Alexa Fluor® 568 Anti-Cdk2 antibody [E304],Abcam,AB312419

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 . How are conjugated primary antibodies validated? This conjugated primary antibody is released using a quantitative quality control method that evaluates binding affinity post-conjugation and efficiency of antibody labeling. For suitable applications and species reactivity, please refer to the unconjugated version of this clone.

Host

Rabbit

Reactivity

Human, Mouse, Rat

Application

Flow Cyt (Intra), ICC/IF, Target Binding Affinity, Antibody Labelling, IHC-P

Conjugate

Alexa Fluor® 568

Platform ID

BAB107981231

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAlexa Fluor® 568 Anti-Cdk2 antibody [E304]
Cat. No.AB312419
HostRabbit
IsotypeIgG
ReactivityHuman, Mouse, Rat
ConjugationAlexa Fluor® 568
ApplicationFlow Cyt (Intra), ICC/IF, Target Binding Affinity, Antibody Labelling, IHC-P
ClonalityMonoclonal
Clone NumberE304
Concentration0.5 mg/mL Batch dependent concentration
ImmunogenThe exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein A
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7.4 Preservative: 0.02% Sodium azide Constituents: PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Storage-20°C
Regulatory StatusResearch Use Only

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, SUV39H1, EZH2 (PubMed : 10499802, PubMed : 10995386, PubMed : 10995387, PubMed : 11051553, PubMed : 11113184, PubMed : 12944431, PubMed : 15800615, PubMed : 19966300, PubMed : 20935635, PubMed : 21262353, PubMed : 21596315, PubMed : 24728993, 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). Acts as a regulator of the phosphatidylinositol 3-kinase/protein kinase B signal transduction by mediating phosphorylation of the C-terminus of protein kinase B (PKB/AKT1 and PKB/AKT2), promoting its activation (PubMed : 24670654). See full target information CDK2

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