CDK2 Antibody (YA3903)
(Synonyms: p33)CDK2 Antibody (YA3903) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to CDK2.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, FC, ELISA
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Reactivity :
Human, Mouse
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Formulation:
Supplied in PBS with 0.05% sodium azide
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
FC
FC: Flow Cytometry
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:1000 | 1:200-1:1000 | 1:200-1:400 | 1:10000 |
Product Details
CDK2 Antibody (YA3903) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to CDK2.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse
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Observed Molecular WeightObserved band size: 34 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 34 kDa
Purified recombinant fragment of human CDK2 aa 197-295.
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS with 0.05% sodium azide
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
Cyclin-dependent kinase 2 (CDK2) is a serine/threonine kinase that forms active complexes with cyclin E and cyclin A to regulate the G1/S transition and S-phase progression during cell-cycle control[1][2]. CDK2 functions within the cyclin-CDK regulatory network that coordinates DNA replication, cell proliferation, and checkpoint signaling, thereby linking cell-cycle progression to genome stability mechanisms[2][3]. Mechanistically, aberrant CDK2 activation promotes uncontrolled proliferation and contributes to tumor development in multiple cancer types, making CDK2 a relevant therapeutic target in oncology research[1][3]. In disease models, elevated CDK2 activity has been associated with tumor growth, while genetic or pharmacological suppression of CDK2 can impair cancer-cell proliferation and enhance antitumor responses[1][4]. Compared with related cell-cycle kinases such as CDK1, CDK2 preferentially associates with cyclins E and A and exhibits distinct conformational and regulatory properties that support selective inhibitor development[5]. This isoform-specific behavior is important because CDK1 can compensate for several cell-cycle functions, whereas CDK2 remains particularly relevant in cyclin E-driven and replication-associated oncogenic contexts[1][3]. For experimental applications, selective CDK2 inhibitors are widely used to investigate cell-cycle regulation, DNA-replication stress, and cancer-cell dependency on cyclin E/CDK2 signaling, supporting both mechanistic studies and therapeutic discovery programs[1][3].
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Subcellular Localization
Cytoplasm, cytoskeleton, microtubule organizing center, centrosome; Nucleus, Cajal body; Cytoplasm; Endosome
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Expression
Induction:Induced transiently by TGFB1 at an early phase of TGFB1-mediated apoptosis -
Isoforms & Post-Translational Modification
P24941 has 2 isomers: P24941-1: 33930 Da (predicted); P24941-2: 30035 Da (predicted).
Phosphorylated at Thr-160 by CDK7 in a CAK complex (PubMed:28666995). Phosphorylation at Thr-160 promotes kinase activity, whereas phosphorylation at Tyr-15 by WEE1 reduces slightly kinase activity. Phosphorylated on Thr-14 and Tyr-15 during S and G2 phases before being dephosphorylated by CDC25A;Nitrosylated after treatment with nitric oxide (DETA-NO) -
Subunit
Found in a complex with CABLES1, CCNA1 and CCNE1. Interacts with CABLES1 (By similarity). Interacts with UHRF2. Part of a complex consisting of UHRF2, CDK2 and CCNE1. Interacts with the Speedy/Ringo proteins SPDYA and SPDYC (PubMed:15611625). Interaction with SPDYA promotes kinase activation via a conformation change that alleviates obstruction of the substrate-binding cleft by the T-loop (PubMed:28666995). Found in a complex with both SPDYA and CDKN1B/KIP1 (PubMed:12972555, PubMed:28666995). Binds to RB1 and CDK7. Binding to CDKN1A (p21) leads to CDK2/cyclin E inactivation at the G1-S phase DNA damage checkpoint, thereby arresting cells at the G1-S transition during DNA repair. Associated with PTPN6 and beta-catenin/CTNNB1. Interacts with CACUL1. May interact with CEP63. Interacts with ANKRD17. Interacts with CEBPA (when phosphorylated) (PubMed:15107404). Forms a ternary complex with CCNA2 and CDKN1B; CDKN1B inhibits the kinase activity of CDK2 through conformational rearrangements (PubMed:24670654, PubMed:8684460). Interacts with cyclins A, B1, B3, D, or E (PubMed:10499802, PubMed:10884347, PubMed:12185076, PubMed:23781148). Interacts with CDK2AP2 (PubMed:23781148)
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SwissProt ID
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Synonyms
p33
Documentation
[1]. Tadesse S, et al. Cyclin-Dependent Kinase 2 Inhibitors in Cancer Therapy: An Update. J Med Chem. 2019 May 9;62(9):4233-4251. [Content Brief]
[2]. Pellarin I, et al. Cyclin-dependent protein kinases and cell cycle regulation in biology and disease. Signal Transduct Target Ther. 2025 Jan 13;10(1):11. doi: 10.1038/s41392-024-02080-z. PMID: 39800748; PMCID: PMC11734941. [Content Brief]
[3]. Asghar U, et al. The history and future of targeting cyclin-dependent kinases in cancer therapy. Nat Rev Drug Discov. 2015 Feb;14(2):130-46. [Content Brief]
[4]. Chen Y, et al. CDK2 inhibition sensitizes anthracycline-induced immunogenic cell death and enhances the efficacy of anti-PD-1 therapy. Front Immunol. 2025 Jun 10;16:1570040. doi: 10.3389/fimmu.2025.1570040. PMID: 40557162; PMCID: PMC12185487. [Content Brief]
[5]. Foster WJ, et al. Hippocampal mGluR1-dependent long-term potentiation requires NAADP-mediated acidic store Ca2+ signaling. Sci Signal. 2018 Nov 27;11(558):eaat9093. [Content Brief]