution (60 mg/kg) on day 1, intraperitoneal injection of saline for 28 days; MCT group: administered intraperitoneal monocrotaline (MCT) (60 mg/kg, Must Bio-Technology, China) on day 1; MCT + DMSO group: administered 28 days of DMSO intraperitoneal injection after MCT administration on day 1; MCT + MCP group: received 28 days of Gal-3 inhibitor PectaSol modified citrus pectin (MCP) (100 mg/kg/d, orally, Econugenics, Santa Rosa, CA, USA) after MCT administration [ ]; MCT + TAK-242 group: received TLR4 receptor inhibitor TAK-242 (3 mg/kg/d, intraperitoneal injection, Aladdin, T125887) for 28 days after MCT administration [ ]; MCT + VP group: received YAP1 inhibitor verteporfin (VP) (4.5 mg/kg, every 2 days, intraperitoneal injection, Aladdin, V129759) for 28 days after MCT administration [ ]; MCT + NC siRNA group: received NC siRNA (0.2 mg/kg/w tail-vein injection, GenePharma, China) for 28 days after MCT administration; MCT + PLK1 siRNA-targeted group: received PLK1 siRNA molecule for 28 days after the injection of MCT; MCT + RO-3306 group: received CDK1 inhibitor RO-3306 (4 mg/kg, every 2 days, orally, MedChemExpress, USA, HY-12529) for 28 days after the injection of MCT [ ]; MCT + PBK-targeted siRNA group: received PBK siRNA molecule for 28 days after the injection of MCT; MCT + PRC1-targeted siRNA group: received PRC1 siRNA molecule for 28 days after the injection of MCT. ..

    Article Title: Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation.
    Article Snippet: .. AR TIC LE IN PR ES S ARTICLE IN PRESS Control group: administered intraperitoneal vehicle solution (60 mg/kg) on day 1, intraperitoneal injection of saline for 28 days; MCT group: administered intraperitoneal monocrotaline (MCT) (60 mg/kg, Must Bio-Technology, China) on day 1; MCT + DMSO group: administered 28 days of DMSO intraperitoneal injection after MCT administration on day 1; MCT + MCP group: received 28 days of Gal3 inhibitor PectaSol modified citrus pectin (MCP) (100 mg/kg/d, orally, Econugenics, Santa Rosa, CA, USA) after MCT administration (36); MCT + TAK-242 group: received TLR4 receptor inhibitor TAK242 (3 mg/kg/d, intraperitoneal injection, Aladdin, T125887) for 28 days after MCT administration (37); MCT + VP group: received YAP1 inhibitor verteporfin (VP) (4.5 mg/kg, every 2 days, intraperitoneal injection, Aladdin, V129759) for 28 days after MCT administration (38); MCT + NC siRNA group: received NC siRNA (0.2 mg/kg/w tailvein injection, GenePharma, China) for 28 days after MCT administration; MCT + PLK1 siRNA-targeted group: received PLK1 siRNA molecule for 28 days after the injection of MCT; MCT + RO3306 group: received CDK1 inhibitor RO-3306 (4 mg/kg, every 2 days, orally, MedChemExpress, USA, HY-12529) for 28 days after the injection of MCT (39); MCT + PBK-targeted siRNA group: received PBK siRNA molecule for 28 days after the injection of MCT; MCT + PRC1-targeted siRNA group: received PRC1 siRNA molecule ..

    Saline:

