共查询到20条相似文献,搜索用时 15 毫秒
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Ming Chen Rui Wang Xi Gan Aiying Lei Chao Li Xiaoli Yu Jun Huang Ting Huang Wanwen Liang 《Molecular biology reports》2010,37(5):2541-2547
Suppression subtractive hybridization library was generated by comparison of cDNA populations isolated from peripheral leukocytes
of pre- and post-immunized tilapia. One cDNA sequence encoding complete inducible cAMP early repressor was obtained from the
library. The sequence was characterized by the presence of the basic structure of ICER IIγ. Expression of ICER was in the
tissues of four types of tilapia was decreased after infection with Streptococcus. After immunization, expression of ICER was initially decreased and then increased after 7 days. In addition, the order for
the overall expression of ICER gene after infection and the increases of ICER expression later after immunization in these
four types of tilapia was positively correlated to the disease resistance and productivity of these four species of tilapia.
Our results provided molecular mechanisms for the different disease resistance capability in different species of tilapia.
In addition, our results also provided reference molecular marker for breeding disease resistant tilapia, cAMP responsive
element modulator. 相似文献
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Yehia G Schlotter F Razavi R Alessandrini A Molina CA 《The Journal of biological chemistry》2001,276(38):35272-35279
Inducible cAMP early repressor (ICER) is an important mediator of cAMP antiproliferative activity that acts as a putative tumor suppressor gene product. In this study, we examined the regulation of ICER protein by phosphorylation and ubiquitination in human choriocarcinoma JEG-3 and mouse pituitary AtT20 cells. We found that cAMP stabilized ICER protein by inhibiting the mitogen-activated protein kinase (MAPK) cascade. Activation of the MAPK pathway increased ICER phosphorylation. ICER phosphorylation was abrogated by inhibition of the MAPK pathway either by cAMP or directly by the MAPK inhibitor PD098059. The MAPKs extracellular signal-regulated kinases 1 and 2 physically interact with ICER and mediated the phosphorylation of ICER on a critical serine residue (Ser-41). A mutant form of ICER in which Ser-41 was substituted by alanine had a half-life 4-5 h longer than its wild-type counterpart. This alteration in stability was due to the inability of the Ser-41-mutant ICER to be efficiently ubiquitinated and degraded via the ubiquitin-proteasome pathway. These results present a novel cell signaling cross-talk mechanism at the cell nucleus between the MAPK and cAMP pathways, whereby MAPK targets a repressor of the cAMP-dependent gene expression for ubiquitination and proteasomal degradation. 相似文献
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McCauslin CS Heath V Colangelo AM Malik R Lee S Mallei A Mocchetti I Johnson PF 《The Journal of biological chemistry》2006,281(26):17681-17688
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Louet JF Hayhurst G Gonzalez FJ Girard J Decaux JF 《The Journal of biological chemistry》2002,277(41):37991-38000
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Valera E Sánchez-Martín FJ Ferrer-Montiel AV Messeguer A Merino JM 《Neurochemistry international》2008,53(5):148-154
N-Methyl-d-aspartate (NMDA) receptors play a critical role in the brain stimulating synaptic plasticity and mediating neurodegeneration; a neuroprotective role has also been described, but its molecular mechanisms in hippocampus are under study. Here, we report that in primary cultures of rat hippocampal neurons exposure to low micromolar NMDA concentrations are neuroprotective against excitotoxic insults, while high micromolar NMDA concentrations provoke neuronal death. Molecular analysis reveals that a toxic concentration of NMDA induced a transient phosphorylation of cAMP-response element-binding protein (pCREB) in 2 min that rapidly decreased below basal levels. In contrast, a nontoxic NMDA concentration gave up to longer (20 min) rise of pCREB, suggesting that neuroprotection could be associated to a relatively prolonged presence of pCREB in the neurons. In support of this tenet, rolipram, an inhibitor of phosphodiesterase IV that increases the levels of cAMP and pCREB, protected against NMDA-induced neuronal death. Similar results were obtained with dibutyrate-cAMP (a cAMP analogue with membrane permeability) that also abrogated NMDA excitotoxicity. Conversely, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89), an inhibitor of protein kinase A (PKA), that prevents the formation of pCREB induced by nontoxic NMDA concentrations, reverted the neuroprotection achieved by preincubation of low micromolar NMDA concentrations. These results substantiate the notion that induction of pCREB via PKA plays an important role in NMDA-mediated neuroprotection. 相似文献
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Ianculescu I Wu DY Siegmund KD Stallcup MR 《The Journal of biological chemistry》2012,287(6):4000-4013
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