INT9953
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
It is concluded that opioids and clonidine promote analgesia after binding to receptors functionally coupled to Gi/G(o) proteins, moreover, the activity of morphine, beta-endorphin and clonidine in this test seems to be counteracted by a process involving activation of Gs alpha transducer proteins. | |||||||||||||||
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This suggests that there is a lower threshold effect, and the low dose did not seem to be sufficient to induce exon skipping in patients with Duchenne muscular dystrophy; therefore, we proceeded straight to the high dose. | |||||||||||||||
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Antisense oligonucleotides have been used for experimental gene silencing and recently as splice-switching oligonucleotides to modify splicing and induce exon skipping,13 particularly in myoblasts from patients with DMD in vitro,14,15 and in mouse and dog models of DMD.16–18 One patient with DMD who had a deletion of exon 20 received an intravenous infusion of a splice-switching oligonucleotide with a phosphorothioate backbone, which induced skipping of exon 19 and restored the DMD open reading frame in lymphocytes but had no effect in skeletal muscle.19 A recent phase 1 clinical study reported encouraging results in four boys with DMD who received a single intramuscular injection of a 2L'O-methyl-ribooligonucleoside-phoshophorothioate splice-switching oligonucleotide that was targeted to skip exon 51. | |||||||||||||||
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When co-expressed with CaMK IV dCT, exon skipping was sharply increased, indicating that CaRRE 2 is also sufficient for CaMK IV–dependent repression (Figure 4B, lanes 1 and 2). | |||||||||||||||
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CaRRE 2 was inserted at the +3 position of the Dup175 exon, the same position relative to the 3? | |||||||||||||||
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After the original duplication event, subsequent accumulation of mutations, presumably in both exon 5a and 5b, have resulted in the two similar but distinct SNAP-25 proteins present in all higher vertebrates. | |||||||||||||||
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Western blot analysis using the C-terminal specific c/ebp Beta antibody showed that the levels of both the LAP and LIP isoforms of c/ebp Beta were increased after treatment with LPS, in accordance with a previous report (14) (Figure 3). | |||||||||||||||
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The c/ebp Beta transcript encodes three isoforms, designated as LAP*, LAP and LIP, that are generated by differential translational initiation (Figure 2A). | |||||||||||||||
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The expression of the three isoforms is regulated in a complex manner, and even differential activation of the c/ebp Beta isoforms upon LPS stimulation has been reported (25). | |||||||||||||||
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Currently available anti-VEGF agents include an aptamer (pegaptanib sodium), which targets the VEGF165 isoform of VEGF-A, and the monoclonal antibody fragment ranibizumab, which targets all VEGF-A isoforms and cleavage products. | |||||||||||||||
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General Comments
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