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Chk2 Antibody Phospho (pS33/35)Rabbit Monoclonal Antibody
| Country | United States
Ordering Information
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| Catalog # | Size | Availability | Price | |
| AJ1543a | 100ul 400 ul | 2-3 days | $ 355.00 | DISCONTINED INQUIRE CLICK INQUIRE Add to cart |
- Specification
- Citiations : 0
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- Backgrounds
Chk2 Antibody Phospho (pS33/35) - Product info | |
| Application | WB
|
| Primary Accession | O96017 |
| Reactivity | Human |
| Clone Names | EPR916(2)Y |
| Calculated MW | 60915 Da |
| Gene ID 11200 | |
| Other Names CHEK2, CHK2, RAD53, Serine/threonine-protein kinase Chk2, Cds1 | |
| Target/Specificity A synthetic phospho-peptide corresponding to residues surrounding Serine 33/35 of human Chk2 was used as immunogen. The antibody only detects Chk2 phosphorylated on Serine 33/35. | |
| Dilution WB~~1:50000~200000 | |
| Format 50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA. | |
| Storage Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. | |
| Precautions Chk2 Antibody Phospho (pS33/35) is for research use only and not for use in diagnostic or therapeutic procedures. | |
Chk2 Antibody Phospho (pS33/35) - Protein Information | |
| Name CHEK2 | |
| Synonyms CDS1, CHK2, RAD53 | |
| Function Serine/threonine-protein kinase which is required for checkpoint-mediated cell cycle arrest, activation of DNA repair and apoptosis in response to the presence of DNA double-strand breaks. May also negatively regulate cell cycle progression during unperturbed cell cycles. Following activation, phosphorylates numerous effectors preferentially at the consensus sequence [L-X- R-X-X-S/T]. Regulates cell cycle checkpoint arrest through phosphorylation of CDC25A, CDC25B and CDC25C, inhibiting their activity. Inhibition of CDC25 phosphatase activity leads to increased inhibitory tyrosine phosphorylation of CDK-cyclin complexes and blocks cell cycle progression. May also phosphorylate NEK6 which is involved in G2/M cell cycle arrest Regulates DNA repair through phosphorylation of BRCA2, enhancing the association of RAD51 with chromatin which promotes DNA repair by homologous recombination. Also stimulates the transcription of genes involved in DNA repair (including BRCA2) through the phosphorylation and activation of the transcription factor FOXM1 Regulates apoptosis through the phosphorylation of p53/TP53, MDM4 and PML. Phosphorylation of p53/TP53 at 'Ser-20' by CHEK2 may alleviate inhibition by MDM2, leading to accumulation of active p53/TP53. Phosphorylation of MDM4 may also reduce degradation of p53/TP53. Also controls the transcription of pro-apoptotic genes through phosphorylation of the transcription factor E2F1. Tumor suppressor, it may also have a DNA damage-independent function in mitotic spindle assembly by phosphorylating BRCA1. Its absence may be a cause of the chromosomal instability observed in some cancer cells | |
| Cellular Location Isoform 2: Nucleus. Note=Isoform 10 is present throughout the cell Isoform 7: Nucleus. Isoform 12: Nucleus. | |
| Tissue Location High expression is found in testis, spleen, colon and peripheral blood leukocytes. Low expression is found in other tissues | |
Chk2 Antibody Phospho (pS33/35) - Related products
AP4999a: CHEK2 Antibody (N-term)
AP7407a: CHK2 Antibody (C-term)
RI11042: CHEK2 predesign siRNA
LY10024a: CHEK2 Over-expression Lysate
BP4999a: CHEK2 Antibody (N-term) Blocking Peptide
BP7407a: CHK2 Antibody (C-term) Blocking Peptide
AT1516a: CHEK2 Antibody (monoclonal) (M01)
Chk2 Antibody Phospho (pS33/35) - Application data
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A. Western blot analysis on HeLa cell lysates using anti-Phospho-Chk2 (pS33/35) RabMAb (Cat. #AJ1543a), 1:500 dilution. Cells were either (A) untreated (B) treated with irradiation
Chk2 Antibody Phospho (pS33/35) - Research Areas
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BACKGROUND
Chk2 is a checkpoint kinase that plays a role in regulating cell cycle progression. In response to DNA damage and DNA replicational stress, Chk1 and Chk2 phosphorylate Cdc25C to prevent entry into mitosis (1,2). Consisting of ionizing radiation (IR), UV irradiation or hydroxyurea treatment, DNA damage induces ATM/ATR to phosphorylate Thr68 and other sites in the amino terminal domain (3). Phosphorylation at Thr68 is a prerequisite for subsequent activation steps.
REFERENCES
1. Blasina, A., et al. Curr Biol. 9: 1
2. Matsuoka, S., et al. Science 282: 1893
3. Matsuoka, S., et al. Proc. Natl. Acad. Sci. USA 97: 10389
