Summary
| Production Name | RASSF1 (19I9) Rabbit Monoclonal Antibody |
| Description | Recombinant rabbit monoclonal antibody |
| Host | Rabbit |
| Application | WB,IHC,IF-P |
| Reactivity | Human |
Performance
| Conjugation | Unconjugated |
| Modification | Unmodified |
| Isotype | IgG |
| Clonality | Monoclonal |
| Form | Liquid |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Buffer | Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% New type preservative N and 50% glycerol. Store at +4°C short term. Store at -20°C long term. Avoid freeze / thaw cycle. |
| Purification | Affinity purification |
Immunogen
| Gene Name | RASSF1 |
| Alternative Names | NORE2A; |
| Gene ID | 11186 |
| SwissProt ID | Q9NS23 |
Application
| Dilution Ratio | WB 1:1000-1:5000,IHC 1:50-1:100,IF-P 1:50-1:100 |
| Molecular Weight | 39kDa |
Background
Potential tumor suppressor. Required for death receptor-dependent apoptosis. Mediates activation of STK3/MST2 and STK4/MST1 during Fas-induced apoptosis by preventing their dephosphorylation. When associated with MOAP1, promotes BAX conformational change and translocation to mitochondrial membranes in response to TNF and TNFSF10 stimulation. Potential tumor suppressor. Required for death receptor- dependent apoptosis. Mediates activation of STK3/MST2 and STK4/MST1 during Fas-induced apoptosis by preventing their dephosphorylation. When associated with MOAP1, promotes BAX conformational change and translocation to mitochondrial membranes in response to TNF and TNFSF10 stimulation. Isoform A interacts with CDC20, an activator of the anaphase-promoting complex, APC, resulting in the inhibition of APC activity and mitotic progression. Inhibits proliferation by negatively regulating cell cycle progression at the level of G1/S-phase transition by regulating accumulation of cyclin D1 protein. Isoform C has been shown not to perform these roles, no function has been identified for this isoform. Isoform A disrupts interactions among MDM2, DAXX and USP7, thus contributing to the efficient activation of TP53 by promoting MDM2 self-ubiquitination in cell-cycle checkpoint control in response to DNA damage.
Research Area