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This paper elucidates a model to regulate glioma cell cycle progression in which hUCBSC acts to control cyclin D1 induction and in concert its partner kinases, Cdk 4 and Cdk 6 by mediating cell cycle arrest at G0-G1 phase.
Carcinogens may induce tumourigenesis partly by mediating cell cycle malfunction.
The p53 tumour suppressor protein inhibits malignant progression by mediating cell cycle arrest, apoptosis or repair following cellular stress.
This is because although AP-1 may stimulate tumor growth and survival by mediating cell cycle progression, inflammation, angiogenesis, and migration, AP-1 may also be instrumental in the induction of apoptosis via the upregulation of FAS, FASL, and TRAIL, as well the differential regulation of BCL2 protein family members.
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Previous studies indicated that miR-34b/c expression is regulated by p53, which mediates cell-cycle arrest and promotes apoptosis [ 17, 38].
Because we showed previously that TGF-β1 and rapamycin cooperate to induce cell cycle arrest [ 20], these results are consistent with the idea that decreases induced in nuclear Cdk2 concentrations by TGF-β1 + rapamycin constitute a novel mechanism by which TGF-β1 mediates cell cycle arrest.
Wee1 is a critical component of the G2/M cell cycle checkpoint machinery and mediates cell cycle arrest by phosphorylation of CDC2.
Unlike deletion of apoptosis genes, genes that mediate cell cycle exit by differentiation are present in myelodysplastic syndrome (MDS) and AML cells but are epigenetically repressed: MDS/AML cells express high levels of key lineage-specifying transcription factors.
It has been shown that in non-irradiated hESC cells (H1 cell line) p21 WAF1/CIP1 mRNA levels are minimal and upon irradiation the level increases up to 300-fold, the p53/p21 WAF1/CIP1 pathway gets activated and may respond to DNA damage and mediate cell cycle arrest by blocking DNA synthesis and allowing DNA repair or entry into apoptosis [42].
The inhibitor of cyclin-dependent kinases WAF1/p21 has been shown to mediate cell cycle arrest by p53 and other factors.
Thus, the string homolog Cdc25B, encoding a dual-specific phosphatase that mediates cell cycle progression by activating cyclin-dependent kinases, has been shown to possess oncogenic potential and is frequently overexpressed in human prostate cancer tissues [ 79].
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