    Article Title: Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation
    Article Snippet: .. Male SD rats (200–220 g) were kept on a 12-h light/dark cycle at 18–22 °C and 40%-60% humidity in the SPF animal laboratory and divided into 11 groups, with 6 rats in each group: Control group: administered intraperitoneal vehicle solution (60 mg/kg) on day 1, intraperitoneal injection of saline for 28 days; MCT group: administered intraperitoneal monocrotaline (MCT) (60 mg/kg, Must Bio-Technology, China) on day 1; MCT + DMSO group: administered 28 days of DMSO intraperitoneal injection after MCT administration on day 1; MCT + MCP group: received 28 days of Gal-3 inhibitor PectaSol modified citrus pectin (MCP) (100 mg/kg/d, orally, Econugenics, Santa Rosa, CA, USA) after MCT administration [ ]; MCT + TAK-242 group: received TLR4 receptor inhibitor TAK-242 (3 mg/kg/d, intraperitoneal injection, Aladdin, T125887) for 28 days after MCT administration [ ]; MCT + VP group: received YAP1 inhibitor verteporfin (VP) (4.5 mg/kg, every 2 days, intraperitoneal injection, Aladdin, V129759) for 28 days after MCT administration [ ]; MCT + NC siRNA group: received NC siRNA (0.2 mg/kg/w tail-vein injection, GenePharma, China) for 28 days after MCT administration; MCT + PLK1 siRNA-targeted group: received PLK1 siRNA molecule for 28 days after the injection of MCT; MCT + RO-3306 group: received CDK1 inhibitor RO-3306 (4 mg/kg, every 2 days, orally, MedChemExpress, USA, HY-12529) for 28 days after the injection of MCT [ ]; MCT + PBK-targeted siRNA group: received PBK siRNA molecule for 28 days after the injection of MCT; MCT + PRC1-targeted siRNA group: received PRC1 siRNA molecule for 28 days after the injection of MCT. ..

    Article Title: Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation.
    Article Snippet: .. AR TIC LE IN PR ES S ARTICLE IN PRESS Control group: administered intraperitoneal vehicle solution (60 mg/kg) on day 1, intraperitoneal injection of saline for 28 days; MCT group: administered intraperitoneal monocrotaline (MCT) (60 mg/kg, Must Bio-Technology, China) on day 1; MCT + DMSO group: administered 28 days of DMSO intraperitoneal injection after MCT administration on day 1; MCT + MCP group: received 28 days of Gal3 inhibitor PectaSol modified citrus pectin (MCP) (100 mg/kg/d, orally, Econugenics, Santa Rosa, CA, USA) after MCT administration (36); MCT + TAK-242 group: received TLR4 receptor inhibitor TAK242 (3 mg/kg/d, intraperitoneal injection, Aladdin, T125887) for 28 days after MCT administration (37); MCT + VP group: received YAP1 inhibitor verteporfin (VP) (4.5 mg/kg, every 2 days, intraperitoneal injection, Aladdin, V129759) for 28 days after MCT administration (38); MCT + NC siRNA group: received NC siRNA (0.2 mg/kg/w tailvein injection, GenePharma, China) for 28 days after MCT administration; MCT + PLK1 siRNA-targeted group: received PLK1 siRNA molecule for 28 days after the injection of MCT; MCT + RO3306 group: received CDK1 inhibitor RO-3306 (4 mg/kg, every 2 days, orally, MedChemExpress, USA, HY-12529) for 28 days after the injection of MCT (39); MCT + PBK-targeted siRNA group: received PBK siRNA molecule for 28 days after the injection of MCT; MCT + PRC1-targeted siRNA group: received PRC1 siRNA molecule ..

    Modification:

    Article Title: Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation
    Article Snippet: .. Male SD rats (200–220 g) were kept on a 12-h light/dark cycle at 18–22 °C and 40%-60% humidity in the SPF animal laboratory and divided into 11 groups, with 6 rats in each group: Control group: administered intraperitoneal vehicle solution (60 mg/kg) on day 1, intraperitoneal injection of saline for 28 days; MCT group: administered intraperitoneal monocrotaline (MCT) (60 mg/kg, Must Bio-Technology, China) on day 1; MCT + DMSO group: administered 28 days of DMSO intraperitoneal injection after MCT administration on day 1; MCT + MCP group: received 28 days of Gal-3 inhibitor PectaSol modified citrus pectin (MCP) (100 mg/kg/d, orally, Econugenics, Santa Rosa, CA, USA) after MCT administration [ ]; MCT + TAK-242 group: received TLR4 receptor inhibitor TAK-242 (3 mg/kg/d, intraperitoneal injection, Aladdin, T125887) for 28 days after MCT administration [ ]; MCT + VP group: received YAP1 inhibitor verteporfin (VP) (4.5 mg/kg, every 2 days, intraperitoneal injection, Aladdin, V129759) for 28 days after MCT administration [ ]; MCT + NC siRNA group: received NC siRNA (0.2 mg/kg/w tail-vein injection, GenePharma, China) for 28 days after MCT administration; MCT + PLK1 siRNA-targeted group: received PLK1 siRNA molecule for 28 days after the injection of MCT; MCT + RO-3306 group: received CDK1 inhibitor RO-3306 (4 mg/kg, every 2 days, orally, MedChemExpress, USA, HY-12529) for 28 days after the injection of MCT [ ]; MCT + PBK-targeted siRNA group: received PBK siRNA molecule for 28 days after the injection of MCT; MCT + PRC1-targeted siRNA group: received PRC1 siRNA molecule for 28 days after the injection of MCT. ..

