Sentence examples for cycle check from inspiring English sources

Ontology editors have reasoning tools to discover such logical errors like discovering redundant links or cycle check routines.

Furthermore, it was demonstrated that 7d induced cell cycle arrest in G2/M phase in MGC-803 cells, and regulated the expression of cell cycle check point proteins, such as cyclin A, cyclin B, CDK1, cdc25c, and p21.

Our observations of increased DNA damage and CML formation are in line with the well-established fact that increased levels of macromolecular damage, whether spontaneously accumulated during serial passaging or induced by high levels of stress, results in the upregulation of several cell cycle check point regulators [25, 29, 30].

These cell cycle check points are G1 (during which cells prepare for replication), S (during which DNA is replicated and a complete copy of each chromosome is made) and G2/M (M is the last phase of the cell cycle during which new chromosomes are equally segregated between two daughter cells before division).

The observed growth arrest in GO-treated cells was further supported by the observation that the levels of the cell cycle check point marker p16 increased by 61% in hMSC-TERT cells treated with 0.75 mM and 1 mM (Figure 6). Figure 5 Frequency of cells in different phases of the cell cycle in untreated control and in GO-treated hMSC-TERT cells (3 days, 1 mM).

In other cell lines, cell cycle check points inhibit re-replication by activating ATR/Chk1 responses.

One of the molecular mechanisms of ErbB2-mediated paclitaxel resistance is that overexpression of the ErbB2 receptor leads to deregulation of the G2/M cell cycle check-point that inhibits paclitaxel-induced apoptosis.

The BRCT domain is found in a diverse group of proteins implicated in DNA repair and cell cycle check-point control (Bork et al, 1997; Callebaut and Mornon, 1997).

Conversely, the phosphorylation of p53 results in its stabilisation and activation [ 5- 7], bringing about its translocation to the nucleus, where it has been shown to bind preferentially to promoters which favour transcription of genes that encode proteins required in stress-induced cell cycle check-point control, DNA repair and apoptosis.

These observations, combined with the 11 cancer and invasion associated genes upregulated in DA, suggest an invasion-favoring profile similar to that described in cancer cells, characterized by reduced expression cell cycle check-point and tumor suppressor genes combined with increased expression of invasion genes.

As prolonged activation of DDR and cell cycle check-points result in permanent cells cycle arrest (cellular senescence; for a review, see [ 65, 66]), we next assessed the presence of senescent cells in cultures exposed to conditioned 'senescent' or control media using established markers of cellular senescence.