F5, also known as Coagulation factor V, is a key regulator of blood coagulation. It is involved in the blood coagulation pathway, playing a crucial role in maintaining hemostasis. Dysregulation of F5 can lead to bleeding or thrombotic disorders [1,2,3].

In a study, a novel heterozygous 832 base pair deletion within F5 exon 13 (F5-Atlanta) was identified in a patient with severe bleeding. This deletion affected F5 and FV expression, leading to elevated levels of total and free TFPI and a FV isoform similar to FV-short described in East Texas bleeding disorder [1].

In breast cancer cells, F5 was found to be an estrogen-responsive gene. Estrogen stimulation increased F5 messenger RNA and FV protein in ERα-positive MCF-7 cells, and high F5 levels in ER-positive breast tumors were associated with increased relapse-free survival [2]. Also, the F5 6665A>G polymorphism was associated with an increased risk of venous thromboembolism in females [3].

In conclusion, F5 is essential for blood coagulation, and its dysregulation can contribute to bleeding and thrombotic disorders. Studies on F5 gene mutations and its regulation in different diseases, such as bleeding disorders and breast cancer, help us understand its role in these pathological conditions, providing insights for diagnosis and potential treatment strategies.