Sentence examples for cell cycle promotion from inspiring English sources

Although MEK5/ERK5 signalling clearly promotes cell cycle promotion in certain context (Kato et al, 1997, 1998), there are situations where ERK5 function does not contribute to proliferation (Squires et al, 2002; Wang et al, 2005).

To further explore the molecular mechanism of CHD1L in cell cycle promotion, expressions of several G1/S phase transition checkpoint related proteins were compared between CHD1L-transgenic and wildtype MEFs.

Bortezomib, the first-in-class proteasome inhibitor, has anticancer properties through wide-ranging mechanisms such as disruption of the cell cycle, promotion of apoptosis, and inhibition of proliferation and angiogenesis (Boccadoro et al, 2005).

However, pretreatment with 10058-F4 (an inhibitor of c-Myc transcriptional activity) or PD98059 (an inhibitor of ERK1/2) suppressed c-Myc expression and ERK1/2 phosphorylation, and inhibited cell cycle promotion by TGFβ1.

To reveal the potential molecular mechanism of GPR39 in cell cycle promotion, expressions of several key cell cycle regulators including p21, cyclin D1, CDK4 and CDK6 were compared between GPR39-c4 and Vec-30 cells.

Katarina Le Blanc pointed out that MSCs differ between foetal and adult tissues, as indicated by the differential expression of genes related to tissue development, cell cycle promotion, chromatin regulation, DNA repair and immunological antigen presentation [ 19].

Renal tubular cells enter in G1 cell arrest to block the effects of molecules contributing to cell-cycle promotion, such as cyclins.

Changes in miRNA levels are also important in PCa progression, as demonstrated by the role of miRNAs in blocking apoptosis, cell-cycle promotion, migration, invasion, and the maintenance of androgen-independent growth [ 6, 7].

Similarly, we demonstrated in this study that GPER/EGFR/ERK signal transduction mediates E2-induced proliferation in breast CAFs, based on the observation that G1 induced similar proliferative and cell-cycle promotion that was blocked not only by GPER interference but also by G15, AG, and U0126 administration.

Recruitment of quiescent cells to re-enter the cell cycle and promotion of cells within the cell cycle to continue dividing are central Cdk4-regulated mechanisms that control reconstitution of β-cell mass.

The effects of an activated TGF-β signalling pathway include inhibition of cell cycle progression, promotion of terminal differentiation and activation of cell death [ 1].