    Article Title: Activation of PBK by Gal-3 contributes to pulmonary artery hypertension by promoting PRC1 activation.
    Article Snippet: .. AR TIC LE IN PR ES S ARTICLE IN PRESS Control group: administered intraperitoneal vehicle solution (60 mg/kg) on day 1, intraperitoneal injection of saline for 28 days; MCT group: administered intraperitoneal monocrotaline (MCT) (60 mg/kg, Must Bio-Technology, China) on day 1; MCT + DMSO group: administered 28 days of DMSO intraperitoneal injection after MCT administration on day 1; MCT + MCP group: received 28 days of Gal3 inhibitor PectaSol modified citrus pectin (MCP) (100 mg/kg/d, orally, Econugenics, Santa Rosa, CA, USA) after MCT administration (36); MCT + TAK-242 group: received TLR4 receptor inhibitor TAK242 (3 mg/kg/d, intraperitoneal injection, Aladdin, T125887) for 28 days after MCT administration (37); MCT + VP group: received YAP1 inhibitor verteporfin (VP) (4.5 mg/kg, every 2 days, intraperitoneal injection, Aladdin, V129759) for 28 days after MCT administration (38); MCT + NC siRNA group: received NC siRNA (0.2 mg/kg/w tailvein injection, GenePharma, China) for 28 days after MCT administration; MCT + PLK1 siRNA-targeted group: received PLK1 siRNA molecule for 28 days after the injection of MCT; MCT + RO3306 group: received CDK1 inhibitor RO-3306 (4 mg/kg, every 2 days, orally, MedChemExpress, USA, HY-12529) for 28 days after the injection of MCT (39); MCT + PBK-targeted siRNA group: received PBK siRNA molecule for 28 days after the injection of MCT; MCT + PRC1-targeted siRNA group: received PRC1 siRNA molecule ..



