References in periodicals archive ?
Calcium influx induced by TRPV1 activation may cause activation or expression of key proteins such as endothelial nitric oxide synthase (eNOS), uncoupling protein 2 (UCP2), KLF2, PPARdelta, PPARgamma, and LXR[alpha] (McCarty et al., 2015).
Tannic acid as a plant-derived polyphenol exerts vasoprotection via enhancing KLF2 expression in endothelial cells.
In a study focusing on the effect of hyperglycemia on embryonic heart development, students Moneera Nasir and Hissa al Thani, supervised by Dr Marwan Abu-Madi and Dr Hussin Yalsin, found that hyperglycemia altered the gene expression of KLF2, grossly changed the heart structure and affected blood flow velocity and ejection throughout the developing heart.
In a study focusing on the effect of hyperglycaemia on embryonic heart development, students Moneera Nasir and Hissa al-Thani, supervised by Dr Marwan Abu-Madi and Dr Hussin Yalsin, found that hyperglycaemia altered the gene expression of KLF2, grossly changed the heart structure and affected blood flow velocity and ejection throughout the developing heart.
Huang et al., "Long noncoding RNA ZFAS1 promotes gastric cancer cells proliferation by epigenetically repressing KLF2 and NKD2 expression," Oncotarget, vol.
In situations of shear stress, it has been shown that the increasing of the Kruppel-like factor (KLF2) transcription factor induced the expression of functional miR-143/miR-145 cluster which was loaded in endothelial cell EVs and taken up by vascular smooth muscle cells in coculture , with acquisition of a contractile phenotype and stabilization of endothelium.
In these conditions, the vascular transcription factor involved in the E-NTPDase 1 is the Kruppel-like factor 2 (KLF2), which can bind near the transcriptional start site of E-NTPDase 1.
The failure of these cells to exit the tissue is currently thought to be due to their low expression of the transcription factor KLF2 and of S1PR1 and to their high expression of the C-type lectin CD69; as a result of these conditions, the cells fail to respond to an "exit cue" provided by S1P (sphingosine-1-phosphate), which is released mainly from lymphatic ECs.
Straight sections of artery that experience normal laminar blood flow are relatively spared from disease through a coordinated modulation of gene expression, predominantly controlled by the transcription factors KLF2 and KLF4 and activation of Nrf2 [29, 32, 114-116].
A potential mediator would have been KLF2, which is directly induced by shear stress via MEF2 and the MAPK signaling pathway, and has been implicated in the induction of eNOS and in keeping endothelial cells in a noninflammatory state [34-36].
Chromosomal translocation involving CDK6 gene at 7q21 as well as allelic loss of 7q31-32 is seen in a significant subset of the splenic MZL cases; NOTCH 2 and KLF2 mutations also might be present .
Qi et al., "Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2," Molecular Cancer, vol.
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