Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study is to compare speech perception performance in Mandarin-speaking Nucleus CI24 implantee using standard behavior MAPs and NRT-based MAPs. Eight Nucleus CI24 users (5 years and older) participated in the study. They all fulfilled the following criteria: (1) behavioral MAP and NRT thresholds can be reliably obtained; (2) had more than 18 functioning electrodes; (3) had at least 6 months experience using CI. All subjects received speech evaluation under three different MAPs: a traditional behavioral MAP, a MAP predicted from the NRT thresholds of the E22 (electrode 22), E19, E15, E11, E8, E5, E1 and a combined MAP based on the information of NRT thresholds and behavioral threshold/comfortable levels of the E11. The speech evaluation package included word recognition test in quiet, in noise, and a Mandarin sentence test in quiet. Results showed that three MAPs are similar in some subjects, but different in other subjects. Compared to the NRT MAPs, the combined MAPs are more similar to the behavioral MAPs. There was no significant difference in the mean score of the word recognition test in quiet, in noise and sentence test under these three MAP conditions. In conclusion, although the behavioral MAPs and the NRT-based MAPs are not identical, the speech performance of Mandarin-speaking CI24 implantee using MAPs predicted from NRT thresholds appeared to be no worse than the traditional behavioral MAPs. Therefore, in certain cases that behavioral MAPs are difficult to obtain (such as in very young or multiple handicapped children), NRT-based MAPs may serve reliably as an initial estimation.
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PMID:Mandarin speech perception in nucleus CI 24 implantees using MAPs based on neural response telemetry. 1558 39

Fibroblast growth factor (FGF) signaling has been shown to be essential for many aspects of normal lung development. To determine epithelial targets of FGF signaling, we cultured embryonic day (E) 11.5 mouse lungs for 24 hr in the presence or absence of the FGF receptor antagonist SU5402, which inhibited branching morphogenesis. Affymetrix gene chip analysis of treated and control epithelia identified several genes regulated by FGF signaling, including Elf5, a member of the Epithelial-specific Ets family of transcription factors. SU5402 reduced Elf5 expression in mesenchyme-free cultures of E12.5 epithelium, demonstrating that the inhibition was direct. In situ hybridization revealed that Elf5 had a dynamic pattern of expression during lung development. We found that expression of Elf5 was induced by FGF7 and FGF10, ligands that primarily bind FGFR2b. To further define the pathways by which FGFs activate Elf5 expression, we cultured E11.5 lung tips in the presence of compounds to inhibit FGF receptors (SU5402), PI3-Kinase/Akt-mediated signaling (LY294002), and MAP Kinase/Erk-mediated signaling (U0126). We found that SU5402 and LY294002 significantly reduced Elf5 expression, whereas U0126 had no effect. LY294002 also reduced Elf5 expression in cultures of purified epithelium. Finally, pAkt was coexpressed with Elf5 in the proximal epithelial airways of E17.5 lungs. These results demonstrate that Elf5 is an FGF-sensitive transcription factor in the lung with a dynamic pattern of expression and that FGF regulation of Elf5 by means of FGFR2b occurs through the PI3-Kinase/Akt pathway.
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PMID:Elf5 is an epithelium-specific, fibroblast growth factor-sensitive transcription factor in the embryonic lung. 1739 8

The nuclear lamina, along with associated nuclear membrane proteins, is a nexus for regulating signaling in the nucleus. Numerous human diseases arise from mutations in lamina proteins, and experimental models for these disorders have revealed aberrant regulation of various signaling pathways. Previously, we reported that the inner nuclear membrane protein Lem2, which is expressed at high levels in muscle, promotes the differentiation of cultured myoblasts by attenuating ERK signaling. Here, we have analyzed mice harboring a disrupted allele for the Lem2 gene (Lemd2). No gross phenotypic defects were seen in heterozygotes, although muscle regeneration induced by cardiotoxin was delayed. By contrast, homozygous Lemd2 knockout mice died by E11.5. Although many normal morphogenetic hallmarks were observed in E10.5 knockout embryos, most tissues were substantially reduced in size. This was accompanied by activation of multiple MAP kinases (ERK1/2, JNK, p38) and AKT. Knockdown of Lem2 expression in C2C12 myoblasts also led to activation of MAP kinases and AKT. These findings indicate that Lemd2 plays an essential role in mouse embryonic development and that it is involved in regulating several signaling pathways. Since increased MAP kinase and AKT/mTORC signaling is found in other animal models for diseases linked to nuclear lamina proteins, LEMD2 should be considered to be another candidate gene for human disease.
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PMID:Nuclear envelope protein Lem2 is required for mouse development and regulates MAP and AKT kinases. 2579 Apr 65