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    96
    Selleck Chemicals cdk1 inhibitor ro 3306
    <t>2,3-BPG-CDK1-EZH2-H3K27me3</t> Axis: BPGM’s epigenetic circuit breaker for cellular migration. (A) Integrated functional metabolomics analysis revealed BPGM-altered metabolites clustered in methyl donor group. Bubble size: metabolites count. (B) Hypothesis of molecular mechanism underlying BPGM regulated BBOX1 expression by post transcriptional modification (PTM). (C) Silencing BPGM significantly reduced the protein level of H3K27me3, while overexpressing BPGM increased its level. Cells stably expressing shBPGM/BPGM and its control cells (shCtrl/Ctrl) were used to detect protein level by western blotting. (D) ChIP assays disclosed that the fragments of BBOX1 and MMP9 promoter precipitated by anti-H3K27me3 antibody were increased upon overexpressing BPGM. SK-HEP-1 cells stably expressing BPGM and its control cells (Ctrl) were employed to ChIP assay. The antibody precipitated DNAs were amplified by qPCR. 5 % of the total DNAs were amplified to serve as the control for DNA content. Values shown are signal of α-H3K27me3-precipitated DNA relative to the input and the mean value of the control group was normalized as 1. (E) Overexpressing BPGM significantly increased the protein level of EZH2 but decreased the protein level of p-EZH2-T 345 in tumor cells. (F) The molecular docking of 2,3-BPG and CDK1. Predicted structure of 2,3-BPG binding with CDK1. Key contact residues: Thr14, Arg127, Arg170. (G) Overexpressing BPGM significantly increased the protein level of p-CDK1-T 14 in tumor cells. Cells stably expressing BPGM (BPGM-OE) and its control cells (Ctrl) were used to detect protein level by western blotting. (H) 2,3-BPG treatment enhanced the phosphorylation of CDK1 at thr14 in tumor cells. The indicated concentration of 2,3-BPG was incubated with the lysate of trophoblasts and tumor cells for 30 minutes followed by western blotting. (I-J) RO-3306 treatment enhanced the phosphorylation of CDK1 at thr14 and reduced the phosphorylation of EZH2 at thr345 in tumor cells. The tumor cells were treated with the indicated concentration of RO-3306 for 12 hours followed by western blotting. (K) The model deciphers the role of BPGM in regulating BBOX1 and MMP9 expression. Error bar: mean ± SEM. P -values are labeled above the bar chart.
    Cdk1 Inhibitor Ro 3306, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cdk1+inhibitor+ro+3306/Ro-3306/pm41785316-359-6-9
    Average 96 stars, based on 1 article reviews
    cdk1 inhibitor ro 3306 - by Bioz Stars, 2026-10
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    cdk1 inhibitor ro 3306 selleckchemicals s7747  (Selleck Chemicals)
    96
    Selleck Chemicals cdk1 inhibitor ro 3306 selleckchemicals s7747
    <t>2,3-BPG-CDK1-EZH2-H3K27me3</t> Axis: BPGM’s epigenetic circuit breaker for cellular migration. (A) Integrated functional metabolomics analysis revealed BPGM-altered metabolites clustered in methyl donor group. Bubble size: metabolites count. (B) Hypothesis of molecular mechanism underlying BPGM regulated BBOX1 expression by post transcriptional modification (PTM). (C) Silencing BPGM significantly reduced the protein level of H3K27me3, while overexpressing BPGM increased its level. Cells stably expressing shBPGM/BPGM and its control cells (shCtrl/Ctrl) were used to detect protein level by western blotting. (D) ChIP assays disclosed that the fragments of BBOX1 and MMP9 promoter precipitated by anti-H3K27me3 antibody were increased upon overexpressing BPGM. SK-HEP-1 cells stably expressing BPGM and its control cells (Ctrl) were employed to ChIP assay. The antibody precipitated DNAs were amplified by qPCR. 5 % of the total DNAs were amplified to serve as the control for DNA content. Values shown are signal of α-H3K27me3-precipitated DNA relative to the input and the mean value of the control group was normalized as 1. (E) Overexpressing BPGM significantly increased the protein level of EZH2 but decreased the protein level of p-EZH2-T 345 in tumor cells. (F) The molecular docking of 2,3-BPG and CDK1. Predicted structure of 2,3-BPG binding with CDK1. Key contact residues: Thr14, Arg127, Arg170. (G) Overexpressing BPGM significantly increased the protein level of p-CDK1-T 14 in tumor cells. Cells stably expressing BPGM (BPGM-OE) and its control cells (Ctrl) were used to detect protein level by western blotting. (H) 2,3-BPG treatment enhanced the phosphorylation of CDK1 at thr14 in tumor cells. The indicated concentration of 2,3-BPG was incubated with the lysate of trophoblasts and tumor cells for 30 minutes followed by western blotting. (I-J) RO-3306 treatment enhanced the phosphorylation of CDK1 at thr14 and reduced the phosphorylation of EZH2 at thr345 in tumor cells. The tumor cells were treated with the indicated concentration of RO-3306 for 12 hours followed by western blotting. (K) The model deciphers the role of BPGM in regulating BBOX1 and MMP9 expression. Error bar: mean ± SEM. P -values are labeled above the bar chart.
