p27, a novel inhibitor of G1 cyclin-Cdk protein kinase activity, is related to p21.

By H. Toyoshima, T. Hunter. 1994

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Citations in the corpus

In silico protein interaction screening uncovers DONSON’s role in replication initiation (2023, background): “The defects seen upon DONSON depletion mirrored the effect of adding the CDK2 inhibitor p27 Kip ( 33 , 34 ) (Fig.1D,lane4,CDKi),suggestingthatDONSON functionsatthefinalstageofCMGassembly.”
The role of the cyclin-dependent kinase inhibitor p21 in apoptosis. (2002, unknown): “also includes p27 (10, 11) and p57 (12, 13).”
Senescence impairs successful reprogramming to pluripotent stem cells. (2009, unknown): “…or CDKN1 family (p21Cip1, p27Kip1 and p57Kip2) (Gu et al., 1993; Harper et al., 1993; Lee et al., 1995; Matsuoka et al., 1995; Polyak et al., 1994; Toyoshima and Hunter, 1994) and the INK4 or CDKN2 family (p16INK4a, p15INK4b, p18INK4c and p19INK4d) (Hannon and Beach, 1994; Hirai et al., 1995;…”
Functional Analysis of Cyclin-Dependent Kinase Inhibitors of Arabidopsis (2001, background): “These CKIs bind to all known G1/S-specific CDKs (Toyoshima and Hunter, 1994; Lee et al., 1995).”
Forkhead Transcription Factor FKHR-L1 Modulates Cytokine-Dependent Transcriptional Regulation of p27KIP1 (2000, background): “p27 is an inhibitor of cell cycle progression, exerting its effect through interaction with cyclinCDK complexes and arresting cells in G0/G1 (53).”
CDK inhibitors: cell cycle regulators and beyond. (2008, unknown): “…et al., 1993; Gu et al., 1993; Harper et al., 1993; Xiong et al., 1993), p27Kip1 (p27, cdkn1b) (Polyak et al., 1994a; Polyak et al., 1994b; Toyoshima and Hunter, 1994), and p57Kip2 (p57, cdkn1c) (Lee et al., 1995; Matsuoka et al., 1995) share a conserved N-terminal domain that mediates…”
Molecular mechanisms underlying ErbB2/HER2 action in breast cancer (2000, background): “Under physiological conditions, it seems that p21Waf1 and p27Kip1, which can act as inhibitors of cyclin E- and A-dependent kinases, also act to positively regulate cyclin D-dependent kinases (Cheng et al., 1999; Polyak et al., 1994; Toyoshima and Hunter, 1994).”
Flexible nets (2005, background): “…is another member of the p21 family of Cdk inhibitors that negatively regulate the cell cycle and thereby contributes to cellular growth and development [125,126]. p27 Kip1 contains an N-terminal Cdk-inhibition domain and a C-terminal domain of unknown function called the QT domain [125,127].”
NPAT links cyclin E-Cdk2 to the regulation of replication-dependent histone gene transcription. (2000, methodology): “We also observed that H4 transcription was inhibited by cotransfection of p27 or a dominant-negative Cdk2, known inhibitors of the G1to-S phase transition (van den Heuvel and Harlow 1993; Polyak et al. 1994; Toyoshima and Hunter 1994), and that this inhibition is H4 SSCS dependent (data not shown).”
BCL-6 represses genes that function in lymphocyte differentiation, inflammation, and cell cycle control. (2000, background): “Given the repression arrests the cell cycle in response to extrinsic signals at the G1-to-S phase transition by binding to G1 cyclinof blimp-1 by BCL-6, downregulation of BCL-6 may be a required first step in the decision of a GC B cell to dependent kinases (Polyak et al., 1994; Toyoshima and Hunter”
Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “p27KIP1 inhibits CYCLIN D1-CDK4/6 activity, thereby preventing cells from progressing to S phase [466].”
Mammalian cell-cycle regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms (2009, background): “…specifically bind to Cdk4 and Cdk6 and prevent D-type cyclin activity and the Cip/Kip family (p21Cip1/Waf1/Sdi1, p27Kip1, p57Kip2) inhibits Cdk2/cyclin E, Cdk2/cyclin A, Cdk1/ cyclin A, as well as Cdk1/cyclin B activity (Toyoshima and Hunter, 1994; Aprelikova et al., 1995; O’Connor, 1997).”