Example sentences for: cyclin-dependent

How can you use “cyclin-dependent” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Taken together, the significantly enriched classes found for both the A549 and the U118 genes in cell culture compared with tumors are highly indicative of processes of cell division and metabolism, with significant MeSH term classes for the two gene sets including 'Cell cycle' (62 genes for A549, 66 genes for U118), 'DNA replication' (30,33), 'Mitosis' (28,37), 'Mitochondria' (38,52), and 'Cyclin-dependent kinases' (21,30); and significant GO terms including 'Cell proliferation' (36,39), 'Metabolism' (108,134), 'Cytokinesis' (8,6), 'Tricarboxylic acid cycle' (3,5), and 'G1/S transition' (5,7).

  • In comparison to the two general alternative mechanisms utilized by known transforming viruses to promote cell-cycle progression, namely, by activating or bypassing endogenous D-type cyclins (herein, referred to as "cyclin D"), it has not been established whether HIV-1 gene products trigger either cyclin D-dependent or cyclin D-independent proliferation in non-lymphoid tissues [ 15 ] . In infected renal epithelium, HIV-1 could disrupt the inhibitory binding of pRb to E2F independent of endogenous cyclin D, analogous to transforming viral mechanisms that bypass and down-regulate endogenous cyclin D, such as SV-40 T antigen binding to pRb [ 16 ] , HHV-8 v -cyclin binding to and activating cyclin-dependent kinase-6 (CDK) [ 17 ] , and activation of cyclin E by EBV-induced c -myc [ 18 ] . Alternatively, HIV-1 could activate cyclin D-dependent proliferation, as exemplified by RSV v -src-mediated signaling [ 19 ] . In most tissues, the selective activation of these cell-cycle pathways is readily discernable.

  • In fission yeast, the checkpoint rad +genes ( hus1 +, rad1 +, rad3 +, rad9 +, rad17 +and rad26 +) and chk1 +manage the sensing and transducing operations of the DNA damage checkpoint [ 1 16 ] . Current data suggest that the Rad26/Rad3-kinase complex initially senses DNA damage by an unknown mechanism [ 17 ] . This response leads to an increase in the kinase activity of the complex [ 18 ] , which phosphorylates and activates the transducing protein kinase, Chk1 [ 19 ] . Finally, Chk1 delays mitotic entry by targeting Cdc25 and Wee1, regulators of cyclin-dependent kinase activity [ 20 21 22 ] .

  • PFD, pelvic floor disorders; p27, p27 kip1; PBS, phosphate-buffered saline; CL, corpus luteum or corpora lutea; cdk, cyclin-dependent kinase; p21, p21 Cip1/WAF1.

  • Candidate mechanisms for the block of proliferation by C/EBPα include 1) activation of the gene promoters of the cyclin-dependent kinase inhibitor p21 [ 37 ] , gadd45 [ 5 6 ] , gas2 and gas3 [ 38 39 ] , 2) post-transcriptional stabilization of p21 [ 22 ] , or 3) interactions of C/EBPα with cell cycle proteins including p21 [ 22 24 25 55 ] , CDK2 [ 25 36 ] , CDK4 [ 36 ] , retinoblastoma [ 54 ] , the retinoblastoma-related protein p107 [ 34 ] and the G1/S-regulating E2F transcription complex [ 26 33 ] (Fig.


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