کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10768104 | 1050804 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Biochemical and medical aspects of the indoleamine 2,3-dioxygenase-initiated l-tryptophan metabolism
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کلمات کلیدی
Age-related cataract - آب مروارید وابسته به سنQuinolinic acid - اسید کینولینیکinterferon-γ - اینترفرون-γAlzheimer’s disease - بیماری آلزایمرTryptophan - تریپتوفانIndoleamine dioxygenase - دیئولزیناز انسولینImmunosuppression - سرکوب سیستم ایمنیDendritic cells - سلول های دندریتیکMetabolism - متابولیسم Neurotoxin - نوروتوکسین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Indoleamine 2,3-dioxygenase (EC 1.13.11.42) is a heme-containing dioxygenase which catalyzes the first and rate-limiting step in the major pathway of l-tryptophan catabolism in mammals. Much attention has recently been focused on the dioxygenase because this metabolic pathway is involved not only in a variety of physiological functions but also in many diseases. In this review, the discovery and unique catalytic properties of dioxygenase are described first, and then the recent findings regarding the dioxygenase-initiated tryptophan metabolism are summarized, with special emphasis on the detrimental role of dioxygenase in side effects of interferon-γ and interleukin-12 (by systemic tryptophan depletion), the escape of malignant tumors from immune surveillance (by immunosuppression caused by tryptophan depletion), several neurodegenerative disorders including Alzheimer's disease (by an aberrant production of neurotoxin, quinolinic acid), and age-related cataract (due to “Kynurenilation,” a novel post-translational modification of lens proteins with tryptophan-derived UV filters).
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 338, Issue 1, 9 December 2005, Pages 12-19
Journal: Biochemical and Biophysical Research Communications - Volume 338, Issue 1, 9 December 2005, Pages 12-19
نویسندگان
Osamu Takikawa,