Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:6743-96-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Gene associated with retinoid-interferon-induced mortality-19 (GRIM-19) has been recognized as a tumor suppressor protein, which regulates cell growth, apoptosis, and migration by signal transducer and activator of transcription 3 (STAT3) signaling pathway and non-STAT3 pathway in glioma cells. Here, we investigated the molecular mechanisms that regulated GRIM-19 expression in glioma cells. By the TargetScan algorithm, four miRNAs, hsa-miR-17-3p, hsa-miR-423-5p, hsa-miR-3184-5p, and hsa-miR-6743-5p, were identified with the potential to bind with 3′-UTR of GRIM-19. Further miRNA inhibitor transfection and luciferase assays revealed that miR-6743-5p was able to directly target the 3′-UTR of GRIM-19. Additionally, miR-6743-5p expression was inversely related with GRIM-19 expression in glioma specimens and cell lines. Moreover, the inhibition of miR-6743-5p caused a significant inhibition of cell proliferation and a marked promotion of cell apoptosis in glioma cells, and this phenotype was rescued by GRIM-19 knockdown. Finally, the inhibition of miR-6743-5p expression suppressed the phosphorylation of STAT3, and the mRNA expression of CyclinD1 and Bcl-2, two target genes of STAT3, while miR-6743-5p mimic had the inversed effects. Treatment with STAT3 inhibitor AG490 partially rescued the proliferation-promoting and anti-apoptosis effects of miR-6743-5p overexpression or GRIM-19 knockdown. Collectively, miR-6743-5p may act as an oncomiRNA in glioma by targetting GRIM-19 and STAT3.
apoptosis, cell proliferation, glioma, GRIM-19, miR-6743-5p, STAT3
miR-6743-5p, as a direct upstream regulator of GRIM-19, enhances proliferation and suppresses apoptosis in glioma cells
Fang Cao,1,* Qiang Zhang,1,* Wei Chen,1 Feng Zheng,1 Qishan Ran,1,2 Yang He,1 Yang Gao,1 and Shengtao Yaocorresponding author2
2017 Dec 22
Pathogenic Yersinia spp. can be subdivided into highly pathogenic (high-pathogenicity) and low-pathogenicity strains. Several genes specific for the high-pathogenicity strains are clustered on a chromosomal fragment designated a “high-pathogenicity island” (HPI). In the present work, the HPI of biotype 1B strain Ye 8081 of Y. enterocolitica was characterized. We demonstrate important differences from the HPI of Y. pestis. The HPI of Y. enterocolitica is smaller (45 kb) and is not flanked by insertion sequences. A copy of the gene coding for the tRNA-Asn is present at one extremity of the HPI and may, as in uropathogenic Escherichia coli, participate in the excision of the island. In addition to the genes encoding the yersiniabactin-pesticin receptor and the high-molecular-weight protein 2, four repeated sequences are present on the HPI of Y. enterocolitica. At least two of them are insertion elements: previously described IS1328 and newly characterized IS1400. Comparison of the HPI of strain Ye 8081 with that of other Y. enterocolitica strains of biotype 1B indicates that most of the island is conserved, apart from 15 kb at the left-hand end which is variable, especially in the region where three repeated sequences are clustered.
Characterization of a large chromosomal "high-pathogenicity island" in biotype 1B Yersinia enterocolitica.
E Carniel, I Guilvout, and M Prentice
Hypothyroidism in polymyalgia rheumatica and giant cell arteritis: lack of any association.
B Dasgupta, E Grundy, and E Stainer
1990 Jul 14;