Dinaciclib, a Cyclin-Dependent Kinase Inhibitor Promotes Proteasomal Degradation of Mcl-1 and Enhances ABT-737-Mediated Cell Death in Malignant Human Glioma Cell Lines (Q35846538)

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scientific article published on 19 November 2015

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English	Dinaciclib, a Cyclin-Dependent Kinase Inhibitor Promotes Proteasomal Degradation of Mcl-1 and Enhances ABT-737-Mediated Cell Death in Malignant Human Glioma Cell Lines	scientific article published on 19 November 2015

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scholarly article

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Europe PubMed Central

PubMed publication ID

10 August 2017

Dinaciclib, a Cyclin-Dependent Kinase Inhibitor Promotes Proteasomal Degradation of Mcl-1 and Enhances ABT-737-Mediated Cell Death in Malignant Human Glioma Cell Lines (English)

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Europe PubMed Central

PubMed publication ID

10 August 2017

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author name string

Esther P Jane

1

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Europe PubMed Central

PubMed publication ID

10 August 2017

Daniel R Premkumar

2

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Europe PubMed Central

PubMed publication ID

10 August 2017

Jonathon M Cavaleri

3

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

Philip A Sutera

4

1 reference

Europe PubMed Central

PubMed publication ID

10 August 2017

Thatchana Rajasekar

5

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Europe PubMed Central

PubMed publication ID

10 August 2017

Ian F Pollack

6

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Europe PubMed Central

PubMed publication ID

10 August 2017

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publication date

19 November 2015

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Europe PubMed Central

PubMed publication ID

10 August 2017

Journal of Pharmacology and Experimental Therapeutics

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Europe PubMed Central

PubMed publication ID

10 August 2017

356

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Europe PubMed Central

PubMed publication ID

10 August 2017

2

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Europe PubMed Central

PubMed publication ID

10 August 2017

354-365

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Europe PubMed Central

PubMed publication ID

10 August 2017

mTOR signaling in glioblastoma: lessons learned from bench to bedside

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Bax forms multispanning monomers that oligomerize to permeabilize membranes during apoptosis

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The history and future of targeting cyclin-dependent kinases in cancer therapy

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Molecular characterizations of glioblastoma, targeted therapy, and clinical results to date

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Recent advances in the molecular understanding of glioblastoma

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ABT-737 is highly effective against molecular subgroups of multiple myeloma

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Mcl-1 down-regulation potentiates ABT-737 lethality by cooperatively inducing Bak activation and Bax translocation

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Quantitative analysis of dose-effect relationships: the combined effects of multiple drugs or enzyme inhibitors

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The CDK inhibitors in cancer research and therapy.

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Clinical study of the novel cyclin-dependent kinase inhibitor dinaciclib in combination with rituximab in relapsed/refractory chronic lymphocytic leukemia patients.

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Co-administration of ABT-737 and SAHA induces apoptosis, mediated by Noxa upregulation, Bax activation and mitochondrial dysfunction in PTEN-intact malignant human glioma cell lines

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Growth suppression of glioma cells by PTEN requires a functional phosphatase catalytic domain

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YM-155 potentiates the effect of ABT-737 in malignant human glioma cells via survivin and Mcl-1 downregulation in an EGFR-dependent context

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Dinaciclib, a novel CDK inhibitor, demonstrates encouraging single-agent activity in patients with relapsed multiple myeloma.

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Phase II study of flavopiridol in relapsed chronic lymphocytic leukemia demonstrating high response rates in genetically high-risk disease

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Mcl-1 ubiquitination: unique regulation of an essential survival protein

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A first-in-human, phase 1, dose-escalation study of dinaciclib, a novel cyclin-dependent kinase inhibitor, administered weekly in subjects with advanced malignancies

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An inhibitor of Bcl-2 family proteins induces regression of solid tumours

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Dinaciclib (SCH 727965), a novel and potent cyclin-dependent kinase inhibitor.

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An integrated genomic analysis of human glioblastoma multiforme

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Clinical response and pharmacokinetics from a phase 1 study of an active dosing schedule of flavopiridol in relapsed chronic lymphocytic leukemia

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Cooperative inhibitory effect of ZD1839 (Iressa) in combination with 17-AAG on glioma cell growth

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ABT-737 synergizes with bortezomib to induce apoptosis, mediated by Bid cleavage, Bax activation, and mitochondrial dysfunction in an Akt-dependent context in malignant human glioma cell lines

1 reference

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Cucurbitacin-I inhibits Aurora kinase A, Aurora kinase B and survivin, induces defects in cell cycle progression and promotes ABT-737-induced cell death in a caspase-independent manner in malignant human glioma cells

1 reference

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1 reference

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Randomized phase 2 study of the cyclin-dependent kinase inhibitor dinaciclib (MK-7965) versus erlotinib in patients with non-small cell lung cancer

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Expression of N-ras gene in gliomas

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The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized.

1 reference

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Bortezomib-induced sensitization of malignant human glioma cells to vorinostat-induced apoptosis depends on reactive oxygen species production, mitochondrial dysfunction, Noxa upregulation, Mcl-1 cleavage, and DNA damage

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1 reference

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12 December 2020

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