Rad17 overexpression 293T裂解物(whole cell)

补充信息

This supplementary information is collated from multiple sources and compiled automatically.

Rad17 also known as CCYC1 is a protein involved in DNA damage checkpoint control. It has an approximate molecular weight of 75 kDa. Rad17 is expressed in various tissues with higher levels in proliferating cells such as cancerous tissues. It functions as a part of the replication factor C (RFC) complex delivering its essential role during the DNA replication and damage response.

Biological function summary

Rad17 plays an important role in maintaining genome stability by activating cell cycle checkpoints. It belongs to the RFC-like complex which identifies DNA damage and initiates the DNA repair process. The complex binds to chromatin and helps recruit the 9-1-1 complex (Rad9-Rad1-Hus1) to sites of DNA damage. This action is important for the cell to halt the cell cycle and commence repair preventing mutations from being passed on during cell division.

Pathways

Rad17 functions in the DNA damage response pathway and is involved in the ATR-Chk1 pathway. Rad17 recruits ATR (ataxia-telangiectasia and Rad3-related protein) to stalled replication forks facilitating the phosphorylation and activation of Chk1 a checkpoint kinase. This signal allows cells to pause the replication process and repair DNA before continuing the cell cycle. Rad17 is closely related to proteins such as ATR and Chk1 through these pathways as they work together to maintain cellular integrity.

Rad17 has links to cancer and genomic instability syndromes. Mutations or malfunctions in Rad17 can disrupt normal checkpoint control and repair mechanisms leading to uncontrolled cell proliferation and tumor development. In cancer Rad17 interacts with proteins such as BRCA1 in pathways that emphasize DNA repair and checkpoint activation. BRCA1 and Rad17 coordinate to preserve genomic stability and disruptions in these proteins' functions can contribute to the onset of certain breast and ovarian cancers.