Cat. # | Size | Price | Inventory |
---|---|---|---|
88873S | 100 µl (50 tests) |
REACTIVITY | H All |
SENSITIVITY | Endogenous |
MW (kDa) | |
Source/Isotype | Rabbit IgG |
Product Information
Application | Dilution |
---|---|
Immunofluorescence (Immunocytochemistry) | 1:50 |
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalently purified water.
NOTE: Cells should be grown, treated, fixed and stained directly in multi-well plates, chamber slides or on coverslips.
NOTE: All subsequent incubations should be carried out at room temperature unless otherwise noted in a humid light-tight box or covered dish/plate to prevent drying and fluorochrome fading.
posted December 2010
Protocol Id: 221
Human, All Species Expected
Monoclonal antibody is produced by immunizing animals with KLH modified on lysines with ADP ribose.
ADP-ribosylation is involved in a variety of cellular processes, including mitotic spindle formation, chromatin decondensation, cell stress response, retroviral silencing, RNA biology, and transcription, but the most well-known function of ADP-ribose chains is to serve as a scaffold for recruiting DNA repair proteins that contain PAR-binding modules to sites of DNA damage (6). X-ray repair cross-complementing protein 1 (XRCC1), histone macroH2A1, the E3 ubiquitin ligase RNF146 (Iduna), and many of the PARPs themselves, among others, contain PAR-binding motifs (PBMs) or domains: WWE, PAR-binding zinc-finger (PBZ), or macrodomains (7). PARylation has a central role in cell survival, and is tightly regulated. PARP deficiency can leave a cell vulnerable to DNA damage-induced apoptosis, while hyper PARylation can lead to parthanatos, a unique form of cell death (8). The role of PARylation in DNA repair has inspired great interest in developing candidate drug inhibitors for PARP, in particular to treat breast, prostate, and small cell lung cancers with mutations in DNA repair genes like BRCA1/2, CHK2, or ATM. Stat1, PERK, p53, G-actin, and Ras are just a few examples of proteins that are functionally modulated by ADP-ribosylation (6,7). Modification by ADP-ribose can block protein interactions or, in the case of P2X7, cause a conformational change that, in the presence of ART2 expression, sensitizes naive murine T-cells to extracellular NAD+, leading to apoptosis (9).
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