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C0620

Sigma-Aldrich

CDK4/Cyclin D1, active, GST tagged human

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

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Synonym(s):
BCL1, CMM3, D11S2878E, MG Cl4458, PRAD1, PSK-J3, U21 B31
UNSPSC Code:
12352200
NACRES:
NA.32

recombinant

expressed in baculovirus infected Sf9 cells

Quality Level

product line

PRECISIO® Kinase

Assay

≥70% (SDS-PAGE)

form

buffered aqueous glycerol solution

specific activity

12-16 nmol/min·mg

mol wt

CDK4 subunit ~57 kDa
cyclin D1 ~61 kDa

UniProt accession no.

shipped in

dry ice

storage temp.

−70°C

Gene Information

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, 0.2 5mM 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

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Regulatory Information

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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
S Mouron et al.
Nature communications, 13(1), 7529-7529 (2022-12-09)
Precision oncology research is challenging outside the contexts of oncogenic addiction and/or targeted therapies. We previously showed that phosphoproteomics is a powerful approach to reveal patient subsets of interest characterized by the activity of a few kinases where the underlying
Noel P Fusté et al.
Nature communications, 7, 11581-11581 (2016-05-18)
Cyclin D1 (Ccnd1) together with its binding partner Cdk4 act as a transcriptional regulator to control cell proliferation and migration, and abnormal Ccnd1·Cdk4 expression promotes tumour growth and metastasis. While different nuclear Ccnd1·Cdk4 targets participating in cell proliferation and tissue

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