p21 in cancer: intricate networks and multiple activities

By T. Abbas, Anindya Dutta. Nature Reviews. Cancer, 2009

2,709 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c6290a2759e13b321b608d77b37ab7bda1d38351

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Citations in the corpus

Multiple functions of p21 in cell cycle, apoptosis and transcriptional regulation after DNA damage. (2016, background): “Consequently, MAPK enhances the p21 transcription in response to growth factor stimulation [1].”
Novel prognostic marker PRMT1 regulates cell growth via downregulation of CDKN1A in HCC (2017, background): “CDKN1A, which is a cyclin dependent kinase inhibitor, drives cell cycle arrest in response to various environmental stimuli [24].”
Overview of MicroRNA Biogenesis, Mechanisms of Actions, and Circulation (2018, background): “For example, cyclin-dependent kinase inhibitor 1A (CDKN1A), a tumor suppressor that is downregulated in multiple cancers (106), is targeted by at least 28 miRNAs and many of which are upregulated together in cancers where CDKN1A has been implicated (107).”
The cytoprotective role of the Keap1–Nrf2 pathway (2011, background): “In addition to promoting cell cycle arrest, p21 is also involved in other cellular processes including senescence, apoptosis and the response to oxidative stress (Esposito et al. 1998; Gartel and Tyner 2002; Abbas and Dutta 2009).”
Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021, background): “Members of the Krüppellike factor (KLF) transcription factor (TF) family can activate the CDKN1A gene by cooperating with p300-CREBBP (AliouatDenis et al., 2005; Abbas and Dutta, 2009).”
PRMT6 increases cytoplasmic localization of p21CDKN1A in cancer cells through arginine methylation and makes more resistant to cytotoxic agents (2015, background): “Three E3 ubiquitin ligase complexes, SCFSKP2 (SKP1-CUL1-SKP2), CRL4CDT2 (CUL4A or CUL4B-DDB1-CDT2) and APC/ CCDC20 poly-ubiquitinate p21, and promote the proteasomedependent proteolysis at specific cell cycle stages [2].”
Hematopoietic stem cell quiescence promotes error prone DNA repair and mutagenesis (2010, background): “We postulate that in HSPCs the high basal level of prosurvival genes coupled with the strong p53-mediated induction of p21 protect against the killing effects of increased proapoptotic gene expression, resulting mainly in growth arrest as already observed in other cellular contexts (Abbas and Dutta,”
The Tumor Suppressor Protein p53 and the Ferroptosis Network (2018, positive): “CDKN1A mediates its activities in cell cycle arrest, primarily by binding to and inhibiting the kinase activity of the cyclindependent kinases (CDKs) [75].”
Cell cycle regulation: p53-p21-RB signaling (2022, background): “In contrast to this main function, p21 has also been shown to function as an assembly factor for complexes of D-type cyclins with CDK4/6 at low stoichiometric concentrations [44].”