TG003 | Clk family kinase inhibitor
NMR (Conforms)
Available Options
| size : | Price | Quantity | |
|---|---|---|---|
| 5 mg | $78.00 | ||
| 25 mg | $300.00 |
TG003 (719277-26-6) is a potent, ATP-competitive inhibitor of Clk-family kinases (IC50‘s = 15, 20 and 200 nM for mClk4, 1 and 2 respectively and >10 μM for mClk3).1 Also inhibits DYRK1A/B (IC50‘s = 24 and 34 nM respectively).2 Suppresses serine/arginine-rich protein phosphorylation, dissociation of nuclear speckles and Clk1/Sty-dependent alternative splicing in mammalian cells.1 TG003 affects the regulation of alternative splicing by phosphorylation of SR protein both in vitro and in vivo. Promotes skipping of exon 31 in the endogenous dystrophin gene.3 TG003 increases levels of Clk1/4 mature mRNAs by promoting splicing of the intron-retaining RNAs.4
References/Citations:
1) Muraki et al. (2004), Manipulation of alternative splicing by a newly developed inhibitor of Clks; J. Biol. Chem., 279 24246
2) Foucourt et al. (2014), Design and synthesis of thiazolo[5,4-f]quinazolines as DYRK1A inhibitors, part II; Molecules, 19 15411
3) Nishida et al. (2011), Chemical treatment enhances skipping of a mutated exon in the dystrophin gene; Nat. Commun., 2 308
4) Ninomiya et al. (2011), Stress-responsive maturation of Clk1/4 pre-mRNAs promotes phosphorylation of SR splicing factor; J. Cell Biol., 195 27
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
TG003 (719277-26-6) is a potent, ATP-competitive inhibitor of Clk-family kinases (IC50‘s = 15, 20 and 200 nM for mClk4, 1 and 2 respectively and >10 μM for mClk3).1 Also inhibits DYRK1A/B (IC50‘s = 24 and 34 nM respectively).2 Suppresses serine/arginine-rich protein phosphorylation, dissociation of nuclear speckles and Clk1/Sty-dependent alternative splicing in mammalian cells.1 TG003 affects the regulation of alternative splicing by phosphorylation of SR protein both in vitro and in vivo. Promotes skipping of exon 31 in the endogenous dystrophin gene.3 TG003 increases levels of Clk1/4 mature mRNAs by promoting splicing of the intron-retaining RNAs.4
References/Citations:
1) Muraki et al. (2004), Manipulation of alternative splicing by a newly developed inhibitor of Clks; J. Biol. Chem., 279 24246
2) Foucourt et al. (2014), Design and synthesis of thiazolo[5,4-f]quinazolines as DYRK1A inhibitors, part II; Molecules, 19 15411
3) Nishida et al. (2011), Chemical treatment enhances skipping of a mutated exon in the dystrophin gene; Nat. Commun., 2 308
4) Ninomiya et al. (2011), Stress-responsive maturation of Clk1/4 pre-mRNAs promotes phosphorylation of SR splicing factor; J. Cell Biol., 195 27
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