Cdkn1a-flox Mouse

Cdkn1a, also known as Cip1/Waf1/p21, is a well-established gene primarily recognized for its crucial role in the cell cycle. It induces cell cycle arrest by inhibiting cyclin-dependent kinases (CDKs), and is also involved in processes like apoptosis, DNA damage response (DDR), and the regulation of stem cell fate [1].

In cisplatin-induced acute kidney injury (AKI), CDKN1A was identified as a key gene associated with ferroptosis in the p53 signaling pathway. Knockdown of CDKN1A in human renal tubular epithelial cells mitigated cisplatin-induced cell injury by reducing oxidative stress and ferroptosis, suggesting its potential as a biomarker for early diagnosis and a therapeutic target in AKI [2]. In esophageal cancer, CDKN1A polymorphisms were found to be associated with the risk of the disease in relation to age. For example, certain genotypes and alleles were significantly associated with EC risk for patients ≤ 55 years old, while different genotypes showed associations in those over 55 [3]. In colorectal cancer, a study in an Iranian population found that the AC genotype of the CDKN1A rs1801270 polymorphism may have a protective role [4].

In conclusion, Cdkn1a is essential for regulating the cell cycle and is involved in multiple biological processes. Its role in diseases such as AKI and various cancers has been revealed through functional studies. These findings from different disease-related research using human cell lines or population-based genetic studies contribute to understanding its biological functions and offer potential directions for disease diagnosis and treatment.