Ikki

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Ikki

 

peasant uprisings in feudal Japan.

The peasant uprisings of the 15th and 16th centuries are divided into the pre-Ikki, Ikko-Ikki, Tokusei-Ikki, and Kuni-Ikki revolts. The pre-Ikki revolts were “land revolts,” that is, peasant uprisings for such demands as the reduction of rents; the most important of these was the 1428 uprising, which encompassed almost all the central provinces. The Ikko-Ikki uprisings were carried out under the banner of the Ikko Buddhist sect. The largest of these uprisings were in the 15th and 16th centuries. The Tokusei-Ikki were urban and peasant uprisings against usurers, and the Kuni-Ikki were “provincial uprisings,” that is, peasant and Samurai uprisings; the most important of these was in the province of Yamashiro in 1485–93. A total of 164 outbreaks are known.

Uprisings that occurred from the 17th century through the 19th were called Hyakusho-Ikki (this concept included not only uprisings but also other antifeudal outbreaks by the peasantry). Throughout the entire Tokugawa period (1603–1867), about 1,640 uprisings and other peasant outbreaks are known. The antifeudal struggle of the peasants weakened the Tokugawa government and facilitated its downfall at the time of the Bourgeois Revolution of 1867–68 (the Meiji Restoration).

References in periodicals archive ?
This signaling culminates with the phosphorylation of immune transcription factors via IKBKE, TBK1, and IKK protein kinases, leading to their nuclear translocation and production of type 1 IFN with subsequent expression of ISGs.
"IKBKE is a newly identified oconogene, a gene linked to cancer," said study lead author Jin Q.
"In our study, we demonstrated that IKBKE is a STAT 3 target gene and is induced by tobacco.
"STAT3 directly binds to the IKBKE promoter and induces IKBKE transcription," he added.
"IKBKE is induced by tobacco carcinogens and mediates tobacco action in promoting lung cancer cell survival.
Of the genes, only IKBKE showed elevated activity, and this occurred in 30 percent of the patients' cancers.
With IKBKE blocked, the cancerous cells slowly withered and died, indicating that the cells depended on it for survival.
The cancerous cells contained a mutation that produced 5 to 10 extra copies of IKBKE, but it remains unclear exactly how that mutation happens or what puts a person at risk of it.
Developing a drug to target IKBKE should be possible, Hahn says, because the enzyme that it produces is a so-called kinase.
Expression miRNA change Function References miR-34 * Downregulation Increase of XIAP involved in [99] resistance to apoptosis miR-203 Upregulation Increase of MMP-1 involved [100] in extracellular matrix degradation Increase of IL-6 involved in inflammation miR-155 Upregulation Decrease of MMP-3 involved [101] in extracellular matrix degradation miR-155 Upregulation Decrease of IKBKE involved [102] in inflammation miR-22 Downregulation Increase of CYR61 involved [103] in cell proliferation and Th17 cell differentiation miR-20a Downregulation Increase of ASK1 involved in [104] TLR4 pathway miR-19b Downregulation Increase of TLR2 involved in [105] innate immunity