research use only
Cat.No.: F8456
This antibody requires an anti-rat secondary antibody.
| Dilution |
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| Application |
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| WB, IP, IF |
| Reactivity |
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| Human, Monkey |
| Source |
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| Rat Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 78 kDa |
| Positive Control | Jurkat cells; HeLa cells |
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| Negative Control |
| Specificity |
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| ORC2 Antibody [P19N22] detects endogenous levels of total ORC2 protein. |
| Clone |
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| P19N22 |
| Synonym(s) |
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| Origin recognition complex subunit 2; ORC2 |
| Background |
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| Origin recognition complex 2 (ORC2) is a core subunit of the hexameric origin recognition complex (ORC), a conserved eukaryotic protein complex that binds to replication origins and nucleates assembly of the pre‑replication complex (pre‑RC) during late M and early G1 phases of the cell cycle. ORC2 integrates into the ORC heterohexamer, which contacts DNA and provides a platform for the sequential recruitment of Cdc6, Cdt1, and the MCM2–7 helicase complex, thereby licensing origins for a single round of DNA replication. ORC2 localizes to the nucleus as well as to centrosomes, centromeres, and heterochromatic regions, where it associates with HP1 and other chromatin‑associated proteins, and this dynamic subnuclear positioning is regulated through the cell cycle, with ORC2‑rich macromolecular assemblies forming at replication origins and heterochromatic domains. Phosphorylation of ORC2 at specific residues such as Thr116 and Thr226 by cyclin‑dependent kinases during S and M phases directly weakens ORC‑2–5 subunit interactions with chromatin and replication origins, leading to ORC dissociation and preventing relicensing within the same cell cycle, while other post‑translational modifications such as SUMOylation contribute to centromeric heterochromatin maintenance and epigenetic regulation. ORC2 participates in non‑replicative chromatin functions, including heterochromatin organization and regional gene‑silencing pathways, and dysregulation of ORC2 phosphorylation, localization, or abundance is linked to replication‑stress phenotypes, chromosome‑instability syndromes, and defects in cell‑cycle progression. |
| References |
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