2. PI3K/Akt/mTOR Stem Cell/Wnt Cell Cycle/DNA Damage Apoptosis
  3. GSK-3 CDK Apoptosis
  4. GTGKT

GTGKT is a CAGE inhibitor. GTGKT binds to CAGE and blocks the binding of CAGE to GSK3β. GTGKT alters the localization of CAGE and inhibits the binding of CAGE to the promoter sequence of Cyclin D1. GTGKT enhances the Apoptotic effect of anticancer agents. GTGKT reduces the expression of Cyclin D1. GTGKT decreases the tumorigenic potential of melanoma and hepatocellular carcinoma cells.

For research use only. We do not sell to patients.

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GTGKT

GTGKT Chemical Structure

CAS No. : 254732-11-1

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GTGKT Related Antibodies

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Description

GTGKT is a CAGE inhibitor. GTGKT binds to CAGE and blocks the binding of CAGE to GSK3β. GTGKT alters the localization of CAGE and inhibits the binding of CAGE to the promoter sequence of Cyclin D1. GTGKT enhances the Apoptotic effect of anticancer agents. GTGKT reduces the expression of Cyclin D1. GTGKT decreases the tumorigenic potential of melanoma and hepatocellular carcinoma cells[1].

IC50 & Target[1]

GSK-3β

 

In Vitro

GTGKT (10 μM; 48 h) reduces the expressions of cyclinD1 and pGSK3βSer9, and inhibits the binding of CAGE-GSK3β in Malme3MR-Taxol cancer cells[1].
GTGKT (10 μM; 48 h) reduces the migration and invasion capacities of anticancer agent-resistant Malme3MR melanoma cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

GTGKT Related Antibodies

Western Blot Analysis[1]

Cell Line: anti-cancer agent-resistant Malme3MR, SNU387R, and Malme3MR-Taxol cancer cells
Concentration: 10 μM
Incubation Time: 48 h
Result: Decreased the expression of cyclinD1 and inactive pGSK3βSer9 without altering CAGE expression in Malme3MR, SNU387R, and Malme3MR-Taxol cells.
Inhibited the binding of CAGE to GSK3β in all three cell lines.
Directly bound to CAGE (but not GSK3β) in Malme3MR and Malme3MR-Taxol cells for biotin-labeled peptide.
In Vivo

GTGKT (10-50 μg/mouse; i.v.; five times; 35 days) dose-dependently reduces subcutaneous melanoma tumor volume in athymic nude mice by decreasing cyclinD1, pGSK3βSer9, and MDR1 expression, increasing phospho-cyclinD1Thr286 expression, and inhibiting CAGE-GSK3β binding[1].
GTGKT (10-50 μg/mouse; i.v.; five times; 35 days) dose-dependently reduces subcutaneous hepatocellular carcinoma tumor volume in athymic nude mice by decreasing cyclinD1, pGSK3βSer9, and MDR1 expression, increasing phospho-cyclinD1Thr286 expression, and inhibiting CAGE-GSK3β binding[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/c nu/nu (5-6-week-old females)[1]
Dosage: 10 μg/mouse; 50 μg/mouse
Administration: i.v.; five times; 35 days
Result: Significantly reduced tumor volume compared to PBS control at 10 μg/mouse.
Resulted in a greater, statistically significant reduction in tumor volume compared to PBS control at 50 μg/mouse.
Decreased expression of cyclinD1, pGSK3βSer9, and MDR1 in tumor lysates.
Increased expression of phospho-cyclinD1Thr286 in tumor lysates.
Inhibited the binding of CAGE to GSK3β in tumor tissue.
Animal Model: BALB/c nu/nu (5-6-week-old females)[1]
Dosage: 10 μg/mouse; 50 μg/mouse
Administration: i.v.; five times; 35 days
Result: Significantly reduced tumor volume compared to PBS control at 10 μg/mouse.
Significantly reduced tumor volume compared to PBS control at 50 μg/mouse, with greater efficacy than the lower dose.
Decreased expression of cyclinD1, pGSK3βSer9, and MDR1 in tumor lysates.
Increased expression of phospho-cyclinD1Thr286 in tumor lysates.
Inhibited the binding of CAGE to GSK3β in tumor tissue.
Animal Model: BALB/c nu/nu (4-week-old females)[1]
Dosage: 50 μg/mouse
Administration: i.v.; five times; 4 weeks
Result: Drastically reduced the number of surface metastatic lung nodules compared to mock and GTGRT peptide controls.
Decreased expression of cyclinD1, pGSK3βSer9, and MDR1 in lung/tumor lysates.
Inhibited the binding of CAGE to GSK3β.
Animal Model: BALB/c nu/nu (5-6-week-old females)[1]
Dosage: 50 μg/mouse
Administration: i.v.; single dose
Result: Detected strong, specific fluorescence in subcutaneous Malme3MR tumors 12 hours after injection.
Observed minimal fluorescence in normal organs (kidney, liver, spleen, lung) 12 hours after injection.
Molecular Weight

462.50

Formula

C18H34N6O8
CAS No.
Sequence

Gly-Thr-Gly-Lys-Thr
Sequence Shortening

GTGKT
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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GTGKT Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

GTGKT254732-11-1GSK-3CDKApoptosisGlycogen synthase kinase-3Glycogen synthase kinase 3Cyclin dependent kinaseanti-cancer drug-resistant cancercyclin D1GSK3βathymic nude miceSNU387RMalme3MR melanoma cellsCAGEcyclin D1 promoter sequencesapoptosisHUVECInhibitorinhibitorinhibit

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