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Recombinant Human Cyclin-dependent kinase 2 (CDK2)

To make this Recombinant Human CDK2 protein, the CDK2 gene was isolated at first and cloned into an expression vector. CUSABIO has built a mature recombinant protein platform. This Recombinant Human CDK2 protein was developed in the platform. It was expressed in E.coli at the region of 1-298aa of the Human CDK2 protein. N-terminal 6xHis tag was fused with the expression vector for affinity and purification purposes. The purity is 90%+ determined by SDS-PAGE. Cyclin-dependent kinase 2 (CDK2) is a member of the larger cell cycle regulating CDK family of kinases, activated by binding partner cyclins as its name suggests. In mitotic cells, CDK2 is activated by phosphorylation and binds to E-type cyclins to progress from G1 into S phase, then subsequently binds A-type cyclins in S phase to advance the cell cycle. In particular, it was thought that CDK2/cyclin E complexes were necessary for the phosphorylation of retinoblastoma (RB) protein and the release of E2F transcription factors to initiate S phase and DNA synthesis. Further analysis reveals that the CDK2 substrate RB remains phosphorylated, even at sites previously thought to be specific to CDK2, suggesting a compensatory mechanism by another kinase. During the last two decades, CDK2 inhibitors have not been developed for contraception but instead predominantly to treat cancer. Multiple CDK2 inhibitors have entered clinical trials, none have been approved by the Food and Drug Administration.

ACP03763

To make this Recombinant Human CDK2 protein, the CDK2 gene was isolated at first and cloned into an expression vector. CUSABIO has built a mature recombinant protein platform. This Recombinant Human CDK2 protein was developed in the platform. It was expressed in E.coli at the region of 1-298aa of the Human CDK2 protein. N-terminal 6xHis tag was fused with the expression vector for affinity and purification purposes. The purity is 90%+ determined by SDS-PAGE. Cyclin-dependent kinase 2 (CDK2) is a member of the larger cell cycle regulating CDK family of kinases, activated by binding partner cyclins as its name suggests. In mitotic cells, CDK2 is activated by phosphorylation and binds to E-type cyclins to progress from G1 into S phase, then subsequently binds A-type cyclins in S phase to advance the cell cycle. In particular, it was thought that CDK2/cyclin E complexes were necessary for the phosphorylation of retinoblastoma (RB) protein and the release of E2F transcription factors to initiate S phase and DNA synthesis. Further analysis reveals that the CDK2 substrate RB remains phosphorylated, even at sites previously thought to be specific to CDK2, suggesting a compensatory mechanism by another kinase. During the last two decades, CDK2 inhibitors have not been developed for contraception but instead predominantly to treat cancer. Multiple CDK2 inhibitors have entered clinical trials, none have been approved by the Food and Drug Administration.

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Specifications


Cat.No ACP03763 Target NameCDK2
FormLiquid or Lyophilized powderExpression SystemE.coli
Expression Range1-298aaMol Weight37.9kDa
Protein LengthFull lengthPurityGreater than 90% as determined by SDS-PAGE.
Storage Buffer5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0.

Immunogen Information


Target SpeciesHumanUniprot IDP24941
Background Information
  • Uniprot Id

    P24941

  • Target Species

    Human

  • Target Name

    CDK2

  • Target Full Name

    Cyclin-dependent kinase 2

  • Target Function

    Serine/threonine-protein kinase involved in the control of the cell cycle; essential for meiosis, but dispensable for mitosis. Phosphorylates CTNNB1, USP37, p53/TP53, NPM1, CDK7, RB1, BRCA2, MYC, NPAT, EZH2. Triggers duplication of centrosomes and DNA. Acts at the G1-S transition to promote the E2F transcriptional program and the initiation of DNA synthesis, and modulates G2 progression; controls the timing of entry into mitosis/meiosis by controlling the subsequent activation of cyclin B/CDK1 by phosphorylation, and coordinates the activation of cyclin B/CDK1 at the centrosome and in the nucleus. Crucial role in orchestrating a fine balance between cellular proliferation, cell death, and DNA repair in human embryonic stem cells (hESCs). Activity of CDK2 is maximal during S phase and G2; activated by interaction with cyclin E during the early stages of DNA synthesis to permit G1-S transition, and subsequently activated by cyclin A2 (cyclin A1 in germ cells) during the late stages of DNA replication to drive the transition from S phase to mitosis, the G2 phase. EZH2 phosphorylation promotes H3K27me3 maintenance and epigenetic gene silencing. Phosphorylates CABLES1. Cyclin E/CDK2 prevents oxidative stress-mediated Ras-induced senescence by phosphorylating MYC. Involved in G1-S phase DNA damage checkpoint that prevents cells with damaged DNA from initiating mitosis; regulates homologous recombination-dependent repair by phosphorylating BRCA2, this phosphorylation is low in S phase when recombination is active, but increases as cells progress towards mitosis. In response to DNA damage, double-strand break repair by homologous recombination a reduction of CDK2-mediated BRCA2 phosphorylation. Phosphorylation of RB1 disturbs its interaction with E2F1. NPM1 phosphorylation by cyclin E/CDK2 promotes its dissociates from unduplicated centrosomes, thus initiating centrosome duplication. Cyclin E/CDK2-mediated phosphorylation of NPAT at G1-S transition and until prophase stimulates the NPAT-mediated activation of histone gene transcription during S phase. Required for vitamin D-mediated growth inhibition by being itself inactivated. Involved in the nitric oxide- (NO) mediated signaling in a nitrosylation/activation-dependent manner. USP37 is activated by phosphorylation and thus triggers G1-S transition. CTNNB1 phosphorylation regulates insulin internalization. Phosphorylates FOXP3 and negatively regulates its transcriptional activity and protein stability. Phosphorylates CDK2AP2. Phosphorylates ERCC6 which is essential for its chromatin remodeling activity at DNA double-strand breaks.

  • Target Subcellular Location

    Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Nucleus, Cajal body. Cytoplasm. Endosome. Note=Localized at the centrosomes in late G2 phase after separation of the centrosomes but before the start of prophase. Nuclear-cytoplasmic trafficking is mediated during the inhibition by 1,25-(OH)(2)D(3).

  • Target Protein Families

    Protein kinase superfamily, CMGC Ser/Thr protein kinase family, CDC2/CDKX subfamily

  • Target Research Area

    Cancer

  • Target Synonyms

    Cdc2 related protein kinase; cdc2-related protein kinase; CDC28; CDC2A; Cdk 2; CDK1; CDK2; CDK2_HUMAN; CDKN2; Cell devision kinase 2; Cell division protein kinase 2; Cyclin dependent kinase 2; cyclin dependent kinase 2-alpha; Cyclin-dependent kinase 2; kinase Cdc2; MPF; p33 protein kinase; p33(CDK2)

  • Target Background

    This gene encodes a member of a family of serine/threonine protein kinases that participate in cell cycle regulation. The encoded protein is the catalytic subunit of the cyclin-dependent protein kinase complex, which regulates progression through the cell cycle. Activity of this protein is especially critical during the G1 to S phase transition. This protein associates with and regulated by other subunits of the complex including cyclin A or E, CDK inhibitor p21Cip1 (CDKN1A), and p27Kip1 (CDKN1B). Alternative splicing results in multiple transcript variants.

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