在對DNA損傷和復制阻滯作出反應時，通過控制關鍵的細胞周期調節器，細胞周期進程停止。該基因編碼的蛋白質是一種細胞周期檢查點調節因子和假定的腫瘤抑制因子。它包含一個叉頭相關蛋白相互作用域，在對DNA損傷作出反應時對激活至關重要，并在對復制阻滯和DNA損傷作出反應時迅速磷酸化。當被激活時，編碼蛋白被認為能抑制CDC25C磷酸酶，防止進入有絲分裂，并已被證明能穩定腫瘤抑制蛋白p53，導致細胞周期在g1停滯。此外，這種蛋白與BRCA1相互作用并磷酸化，使BRCA1在DNA損傷后恢復生存。這種基因的突變與李夫瑯梅尼綜合征有關，李夫瑯梅尼綜合征是一種高度滲透性的家族性癌癥表型，通常與TP53的遺傳突變有關。而且，這種基因的突變被認為是導致肉瘤、乳腺癌和腦腫瘤的一種傾向。這種核蛋白是絲氨酸/蘇氨酸蛋白激酶CDS1亞家族的成員。一些轉錄變體編碼不同的亞型已被發現的這個基因。
In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. The protein encoded by this gene is a cell cycle checkpoint regulator and putative tumor suppressor. It contains a forkhead-associated protein interaction domain essential for activation in response to DNA damage and is rapidly phosphorylated in response to replication blocks and DNA damage. When activated, the encoded protein is known to inhibit CDC25C phosphatase, preventing entry into mitosis, and has been shown to stabilize the tumor suppressor protein p53, leading to cell cycle arrest in G1. In addition, this protein interacts with and phosphorylates BRCA1, allowing BRCA1 to restore survival after DNA damage. Mutations in this gene have been linked with Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53. Also, mutations in this gene are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors. This nuclear protein is a member of the CDS1 subfamily of serine/threonine protein kinases. Several transcript variants encoding different isoforms have been found for this gene.