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C1249

Sigma-Aldrich

CDK4/CyclinD3, active, GST tagged human

PRECISIO® Kinase, recombinant, expressed in baculovirus infected Sf9 cells, ≥70% (SDS-PAGE), buffered aqueous glycerol solution

Synonym(s):

CCND3, CMM3, MGC14458, PSK-J3

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About This Item

UNSPSC Code:
51111800
NACRES:
NA.32

recombinant

expressed in baculovirus infected Sf9 cells

Quality Level

200

product line

PRECISIO® Kinase

assay

≥70% (SDS-PAGE)

form

buffered aqueous glycerol solution

specific activity

13-19 nmol/min·mg

mol wt

CDK4 subunit ~58 kDa
cyclin D3 ~58 kDa

UniProt accession no.

P11802
P30281

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... CCND3(896) , CDK4(1019)

Biochem/physiol Actions

CDK4 is a member of the cyclin-dependent protein kinase family and is involved in the control of cell proliferation during the G1 phase of cell cycle. CDK4 forms a complex with the D-type cyclins and is inhibited by p16 (cyclin-dependent kinase inhibitor-2). CDK4 can mediate phosphorylation of the C-terminal region of Rb protein leading to an active transcriptional repression of E2F complex. CDC37 and HSP90 can preferentially associate with the fraction of CDK4 not bound to D-type cyclins. SMAD3 is a major physiologic substrate of the G1 cyclin-dependent kinases CDK4 and CDK2.

Physical form

Supplied in 50 mM Tris-HCl, pH 7.5, with 150 mM NaCl, 0.25 mM DTT, 0.1 mM EGTA, 0.1 mM EDTA, 0.1 mM PMSF, and 25% glycerol.

Legal Information

PRECISIO is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificates of Analysis (COA)

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J W Harbour et al.
Cell, 98(6), 859-869 (1999-09-28)
We present evidence that phosphorylation of the C-terminal region of Rb by Cdk4/6 initiates successive intramolecular interactions between the C-terminal region and the central pocket. The initial interaction displaces histone deacetylase from the pocket, blocking active transcriptional repression by Rb.
Isao Matsuura et al.
Nature, 430(6996), 226-231 (2004-07-09)
Transforming growth factor-beta (TGF-beta) potently inhibits cell cycle progression at the G1 phase. Smad3 has a key function in mediating the TGF-beta growth-inhibitory response. Here we show that Smad3 is a major physiological substrate of the G1 cyclin-dependent kinases CDK4

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