research use only
Cat.No.: F6758
| Dilution |
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| Application |
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| WB, IP |
| Reactivity |
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| Human, Mouse, Rat, Hamster, 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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| 28 kDa |
| Positive Control | Jurkat cells; C6 cells; HeLa cells; HUVEC cells; NIH/3T3 cells |
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| Negative Control |
| Specificity |
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| ORC6 Antibody [E10G21] detects endogenous levels of total ORC6 protein. |
| Clone |
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| E10G21 |
| Synonym(s) |
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| Origin recognition complex subunit 6; ORC6; ORC6L |
| Background |
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| ORC6 (Origin Recognition Complex Subunit 6) is an essential component of the heterohexameric Origin Recognition Complex that binds replication origins in G1 phase, recruiting Cdc6 and Cdt1 to assemble pre-replicative complexes and license chromosomal origins for accurate S-phase firing, while stabilizing MCM2-7 helicase association with chromatin to ensure complete genome duplication. ORC6 localizes to replication forks as an accessory factor in mismatch repair, directly recruiting MutSα (MSH2-MSH6) and MutLα (MLH1-PMS2) to facilitate DNA lesion recognition, MutLα activation, and ATR-mediated damage signaling, thereby preserving genomic integrity during replication stress. It features an N-terminal TFIIB-like helical repeat region containing DNA-binding residues Q129, R137, and K168, and a C-terminal cytokinesis domain that interacts with septins at the midbody to physically separate daughter cells and prevent binucleation. Mutations in ORC6 disrupt pre-RC assembly, causing Meier-Gorlin syndrome, a disorder marked by profound developmental defects including microcephaly, primordial dwarfism, and kneecap hypoplasia due to replication licensing failure. ORC6 overexpression hyperactivates replication origins, driving uncontrolled proliferation, migration, and invasion with poor prognosis in non-small cell lung cancer, hepatocellular carcinoma, renal cell carcinoma, and breast cancer, as well as emerging NFκB-mediated inflammatory roles in immune dysregulation. |
| References |
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