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Rabbit Polyclonal Phospho-Cdk2 (T160) antibody (STJ90220)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IHC, ELISA
Recommended dilution: WB 1:500-1:2000; IHC 1:100-1:300; ELISA 1:5000;
Recommended protocols: check protocols
Click or hover above images to see image description for Cdk2 (phospho Thr160) Polyclonal Antibody.
Check alternative names for the antibodyExpand
CDK2 antibody, CDKN2 antibody,|CDC28 antibody|CDC2A antibody|Cdk 2 antibody|CDK1 antibody|CDK2 antibody|CDK2_HUMAN antibody|CDKN2 antibody|Cell devision kinase 2 antibody|Cell division protein kinase 2 antibody|Cyclin dependent kinase 2 antibody|cyclin dependent kinase 2-alpha antibody|Cyclin-dependent kinase 2 antibody|kinase Cdc2 antibody|MPF antibody|p33 protein kinase antibody|p33(CDK2) antibody|Anti-Cdk2 antibody [E304] (ab32147)
SCBT cat No: sc-70829|sc-136191|sc-53220|sc-6248|sc-748|sc-163|sc-515036|sc-390283|sc-48131|sc-81836|
Cdk2 (phospho Thr160) Polyclonal Antibody
|Catalogue No.|| |
Human, Mouse, Rat
Phospho-Cdk2 (T160) Polyclonal Antibody detects endogenous levels of Cdk2 protein only when phosphorylated at T160.
Synthesized phospho-peptide derived from human Cdk2 around the phosphorylation site of T160
WB, IHC, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IHC 1:100-1:300; ELISA 1:5000;
|Molecular weight|| |
Cdk2 (phospho Thr160) Antibody was tube-contained. Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Cdk2 (phospho Thr160) Antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Cyclin-dependent kinase 2 antibody, Cell division protein kinase 2 antibody, p33 protein kinase antibody
|Protein names|| |
Cyclin-dependent kinase 2 , Cell division protein kinase 2 , p33 protein kinase
|Protein 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. Interacts with cyclins A, B1, B3, D, or E. 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 (By similarity). 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 (By similarity). / ATP + a protein = ADP + a phosphoprotein. / Mg2+ / Phosphorylation at Thr-14 or Tyr-15 inactivates the enzyme, while phosphorylation at Thr-160 activates it. Inhibited by 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), AG-024322, N-(4-Piperidinyl)-4-(2,6-dichlorobenzoylamino)-1H-pyrazole-3-carboxamide (AT7519), R547 (Ro-4584820), purine, pyrimidine and pyridine derivatives, 2-aminopyrimidines, paullones, thiazo derivatives, macrocyclic quinoxalin-2-one, pyrazolo[1,5-a]-1,3,5-triazine, pyrazolo[1,5-a]pyrimidine, 2-(1-ethyl-2-hydroxyethylamino)-6-benzylamino-9-isopropylpurine (roscovitine, seliciclib and CYC202), SNS-032 (BMS-387032), triazolo[1,5-a]pyrimidines, staurosporine and olomoucine. Stimulated by MYC. Inactivated by CDKN1A (p21).
|Protein tissue specificity|| |
Induced transiently by TGFB1 at an early phase of TGFB1-mediated apoptosis.
|Protein sequence and domain|| |
Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. CDC2/CDKX subfamily. / Contains 1 protein kinase domain.
|Protein post-translational modifications|| |
Phosphorylated at Thr-160 by CDK7 in a CAK complex. 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).
|Protein cellular localization|| |
Cytoplasm > cytoskeleton > microtubule organizing center > centrosome / Nucleus > Cajal body / Cytoplasm / Endosome
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St John’s Laboratory Ltd.
|Product type|| |
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