Not more than 1500 words
(1) Background of the gene product
(2) Background of the SNP
(3) Population variations of the SNP
(4) Impact of the SNP on the different splice variants
(5) References (from 3 to 5)
( gene is Rad17 (DNA Damage Checkpoint))
Please use Harvard style for referencing
This material may consist of step-by-step explanations on how to solve a problem or examples of proper writing, including the use of citations, references, bibliographies, and formatting. This material is made available for the sole purpose of studying and learning - misuse is strictly forbidden.Rad17 is a DNA damage checkpoint protein. The DNA-damage induced checkpoint process is a process in which the cell halts its replication and division if it detects DNA damage, in order to attempt to repair that damage. If the DNA damage cannot be repaired, the cell will initiate apoptosis and die. This mechanism ensures the integrity the DNA and prevents replication in case the damage to the cell’s DNA is extensive and beyond repair. This mechanism is especially important in multicellular organisms, as it is one of the organism’s safeguards against proliferation of DNA-damaged cells, i.e. it helps protect the body from tumor formation. Rad17 interacts with 3 other checkpoint proteins (Rad1, Hus1 and Rad9) early in the DNA damage-induced signaling pathway (Rauen et al, 2000). While all four proteins act as “sensors” that detect DNA damage, the three other proteins form a complex that detects DNA damage that resembles a sliding clamp, similar to the proliferating cell nucleus antigen; Rad17 interacts with 4 replication factor c (RFC) subunits to form a complex in the form of a clamp loader, that interacts with the Rad1-Hus1-Rad9 complex and initiates the signal transduction process for arresting cell cycle (Hiroyuki, N. and Makoto, N., 2006).
Single nucleotide polymorphisms...