Anti-CDK2 antibody [EPR24495-145] - BSA and Azide free (Detector),Abcam,AB300171
Sandwich ELISA The recommended antibody orientation is based on internal optimization for ELISA-based assays. Antibody orientation is assay dependent and needs to be optimized for each assay type. Please note that the range provided for this antibody is only an estimation based on the performance of the product using the recommended antibody pair. Performance of the antibody pair will depend on the specific characteristics of your assay. We guarantee the product works in sandwich ELISA, but we do not guarantee the sensitivity or dynamic range of the antibody in your assay. Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents . What are the advantages of a recombinant monoclonal antibody? This product is a recombinant monoclonal antibody, which offers several advantages including: - High batch-to-batch consistency and reproducibility - Improved sensitivity and specificity - Long-term security of supply - Animal-free batch production For more information, read more on recombinant antibodies . Conjugation ready Our carrier-free antibodies are typically supplied in a PBS-only formulation, purified and free of BSA, sodium azide and glycerol. This conjugation-ready format is designed for use with fluorochromes, metal isotopes, oligonucleotides, and enzymes, which makes them ideal for antibody labelling, functional and cell-based assays, flow-based assays (e.g. mass cytometry) and Multiplex Imaging applications. Use our conjugation kits for antibody conjugates that are ready-to-use in as little as 20 minutes with 1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.
Host
Rabbit
Reactivity
Rat, Mouse, Human
Application
sELISA
Platform ID
BAB320501701

Abcam
Contact
Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215
Email:
Specifications
Scientific Background
Target data Serine/threonine-protein kinase involved in the control of the cell cycle; essential for meiosis, but dispensable for mitosis (PubMed : 10499802, PubMed : 10884347, PubMed : 10995386, PubMed : 10995387, PubMed : 11051553, PubMed : 11113184, PubMed : 12944431, PubMed : 15800615, PubMed : 17495531, PubMed : 19966300, PubMed : 20935635, PubMed : 21262353, PubMed : 21596315, PubMed : 28216226, PubMed : 28666995). Phosphorylates CABLES1, CTNNB1, CDK2AP2, ERCC6, NBN, USP37, p53/TP53, NPM1, CDK7, RB1, BRCA2, MYC, NPAT, EZH2 (PubMed : 10499802, PubMed : 10995386, PubMed : 10995387, PubMed : 11051553, PubMed : 11113184, PubMed : 12944431, PubMed : 15800615, PubMed : 19966300, PubMed : 20935635, PubMed : 21262353, PubMed : 21596315, PubMed : 28216226). Triggers duplication of centrosomes and DNA (PubMed : 11051553). 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 (PubMed : 18372919, PubMed : 19238148, PubMed : 19561645). Crucial role in orchestrating a fine balance between cellular proliferation, cell death, and DNA repair in embryonic stem cells (ESCs) (PubMed : 18372919, PubMed : 19238148, PubMed : 19561645). 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 (PubMed : 18372919, PubMed : 19238148, PubMed : 19561645). EZH2 phosphorylation promotes H3K27me3 maintenance and epigenetic gene silencing (PubMed : 20935635). Cyclin E/CDK2 prevents oxidative stress-mediated Ras-induced senescence by phosphorylating MYC (PubMed : 19966300). 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 (PubMed : 15800615, PubMed : 20195506, PubMed : 21319273). In response to DNA damage, double-strand break repair by homologous recombination a reduction of CDK2-mediated BRCA2 phosphorylation (PubMed : 15800615). Involved in regulation of telomere repair by mediating phosphorylation of NBN (PubMed : 28216226). Phosphorylation of RB1 disturbs its interaction with E2F1 (PubMed : 10499802). NPM1 phosphorylation by cyclin E/CDK2 promotes its dissociates from unduplicated centrosomes, thus initiating centrosome duplication (PubMed : 11051553). 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 (PubMed : 10995386, PubMed : 10995387). Required for vitamin D-mediated growth inhibition by being itself inactivated (PubMed : 20147522). Involved in the nitric oxide- (NO) mediated signaling in a nitrosylation/activation-dependent manner (PubMed : 20079829). USP37 is activated by phosphorylation and thus triggers G1-S transition (PubMed : 21596315). CTNNB1 phosphorylation regulates insulin internalization (PubMed : 21262353). Phosphorylates FOXP3 and negatively regulates its transcriptional activity and protein stability (By similarity). Phosphorylates ERCC6 which is essential for its chromatin remodeling activity at DNA double-strand breaks (PubMed : 29203878). See full target information CDK2
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