摘要未折叠蛋白反应(unfolded protein response,UPR)是细胞在进化过程中产生的一条高度保守的自我保护信号传导通路。UPR不仅参与蛋白质的修饰,还与细胞周期的停滞和凋亡等有关。已知UPR与脑缺血、糖尿病等多种疾病的发病有关。近年来研究发现,UPR与惊厥性脑损伤的关系密切,该文着重综述了UPR通路及其在惊厥性脑损伤中的可能作用。
1Ninomiya-Tsuji J,Kishimoto K,Hiyama A,Inoue J,Cao Z,Matsumoto K.The kinase TAK1 can activate the NIK-IκB as well as the MAP kinase cascade in the IL-1 signalling pathway[].Nature.1999
2Baeuerle PA,Baltimore D.A 65-kD subunit of active NF-κB is required for inhibition of NF-κB by IκB[].Genes and Development.1989
3Carty M,Goodbody R,Schroder M,Stack J,Moynagh PN,Bowie AG.The human adaptor SARM negatively regulates adaptor protein TRIF-dependent Toll-like receptor signaling[].Nature Immunology.2006
4Qin J,Jiang Z,Qian Y,Casanova JL,Li X.IRAK4 kinase activity is redundant for interleukin-1 (IL-1) receptor-associated kinase phosphorylation and IL-1 responsiveness[].Journal of Biological Chemistry.2004
5Kobayashi K,Hernandez LD,Galan JE,Janeway CA Jr,Medzhitov R,Flavell RA.IRAK-M is a negative regulator of Toll-like receptor signaling[].Cell.2002
6Burns K,Janssens S,Brissoni B,Olivos N,Beyaert R,Tschopp J.Inhibition of interleukin 1 receptor/Toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4[].The Journal of Experimental Medicine.2003
7Bohuslav J,Chen LF,Kwon H,Mu Y,Greene WC.p53 induces NF-κB activation by an IκB kinase-independent mechanism involving phosphorylation of p65 by ribosomal S6 kinase 1[].Journal of Biological Chemistry.2004
8Jiang Z,Mak TW,Sen G,Li X.Toll-like receptor 3-mediated activation of NF-κB and IRF3 diverges at Toll-IL-1 receptor domain-containing adapter inducing IFN-β[].Proceedings of the National Academy of Sciences of the United States of America.2004
9Vidal S,Khush RS,Leulier F,Tzou P,Nakamura M,Lemaitre B.Mutations in the Drosophila dTAK1 gene reveal a conserved function for MAPKKKs in the control of rel/NF-κB-dependent innate immune responses[].Genes and Development.2001
10Kawai T,Takeuchi O,Fujita T, et al.Lipopolysaccharide stimulates the MyD88-independent pathway and results in activation of IFN-regulatory factor 3 and the expression of a subset of lipopolysaccharide-inducible genes[].J Immunol.2001
3Bengzon J, Mohapel P, Ekdahl C T, et al. Neuronal apoptosis after brief and prolonged seizures[J]. Prog Brain Res, 2002,135:111- 119.
4Santin G, Piccolini V M, Veneroni P, et al. Different patterns of apoptosis in response to eisplatin in B 50 neuroblastoma rat cells[J]. Histol Histopathol,2011,26(7) :831-842.
5Henshall D C, Simon R P. Epilepsy and apoptosis pathways [J].JCerebBioodFlowMetab, 2005,25(12):1557 -1572.
6Yoshida H, Haze K, Yanagi H, et al. Identification of the cis- acting endoplasmic reticulum stress response element responsi ble for transcriptional induction of mammalian glucose regula- ted proteins involvement of basic leucine zipper transcription Iactors[J]. J Biol Chem,1998,273(50) :33741-33749.
7Racine R J, Steingart M, Mclntyre D C. Development of kin riling-prone and kinding-resistant rats: selective breeding and electrophysiological studies[J]. Epilepsy Res, 1999,35 (3) : 183-195.
8Lee A S. The ER chaperone and signaling regulator GRP 78/ BiP as a monitor of endoplasmic reticulum stress[J]. Me thods, 2005,35 (4) : 373 - 381.
9Zinszner H, Kuroda M, Wang X, et al. CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum[J]. Genes Dev, 1998,12(7) : 982- 995.
10McCullough K D, Martindale J L, Klotz L O, et al. GADD 153 sensitizes cells to endoplasmic reticulum stress by down- regulating Bcl-2 and perturbing the cellular redox state [J]. MolCellBiol,2001,21(4):1249 1259.
