|Calculated MW||77055 Da|
|Other Names||Cell cycle checkpoint protein RAD17, hRad17, RF-C/activator 1 homolog, RAD17, R24L|
|Target/Specificity||A phospho-specific peptide corresponding to residues surrounding Serine 645 of human Rad17 was used as immunogen. The antibody only detects Rad17 phosphorylated on Serine 645.|
|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||Rad17 Antibody Phospho (pS645) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Essential for sustained cell growth, maintenance of chromosomal stability, and ATR-dependent checkpoint activation upon DNA damage. Has a weak ATPase activity required for binding to chromatin. Participates in the recruitment of the RAD1-RAD9- HUS1 complex and RHNO1 onto chromatin, and in CHEK1 activation. May also serve as a sensor of DNA replication progression, and may be involved in homologous recombination.|
|Cellular Location||Nucleus. Note=Phosphorylated form redistributes to discrete nuclear foci upon DNA damage|
|Tissue Location||Overexpressed in various cancer cell lines and in colon carcinoma (at protein level). Isoform 2 and isoform 3 are the most abundant isoforms in non irradiated cells (at protein level). Ubiquitous at low levels. Highly expressed in testis, where it is expressed within the germinal epithelium of the seminiferous tubuli. Weakly expressed in seminomas (testicular tumors).|
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Provided below are standard protocols that you may find useful for product applications.
Checkpoint Rad proteins function early in the DNA damage signaling cascade to arrest cell cycle progression in response to DNA damage (1). There is a direct regulatory linkage between the Rad17 homologue and the checkpoint kinases, ATM and ATR (2). ATR but not ATM phosphorylates the Rad17 checkpoint protein on Ser635 and Ser645 in vitro. In undamaged synchronized human cells, these two sites were phosphorylated in late G(1), S, and G(2)/M, but not in early-mid G(1). Treatment of cells with genotoxic stress induced phosphorylation of Rad17 in cells in early-mid G(1). This suggests that ATR and Rad17 are essential components of a DNA damage response pathway in mammalian cells (3).
1. Lindsey-Boltz LA, et al. Proc Natl Acad Sci U S A. 98(20):11236-41, 2001
2. Bao S, et al. Nature 411(6840):969-74, 2001
3. Post S, et al. Proc Natl Acad Sci U S A. 98(23):13102-7, 2001
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