    Cdk1 Inhibitor Ro 3306 Selleckchemicals S7747, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cdk1+inhibitor+ro+3306/Ro-3306/pm41785087-710-20-23
    Average 96 stars, based on 1 article reviews
    cdk1 inhibitor ro 3306 selleckchemicals s7747 - by Bioz Stars, 2026-10
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    cdk1 specific inhibitor ro 3306  (MedChemExpress)
    97
    MedChemExpress cdk1 specific inhibitor ro 3306
    PPP1R14C promotes LUSC cell proliferation and invasion via <t>CDK1</t> activation. ( A ) Overexpression of PPP1R14C activates CDK1 through T161-CDK1 phosphorylation. Western blot analysis revealed that compared to the control group, overexpression of PPP1R14C in NCI-H520 cells significantly increased the phosphorylation levels of T161-CDK1 and histone H1 (p-CDK1, P-T161(CDK1), and p-Histone H1). ( B ) PPP1R14C knockdown inhibits CDK1 activation by reducing T161-CDK1 phosphorylation. Western blot analysis showed that compared to the control group, PPP1R14C knockdown (shPPP1R14C) significantly reduced the expression levels of p-CDK1, P-T161(CDK1), and p-Histone H1. ( C ) Interaction between PPP1R14C and PP1α. Co-immunoprecipitation experiments showed that PPP1R14C antibodies pulled down PP1α, while isotype control IgG did not detect PP1α signals, indicating that PPP1R14C can directly bind to PP1α. ( D ) Overexpression of PPP1R14C inhibits the binding of CDK1 to PP1α. Co-immunoprecipitation experiments showed that PP1α could co-precipitate with CDK1 in cells expressing the empty vector, while overexpression of PPP1R14C inhibited the binding of CDK1 to PP1α. ( E ) CDK1 inhibition abolished PPP1R14C-mediated proliferation. CCK-8 proliferation assays showed that the growth advantage conferred by PPP1R14C overexpression was completely abolished by the CDK1 <t>inhibitor</t> <t>RO-3306</t> (* p < 0.05, ** p < 0.01, **** p < 0.0001). ( F ) CDK1 activity is critical for PPP1R14C-driven clonogenicity. Colony formation experiments showed that inhibition of CDK1 with RO-3306 neutralized PPP1R14C-driven clonogenic growth (* p < 0.05, **** p < 0.0001). ( G ) CDK1 inhibition attenuated the invasive ability enhanced by PPP1R14C. Transwell invasion assays showed that blocking CDK1 with RO-3306 could inhibit the pro-invasive effect of PPP1R14C overexpression (* p < 0.05, **** p < 0.0001).
    Cdk1 Specific Inhibitor Ro 3306, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cdk1+inhibitor+ro+3306/Ro-3306/pmc13000272-44-1-4
    Average 97 stars, based on 1 article reviews
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    2,3-BPG-CDK1-EZH2-H3K27me3 Axis: BPGM’s epigenetic circuit breaker for cellular migration. (A) Integrated functional metabolomics analysis revealed BPGM-altered metabolites clustered in methyl donor group. Bubble size: metabolites count. (B) Hypothesis of molecular mechanism underlying BPGM regulated BBOX1 expression by post transcriptional modification (PTM). (C) Silencing BPGM significantly reduced the protein level of H3K27me3, while overexpressing BPGM increased its level. Cells stably expressing shBPGM/BPGM and its control cells (shCtrl/Ctrl) were used to detect protein level by western blotting. (D) ChIP assays disclosed that the fragments of BBOX1 and MMP9 promoter precipitated by anti-H3K27me3 antibody were increased upon overexpressing BPGM. SK-HEP-1 cells stably expressing BPGM and its control cells (Ctrl) were employed to ChIP assay. The antibody precipitated DNAs were amplified by qPCR. 5 % of the total DNAs were amplified to serve as the control for DNA content. Values shown are signal of α-H3K27me3-precipitated DNA relative to the input and the mean value of the control group was normalized as 1. (E) Overexpressing BPGM significantly increased the protein level of EZH2 but decreased the protein level of p-EZH2-T 345 in tumor cells. (F) The molecular docking of 2,3-BPG and CDK1. Predicted structure of 2,3-BPG binding with CDK1. Key contact residues: Thr14, Arg127, Arg170. (G) Overexpressing BPGM significantly increased the protein level of p-CDK1-T 14 in tumor cells. Cells stably expressing BPGM (BPGM-OE) and its control cells (Ctrl) were used to detect protein level by western blotting. (H) 2,3-BPG treatment enhanced the phosphorylation of CDK1 at thr14 in tumor cells. The indicated concentration of 2,3-BPG was incubated with the lysate of trophoblasts and tumor cells for 30 minutes followed by western blotting. (I-J) RO-3306 treatment enhanced the phosphorylation of CDK1 at thr14 and reduced the phosphorylation of EZH2 at thr345 in tumor cells. The tumor cells were treated with the indicated concentration of RO-3306 for 12 hours followed by western blotting. (K) The model deciphers the role of BPGM in regulating BBOX1 and MMP9 expression. Error bar: mean ± SEM. P -values are labeled above the bar chart.

