protein
| interacts with RAD9 and ATR |
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CHEK1-interacting protein that participates in the DNA replication checkpoint |
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interacts with CDC7 (CDC7 is potentially required for activation of the ATR-CHEK1 checkpoint pathway through regulation of Claspin) |
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acts synergistically with damaged DNA to increase phosphorylation of CHEK1 by ATR |
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RAD9A-mediated Claspin localization is a vital step during checkpoint activation |
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RAD9A, RAD9B plays a role in locating Claspin to sites of DNA damage, facilitating its role during the CHEK1-mediated checkpoint response |
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mediates the phosphorylation and activation of CHEK1 by ATR |
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TIMELESS associates with S phase replication checkpoint proteins CLSPN and TIPIN , and plays an important role in maintaining replication fork stability at physical barriers, like centromeres, telomeres and ribosomal DNA repeats, as well as at termination sites |
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interacts with many factors involved in checkpoint regulation and replication fork machinery, including ATR, ATM, CHEK1, Tim, MCM4, MCM10, CDC45, CDC7K, DNA polymerases |
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in the presence of BRCA1, HERC2 interacts with CLSPN, a protein essential for G(2)-M checkpoint activation and replication fork stability |
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Claspin and RAD17 are reportedly involved in the DNA damage-induced phosphorylation of CHEK1, a hallmark of checkpoint activation |
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function of HERC2/USP20 in coordinating CHEK1 activation by modulating CLSPN stability, which ultimately promotes genome stability and suppresses tumor growth |
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USP20 is a positive regulator of CLSPN and suppresses the malignant characteristics of gastric cancer cells |
Other
| phosphorylation in response to replication stress is required for its association with CHEK1 |
| regulated by cell cycle |
| regulated by ATR in response to DNA damage |
| levels are controlled by proteasomal degradation, and this is regulated by PLK1 |
| cleavage by caspases, and proteasome-dependent degradation under apoptotic conditions, resulting in a reduction of the levels of both full-length claspin and its cleavage products |
| REL directly controls Claspin gene transcription |
| IKK complex(IKBKG, IKBKB) can regulate Claspin levels by controlling its mRNA expression |