Recycling the Cell Cycle Cyclins Revisited

By Andrew W. Murray. Cell, 2004

768 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/6f1e11792e7c2275e96699297f33b5c589276650

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Citations in the corpus

A hyperfused mitochondrial state achieved at G1–S regulates cyclin E buildup and entry into S phase (2009, positive): “For example, buildup of cyclin E at G1–S transition leads to the initiation of DNA replication, after which cells commit to mitosis (9).”
Control of cell proliferation and apoptosis by mob as tumor suppressor, mats. (2005, neutral): “During normal development of multicellular organisms, appropriate cell number and organ size are determined by coordinated cell growth, cell proliferation, and apoptosis (reviewed by Danial and Korsmeyer, 2004; Murray 2004; Sherr, 2004).”
MicroRNA and cancer (2012, neutral): “CDK activity subsequently triggers progression through sequential phases of the cell cycle (Murray, 2004).”
Living with or without cyclins and cyclin-dependent kinases. (2004, positive): “The current thinking is that the major differences between cyclins reflect their timing of expression, their subcellular localization, and other biochemical differences that help to mediate Cdk substrate access and selection, thereby allowing a more refined tuning of the cell cycle oscillator (Rober”
p38 MAP kinase inhibition enables proliferation of adult mammalian cardiomyocytes. (2005, neutral): “GENES & DEVELOPMENT 19:1175–1187 © 2005 by Cold Spring Harbor Laboratory Press ISSN 0890-9369/05; www.genesdev.org 1175 ferentiation of many cell types (Nebreda and Porras 2000; Wu et al. 2000; Ambrosino and Nebreda 2001; Bulavin et al. 2002; Shi and Gaestel 2002), including differentiation of P19…”
Stochastic model of yeast cell-cycle network (2006, neutral): “The stochasticity in the model is controlled by a temperature-like parameter β.”