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- W2806777665 abstract "Inositol-requiring transmembrane kinase/endoribonuclease 1α (IRE1α) is the most prominent and evolutionarily conserved endoplasmic reticulum (ER) membrane protein. This transduces the signal of misfolded protein accumulation in the ER, named as ER stress, to the nucleus as unfolded protein response (UPR). The ER stress-mediated IRE1α signaling pathway arbitrates the yin and yang of cell life. IRE1α has been implicated in several physiological as well as pathological conditions, including immune disorders. Autoimmune diseases are caused by abnormal immune responses that develop due to genetic mutations and several environmental factors, including infections and chemicals. These factors dysregulate the cell immune reactions, such as cytokine secretion, antigen presentation, and autoantigen generation. However, the mechanisms involved, in which these factors induce the onset of autoimmune diseases, are remaining unknown. Considering that these environmental factors also induce the UPR, which is expected to have significant role in secretory cells and immune cells. The role of the major UPR molecule, IRE1α, in causing immune responses is well identified, but its role in inducing autoimmunity and the pathogenesis of autoimmune diseases has not been clearly elucidated. Hence, a better understanding of the role of IRE1α and its regulatory mechanisms in causing autoimmune diseases could help to identify and develop the appropriate therapeutic strategies. In this review, we mainly center the discussion on the molecular mechanisms of IRE1α in the pathophysiology of autoimmune diseases." @default.
- W2806777665 created "2018-06-13" @default.
- W2806777665 creator A5029333655 @default.
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- W2806777665 creator A5045460414 @default.
- W2806777665 creator A5068304729 @default.
- W2806777665 creator A5077043027 @default.
- W2806777665 date "2018-06-06" @default.
- W2806777665 modified "2023-10-16" @default.
- W2806777665 title "IRE1α Implications in Endoplasmic Reticulum Stress-Mediated Development and Pathogenesis of Autoimmune Diseases" @default.
- W2806777665 cites W1497659049 @default.
- W2806777665 cites W150569175 @default.
- W2806777665 cites W1505701939 @default.
- W2806777665 cites W1530495975 @default.
- W2806777665 cites W1534272867 @default.
- W2806777665 cites W1537983046 @default.
- W2806777665 cites W1540298277 @default.
- W2806777665 cites W1561041814 @default.
- W2806777665 cites W1561349380 @default.
- W2806777665 cites W1569236547 @default.
- W2806777665 cites W1573568265 @default.
- W2806777665 cites W1573805380 @default.
- W2806777665 cites W1575156763 @default.
- W2806777665 cites W1579851397 @default.
- W2806777665 cites W1579942073 @default.
- W2806777665 cites W1583798678 @default.
- W2806777665 cites W1598330158 @default.
- W2806777665 cites W1616384098 @default.
- W2806777665 cites W1646704914 @default.
- W2806777665 cites W1651776210 @default.
- W2806777665 cites W1653604424 @default.
- W2806777665 cites W1672219033 @default.
- W2806777665 cites W1676144893 @default.
- W2806777665 cites W1765185969 @default.
- W2806777665 cites W1799806109 @default.
- W2806777665 cites W1820973630 @default.
- W2806777665 cites W1822514482 @default.
- W2806777665 cites W1823288226 @default.
- W2806777665 cites W1833135903 @default.
- W2806777665 cites W1840914099 @default.
- W2806777665 cites W1856950927 @default.
- W2806777665 cites W1863320924 @default.
- W2806777665 cites W1883890187 @default.
- W2806777665 cites W1901580941 @default.
- W2806777665 cites W1903866035 @default.
- W2806777665 cites W1905806846 @default.
- W2806777665 cites W1942558899 @default.
- W2806777665 cites W1955652166 @default.
- W2806777665 cites W1957936329 @default.
- W2806777665 cites W1965021089 @default.
- W2806777665 cites W1965364089 @default.
- W2806777665 cites W1966157599 @default.
- W2806777665 cites W1966346152 @default.
- W2806777665 cites W1967188261 @default.
- W2806777665 cites W1967786181 @default.
- W2806777665 cites W1969601520 @default.
- W2806777665 cites W1970891118 @default.
- W2806777665 cites W1973400283 @default.
- W2806777665 cites W1974835124 @default.
- W2806777665 cites W1974943986 @default.
- W2806777665 cites W1977603207 @default.
- W2806777665 cites W1979228875 @default.
- W2806777665 cites W1979241625 @default.
- W2806777665 cites W1980153386 @default.
- W2806777665 cites W1980819818 @default.
- W2806777665 cites W1980998023 @default.
- W2806777665 cites W1981515291 @default.
- W2806777665 cites W1982844430 @default.
- W2806777665 cites W1983012315 @default.
- W2806777665 cites W1983712394 @default.
- W2806777665 cites W1985803879 @default.
- W2806777665 cites W1985886168 @default.
- W2806777665 cites W1985920465 @default.
- W2806777665 cites W1986290768 @default.
- W2806777665 cites W1986737010 @default.
- W2806777665 cites W1986836799 @default.
- W2806777665 cites W1988285559 @default.
- W2806777665 cites W1988561408 @default.
- W2806777665 cites W1988988264 @default.
- W2806777665 cites W1989969667 @default.
- W2806777665 cites W1990136127 @default.
- W2806777665 cites W1990400035 @default.
- W2806777665 cites W1991242352 @default.
- W2806777665 cites W1991288178 @default.
- W2806777665 cites W1991704577 @default.
- W2806777665 cites W1993305863 @default.
- W2806777665 cites W1993688639 @default.
- W2806777665 cites W1993697882 @default.
- W2806777665 cites W1994422443 @default.
- W2806777665 cites W1995054388 @default.
- W2806777665 cites W1995411333 @default.
- W2806777665 cites W1997552767 @default.
- W2806777665 cites W1998392642 @default.
- W2806777665 cites W1998986309 @default.
- W2806777665 cites W1999634145 @default.
- W2806777665 cites W2000468514 @default.
- W2806777665 cites W2001712980 @default.
- W2806777665 cites W2002207827 @default.
- W2806777665 cites W2002439304 @default.
- W2806777665 cites W2003755766 @default.