کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9425639 | 1295885 | 2005 | 18 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The NR1-4 C-terminus interferes with N-methyl-d-aspartate receptor-mediated excitotoxicity: Evidence against a typical T/SXV-PDZ interaction
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کلمات کلیدی
PSD-95Discosoma sp. Red fluorescent proteinmembrane-associated guanylate kinasesECFPEYFPPDZNMDARNOSeGFPMAGUK - آنهاenhanced cyan fluorescent protein - افزایش پروتئین فلورسنت سیانوژنexcitotoxicity - اکسید سمیتpostsynaptic density-95 - تراکم پست سیناپتیک 95long term potentiation - تقویت طولانی مدتLTP - تقویت طولانی مدت یا LTP endoplasmic reticulum - شبکه آندوپلاسمی Flow cytometry - فلوسیتومتریnitric oxide synthase - نیتریک اکسید سنتازenhanced yellow fluorescent protein - پروتئین فلورسنت زرد افزایش یافته استgreen fluorescent protein - پروتئین فلورسنت سبزenhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استN-methyl-d-aspartate receptor - گیرنده N-methyl-d-aspartateGlutamate receptor - گیرنده گلومات
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: The NR1-4 C-terminus interferes with N-methyl-d-aspartate receptor-mediated excitotoxicity: Evidence against a typical T/SXV-PDZ interaction The NR1-4 C-terminus interferes with N-methyl-d-aspartate receptor-mediated excitotoxicity: Evidence against a typical T/SXV-PDZ interaction](/preview/png/9425639.png)
چکیده انگلیسی
The N-methyl-d-aspartate receptor (NMDAR) plays a key role in the neural plasticity that underlies learning and memory in vivo. The plasticity exhibited by NMDARs may also contribute to disease pathogenesis, as a number of disorders are caused or exacerbated by exaggerated NMDAR activity. The NMDAR is composed of two obligatory types of subunits, NR1 and NR2. These transmembrane proteins include large intracellular C-termini that have yet to be fully characterized. We have developed a three-color fluorescence system in order to visualize NMDAR expression in living cells. Using excitotoxicity as a proxy for exaggerated NMDAR activity, we analyzed the effect of over-expressing NR1-4 and NR2A C-terminal domains on exaggerated NMDAR function. We demonstrate that a determinant within the C-terminal domain of NR1-4 (C02â²) is important for NMDAR excitotoxicity, whereas no novel determinants were identified in the NR2A C-terminus. Through the use of heterologous cells, and by examining the interaction between the prototypical NMDAR-binding partner postsynaptic density-95 (PSD-95), we show that this effect is unlikely to be mediated through a classical interaction with PSD-95.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 132, Issue 2, 2005, Pages 281-298
Journal: Neuroscience - Volume 132, Issue 2, 2005, Pages 281-298
نویسندگان
P.A. Mattar, K.D. Holmes, G.A. Dekaban,