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Merck
Összes fotó(2)

Fontos dokumentumok

SRP0356

Sigma-Aldrich

GSK3β active human

recombinant, expressed in baculovirus infected Sf9 cells, ≥80% (SDS-PAGE)

Szinonimák:

glycogen synthase kinase 3 beta

Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez


About This Item

CAS-szám:
UNSPSC kód:
12352200
NACRES:
NA.32

biológiai forrás

human

rekombináns

expressed in baculovirus infected Sf9 cells

Teszt

≥80% (SDS-PAGE)

Forma

aqueous solution

specifikus aktivitás

≥500 pmol/min-μg

molekulatömeg

73 kDa

kiszerelés

pkg of 10 μg

technika/technikák

activity assay: suitable
inhibition assay: suitable

NCBI elérési szám

UniProt elérési szám

kiszállítva

dry ice

tárolási hőmérséklet

−70°C

Géninformáció

human ... GSK3B(2932)

Általános leírás

Glycogen Synthase Kinase 3β (GSK3β) is one of the two isoforms of GSK3 enzyme, both of which are encoded by different genes. This protein is predominantly cytoplasmic, but is also found to be localized to nucleus and mitochondria. It is a protein-serine kinase. This protein contains a protein kinase domain in its core, and is composed of 482 amino acids with a molecular weight of 46,712Da. It shows a wide range of tissue expression with the highest expression in brain.
Human GSK3beta GenBank Accession No. NM_002093), full length with N-terminal GST-tag, MW=73 kDa, expressed in a Baculovirus infected Sf9 cell expression system.

Alkalmazás

Useful for the study of enzyme kinetics, screening inhibitors, and selectivity profiling.

Biokémiai/fiziológiai hatások

Glycogen Synthase Kinase 3β (GSK3β) is responsible for rapid cyclin D1 turnover by phosphorylating it on Thr-286. It functions as a negative regulator of Wnt signaling during embryonic development and cell proliferation in adult tissues. This protein phosphorylates and regulates multiple proteins such as glycogen synthase, insulin receptor substrate-1, axin and APC (adenomatous polyposis coli). This protein is also shown to interact with multiple protein which are linked with Alzheimer′s disease (AD).

Tárolási osztály kódja

12 - Non Combustible Liquids

WGK

WGK 1

Lobbanási pont (F)

Not applicable

Lobbanási pont (C)

Not applicable


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Analitikai tanúsítványok (COA)

Lot/Batch Number

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Dokumentumtár megtekintése

B R Sperber et al.
Neuroscience letters, 197(2), 149-153 (1995-09-08)
Hyperphosphorylated tau protein is the major constituent of the paired helical filament (PHF), the major fibrous component of the neurofibrillary lesions of Alzheimer's disease (AD). Hyperphosphorylation of tau is believed to be the critical event that leads to filament assembly.
C Sutherland et al.
The Biochemical journal, 296 ( Pt 1), 15-19 (1993-11-15)
The beta-isoform of glycogen synthase kinase-3 (GSK3 beta) isolated from rabbit skeletal muscle was inactivated 90-95% following incubation with MgATP and either MAP kinase-activated protein kinase-1 (MAPKAP kinase-1, also termed RSK-2) or p70 S6 kinase (p70S6K), and re-activated with protein
Richard S Jope et al.
Trends in biochemical sciences, 29(2), 95-102 (2004-04-23)
Glycogen synthase kinase-3 (GSK3) is now recognized as a key component of a surprisingly large number of cellular processes and diseases. Several mechanisms play a part in controlling the actions of GSK3, including phosphorylation, protein complex formation, and subcellular distribution.
C A Grimes et al.
Progress in neurobiology, 65(4), 391-426 (2001-08-31)
Glycogen synthase kinase-3beta (GSK3beta) is a fascinating enzyme with an astoundingly diverse number of actions in intracellular signaling systems. GSK3beta activity is regulated by serine (inhibitory) and tyrosine (stimulatory) phosphorylation, by protein complex formation, and by its intracellular localization. GSK3beta
J A Diehl et al.
Genes & development, 12(22), 3499-3511 (1998-12-01)
The activities of cyclin D-dependent kinases serve to integrate extracellular signaling during G1 phase with the cell-cycle engine that regulates DNA replication and mitosis. Induction of D-type cyclins and their assembly into holoenzyme complexes depend on mitogen stimulation. Conversely, the

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