    Journal: Neoplasia (New York, N.Y.)

    Article Title: BPGM as an intrinsic brake to constrain metastasis through phospho-epigenetic-mediated carnitine biosynthesis suppression

    doi: 10.1016/j.neo.2026.101299

    Figure Lengend Snippet: 2,3-BPG-CDK1-EZH2-H3K27me3 Axis: BPGM’s epigenetic circuit breaker for cellular migration. (A) Integrated functional metabolomics analysis revealed BPGM-altered metabolites clustered in methyl donor group. Bubble size: metabolites count. (B) Hypothesis of molecular mechanism underlying BPGM regulated BBOX1 expression by post transcriptional modification (PTM). (C) Silencing BPGM significantly reduced the protein level of H3K27me3, while overexpressing BPGM increased its level. Cells stably expressing shBPGM/BPGM and its control cells (shCtrl/Ctrl) were used to detect protein level by western blotting. (D) ChIP assays disclosed that the fragments of BBOX1 and MMP9 promoter precipitated by anti-H3K27me3 antibody were increased upon overexpressing BPGM. SK-HEP-1 cells stably expressing BPGM and its control cells (Ctrl) were employed to ChIP assay. The antibody precipitated DNAs were amplified by qPCR. 5 % of the total DNAs were amplified to serve as the control for DNA content. Values shown are signal of α-H3K27me3-precipitated DNA relative to the input and the mean value of the control group was normalized as 1. (E) Overexpressing BPGM significantly increased the protein level of EZH2 but decreased the protein level of p-EZH2-T 345 in tumor cells. (F) The molecular docking of 2,3-BPG and CDK1. Predicted structure of 2,3-BPG binding with CDK1. Key contact residues: Thr14, Arg127, Arg170. (G) Overexpressing BPGM significantly increased the protein level of p-CDK1-T 14 in tumor cells. Cells stably expressing BPGM (BPGM-OE) and its control cells (Ctrl) were used to detect protein level by western blotting. (H) 2,3-BPG treatment enhanced the phosphorylation of CDK1 at thr14 in tumor cells. The indicated concentration of 2,3-BPG was incubated with the lysate of trophoblasts and tumor cells for 30 minutes followed by western blotting. (I-J) RO-3306 treatment enhanced the phosphorylation of CDK1 at thr14 and reduced the phosphorylation of EZH2 at thr345 in tumor cells. The tumor cells were treated with the indicated concentration of RO-3306 for 12 hours followed by western blotting. (K) The model deciphers the role of BPGM in regulating BBOX1 and MMP9 expression. Error bar: mean ± SEM. P -values are labeled above the bar chart.

    Article Snippet: The following reagents were used: l -carnitine (541-15-1, Sigma-Aldrich, Saint Louis, MO, USA); 2,3-BPG (D5764, Sigma-Aldrich); CDK1 inhibitor, RO-3306 (S7747, Selleck, Shanghai, China).

    Techniques: Migration, Functional Assay, Expressing, Modification, Stable Transfection, Control, Western Blot, Amplification, Binding Assay, Phospho-proteomics, Concentration Assay, Incubation, Labeling

