Control of cell cycle transcription during G1 and S phases

Abstract

The accurate transition from G1 phase of the cell cycle to S phase is crucial for the control of eukaryotic cell proliferation, and its misregulation promotes oncogenesis. During G1 phase, growth-dependent cyclin-dependent kinase (CDK) activity promotes DNA replication and initiates G1-to-S phase transition. CDK activation initiates a positive feedback loop that further increases CDK activity, and this commits the cell to division by inducing genome-wide transcriptional changes. G1–S transcripts encode proteins that regulate downstream cell cycle events. Recent work is beginning to reveal the complex molecular mechanisms that control the temporal order of transcriptional activation and inactivation, determine distinct functional subgroups of genes and link cell cycle-dependent transcription to DNA replication stress in yeast and mammals.

Astrocyte reactivity after brain injury—: The role of galectins 1 and 3

“…Although the level of Ptch1 expression in reactive astrocytes was not significantly changed, it is possible that binding of extracellular Shh can disrupt interaction between Ptch1 and phosphorylated cyclin B1, thus allowing the complex to localize to the nucleus where it stimulates the G2 to M‐phase transition, as has been shown for Shh‐treated cells in vitro (Barnes et al, 2001; Ruiz i Altaba et al, 2002). As transcriptional regulation during G1‐to‐S transition is dependent on E2F transcription factors family (for review, see Bertoli et al, 2013), it is relevant to note that E2F2 and E2F8 were also strongly induced in reactive astrocytes. Thus, proliferation of reactive astrocytes is regulated at the transcriptional level by increasing the transcription of several proproliferative components, while their regulation by the Shh pathway is not reflected at the transcriptome level at least at this time point.…”

Cyclin E-CDK2 Protein Phosphorylates Plant Homeodomain Finger Protein 8 (PHF8) and Regulates Its Function in the Cell Cycle

“…E-4), ␤-actin catalog no. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19], and lamin B (catalog no. M-20) antibodies were purchased from Santa Cruz Biotechnology.…”

“…Multiple cyclin E-CDK2 substrates are cell division regulators. Cyclin E-CDK2 assists cyclin D-CDK4 in phosphorylating retinoblastoma protein, which leads to the release of E2F transcriptional factors from retinoblastoma protein-dependent inhibition to promote the expression of genes (such as cyclin E, myc, and DNA polymerase) that drive cells to enter S phase (8,9). Cyclin E-CDK2 also phosphorylates the CDK inhibitor p27 to promote its degradation (10).…”

microRNA-186 inhibits cell proliferation and induces apoptosis in human esophageal squamous cell carcinoma by targeting SKP2

“…13 S-phase kinase-associated protein 2 (SKP2), a part of SKP1-CUL1-F-box (SCF) complexes, is the specificity factor of an E3 ligase involved in cell-cycle regulation through degradation of the CKIs, 14 such as p21 cip1 , p27 kip1 , and p57 kip2 . Skp2 has a critical role in regulating many cellular processes such as cell-cycle regulation, cell proliferation, apoptosis, differentiation, and survival, all of which are closely related to cancer development through degradation of its substrates.…”