[KO Validated] CDKN1A/p21 Rabbit mAb

The p53-p21-RB axis regulates the transcription of numerous genes critical for cell cycle control. p53 activation induces p21/CDKN1A, which inhibits cyclin-CDK complexes, leading to RB hypophosphorylation and repression of E2F-dependent genes, causing cell cycle arrest. Loss of p53 or RB function disrupts the cell cycle, promoting uncontrolled proliferation and tumorigenesis. Interestingly, in some p53-deficient tumor cells, p21 can still be highly expressed and may acquire oncogenic properties, potentially by disrupting DNA replication licensing. [1]

ABclonal A19094 (KO-Validated CDKN1A/p21 Rabbit mAb) was cited in the study by Dr. Ji, Dr. Cheng, and Dr. Zhao's research groups from Shanghai Jiao Tong University School of Medicine, titled CircHAS2 activates CCNE2 to promote cell proliferation and sensitizes the response of colorectal cancer to anlotinib, published in Molecular Cancer on March 21, 2024. In this study, CircHAS2 was shown to disrupt the USP10-p53 interaction, leading to reduced p53 stability and diminished expression of its downstream target, p21, while upregulating CCNE2. This facilitates cell cycle progression and proliferation. Anlotinib suppresses tumor growth by downregulating circHAS2, which in turn restores p53 function and its regulatory effects on cell cycle control.

Fig. 1 p53-p21-RB signaling. [1]

1. Engeland, Kurt. "Cell cycle regulation: p53-p21-RB signaling." Cell Death & Differentiation 29.5 (2022): 946-960.

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