    PPP1R14C promotes LUSC cell proliferation and invasion via CDK1 activation. ( A ) Overexpression of PPP1R14C activates CDK1 through T161-CDK1 phosphorylation. Western blot analysis revealed that compared to the control group, overexpression of PPP1R14C in NCI-H520 cells significantly increased the phosphorylation levels of T161-CDK1 and histone H1 (p-CDK1, P-T161(CDK1), and p-Histone H1). ( B ) PPP1R14C knockdown inhibits CDK1 activation by reducing T161-CDK1 phosphorylation. Western blot analysis showed that compared to the control group, PPP1R14C knockdown (shPPP1R14C) significantly reduced the expression levels of p-CDK1, P-T161(CDK1), and p-Histone H1. ( C ) Interaction between PPP1R14C and PP1α. Co-immunoprecipitation experiments showed that PPP1R14C antibodies pulled down PP1α, while isotype control IgG did not detect PP1α signals, indicating that PPP1R14C can directly bind to PP1α. ( D ) Overexpression of PPP1R14C inhibits the binding of CDK1 to PP1α. Co-immunoprecipitation experiments showed that PP1α could co-precipitate with CDK1 in cells expressing the empty vector, while overexpression of PPP1R14C inhibited the binding of CDK1 to PP1α. ( E ) CDK1 inhibition abolished PPP1R14C-mediated proliferation. CCK-8 proliferation assays showed that the growth advantage conferred by PPP1R14C overexpression was completely abolished by the CDK1 inhibitor RO-3306 (* p < 0.05, ** p < 0.01, **** p < 0.0001). ( F ) CDK1 activity is critical for PPP1R14C-driven clonogenicity. Colony formation experiments showed that inhibition of CDK1 with RO-3306 neutralized PPP1R14C-driven clonogenic growth (* p < 0.05, **** p < 0.0001). ( G ) CDK1 inhibition attenuated the invasive ability enhanced by PPP1R14C. Transwell invasion assays showed that blocking CDK1 with RO-3306 could inhibit the pro-invasive effect of PPP1R14C overexpression (* p < 0.05, **** p < 0.0001).

    Journal: Scientific Reports

    Article Title: Transcriptional activation of PPP1R14C by KLF7 unleashes CDK1 activity to promote lung squamous cell carcinoma

    doi: 10.1038/s41598-026-39174-3

    Figure Lengend Snippet: PPP1R14C promotes LUSC cell proliferation and invasion via CDK1 activation. ( A ) Overexpression of PPP1R14C activates CDK1 through T161-CDK1 phosphorylation. Western blot analysis revealed that compared to the control group, overexpression of PPP1R14C in NCI-H520 cells significantly increased the phosphorylation levels of T161-CDK1 and histone H1 (p-CDK1, P-T161(CDK1), and p-Histone H1). ( B ) PPP1R14C knockdown inhibits CDK1 activation by reducing T161-CDK1 phosphorylation. Western blot analysis showed that compared to the control group, PPP1R14C knockdown (shPPP1R14C) significantly reduced the expression levels of p-CDK1, P-T161(CDK1), and p-Histone H1. ( C ) Interaction between PPP1R14C and PP1α. Co-immunoprecipitation experiments showed that PPP1R14C antibodies pulled down PP1α, while isotype control IgG did not detect PP1α signals, indicating that PPP1R14C can directly bind to PP1α. ( D ) Overexpression of PPP1R14C inhibits the binding of CDK1 to PP1α. Co-immunoprecipitation experiments showed that PP1α could co-precipitate with CDK1 in cells expressing the empty vector, while overexpression of PPP1R14C inhibited the binding of CDK1 to PP1α. ( E ) CDK1 inhibition abolished PPP1R14C-mediated proliferation. CCK-8 proliferation assays showed that the growth advantage conferred by PPP1R14C overexpression was completely abolished by the CDK1 inhibitor RO-3306 (* p < 0.05, ** p < 0.01, **** p < 0.0001). ( F ) CDK1 activity is critical for PPP1R14C-driven clonogenicity. Colony formation experiments showed that inhibition of CDK1 with RO-3306 neutralized PPP1R14C-driven clonogenic growth (* p < 0.05, **** p < 0.0001). ( G ) CDK1 inhibition attenuated the invasive ability enhanced by PPP1R14C. Transwell invasion assays showed that blocking CDK1 with RO-3306 could inhibit the pro-invasive effect of PPP1R14C overexpression (* p < 0.05, **** p < 0.0001).

    Article Snippet: The CDK1-specific inhibitor RO-3306 (MedChemExpress) was dissolved in DMSO to a 10 mM stock solution and used at a final concentration of 10 μM for in vitro assays.

    Techniques: Activation Assay, Over Expression, Phospho-proteomics, Western Blot, Control, Knockdown, Expressing, Immunoprecipitation, Binding Assay, Plasmid Preparation, Inhibition, CCK-8 Assay, Activity Assay, Blocking Assay