γがんま-干ひ扰素

現有げんゆう可用かよう的てき蛋白たんぱく結構けっこう：
Pfam	結構けっこう（旧版きゅうばん） / ECOD
PDB	RCSB PDB; PDBe; PDBj
PDBsum（英えい语：PDBsum）	結構けっこう概要がいよう

IFN-γがんま
	Crystal structure of a biologically active single chain mutant of human interferon gamma
鑑定かんてい
標しるべ誌し	?
Pfam	PF00714（旧版きゅうばん）
Pfam宗むね系けい	CL0053（旧版きゅうばん）
InterPro（英えい语：InterPro）	IPR002069
SCOP（英えい语：Structural Classification of Proteins）	1rfb / SUPFAM
現有げんゆう可用かよう的てき蛋白たんぱく結構けっこう：
Pfam	結構けっこう（旧版きゅうばん） / ECOD
PDB	RCSB PDB; PDBe; PDBj
PDBsum（英えい语：PDBsum）	結構けっこう概要がいよう

干ひ扰素-γがんま
	γがんま-干ひ擾素晶あきら體たい結構けっこう線せん狀じょう表示ひょうじ
有效ゆうこう结构
PDB	直系ちょっけい同どう源みなもと检索：PDBe, RCSB
PDB查询代だい码列表ひょう
	1EKU, 1FG9, 1FYH, 1HIG, 3BES
标识
代だい号ごう	IFNG; IFG; IFI
扩展标识	遗传学がく：147570 鼠ねずみ基もと因いん：107656 同どう源みなもと基はじめ因いん：55526 GeneCards: IFNG Gene
基もと因いん本体ほんたい论描述じゅつ
分子ぶんし功こう能のう	· cytokine activity; · interferon-gamma receptor binding;
细胞成分せいぶん	· extracellular region; · extracellular space; · external side of plasma membrane;
生物せいぶつ过程	· protein import into nucleus, translocation; · negative regulation of transcription from RNA polymerase II promoter; · neutrophil apoptotic process; · regulation of the force of heart contraction; · positive regulation of mesenchymal cell proliferation; · adaptive immune response; · CD8-positive, alpha-beta T cell differentiation involved in immune response; · negative regulation of mesenchymal to epithelial transition involved in metanephros morphogenesis; · apoptotic process; · cellular component movement; · humoral immune response; · cell cycle arrest; · cell surface receptor signaling pathway; · response to virus; · cytokine-mediated signaling pathway; · antigen processing and presentation; · neutrophil chemotaxis; · endoplasmic reticulum unfolded protein response; · negative regulation of myelination; · positive regulation of synaptic transmission, cholinergic; · negative regulation of interleukin-17 production; · positive regulation of interleukin-12 production; · positive regulation of interleukin-23 production; · positive regulation of tumor necrosis factor production; · positive regulation of peptidyl-serine phosphorylation of STAT protein; · positive regulation of smooth muscle cell apoptotic process; · positive regulation of T cell proliferation; · response to drug; · positive regulation of tyrosine phosphorylation of Stat1 protein; · defense response to bacterium; · defense response to protozoan; · negative regulation of growth of symbiont in host; · positive regulation of chemokine biosynthetic process; · positive regulation of interleukin-12 biosynthetic process; · positive regulation of MHC class II biosynthetic process; · positive regulation of interleukin-6 biosynthetic process; · positive regulation of nitric oxide biosynthetic process; · positive regulation of neuron differentiation; · positive regulation of osteoclast differentiation; · positive regulation of cell adhesion; · positive regulation of transcription from RNA polymerase II promoter; · positive regulation of isotype switching to IgG isotypes; · negative regulation of smooth muscle cell proliferation; · positive regulation of interleukin-1 beta secretion; · regulation of insulin secretion; · positive regulation of membrane protein ectodomain proteolysis; · defense response to virus; · positive regulation of killing of cells of other organism; · interferon-gamma-mediated signaling pathway; · regulation of interferon-gamma-mediated signaling pathway; · positive regulation of fructose 1,6-bisphosphate 1-phosphatase activity; · positive regulation of fructose 1,6-bisphosphate metabolic process; · positive regulation of vitamin D biosynthetic process; · positive regulation of calcidiol 1-monooxygenase activity; · cellular response to lipopolysaccharide; · cellular response to interleukin-18; · negative regulation of metanephric nephron tubule epithelial cell differentiation; · positive regulation of tumor necrosis factor (ligand) superfamily member 11 production;
	Sources: Amigo / QuickGO
RNA表ひょう达模式しき
	更さら多た表ひょう达数据すえ
直系ちょっけい同どう源みなもと体たい
	查; 论; 编;

**Γがんま-干ひ扰素**
臨床りんしょう資料しりょう
商品しょうひん名めい（英えい语：Drug nomenclature）	Actimmune
AHFS/Drugs.com	Monograph
MedlinePlus	a601152
ATC碼	L03AB03 (WHO)
识别信しん息いき
IUPAC命名めいめい法ほう Human interferon gamma-1b
CAS号ごう	82115-62-6 ^Y 98059-61-1
DrugBank	DB00033^N
ChemSpider	NA^Y
ChEMBL	ChEMBL1201564^N
化学かがく信しん息いき
化学かがく式しき	C₇₆₁H₁₂₀₆N₂₁₄O₂₂₅S₆
摩ま尔质量りょう	17145.6 g/mol

干ひ扰素-γがんま（Interferon gamma、Interferon-γがんま、IFNG、IFNγがんま）是これ水溶すいよう性せい二に聚体的てき细胞因子いんし^[2]。是ぜII型がた干ひ扰素的てき唯ただ一成いっせい员^[3]曾被称しょう为巨きょ噬细胞活化か因子いんし。

结构[编辑]

干ひ扰素-γ的てき单体是ぜ由よし六ろく个αあるふぁ螺旋らせん组成一いち个核心こころ^[4]和かず在ざいC端はし区く延伸えんしん展てん开的片へん断だん序列じょれつ。

生物せいぶつ活性かっせい的てき二に聚体是ぜ由よし两个反はん平行へいこう相互そうご锁定的てき单体形成けいせい。

生物せいぶつ活性かっせい[编辑]

所有しょゆう的てき细胞都と可か以产生せい干ひ扰素-αあるふぁ（英えい语：Interferon alfa）和わ干ひ扰素-βべーた，而干扰素-γがんま只ただ由ゆかり自然しぜん杀伤细胞（NK细胞）和かず活かつ化か的てきT细胞产生。I型がた干ひ扰素对酸稳定，而干扰素-γがんま则遇酸さん变性。

干ひ扰素-γがんま具有ぐゆう抗こう病毒びょうどく、免疫めんえき调节及抗肿瘤特性とくせい^[5]。干ひ扰素-γがんま可か以与干ひ扰素伽とぎ玛受体たい（英えい语：Interferon-gamma receptor）(IFNGR)结合，进而调节JAK-STAT通路つうろ。干ひ扰素-γがんま激げき活かつ抗原こうげん提ひさげ呈てい细胞，通つう过上调转录因子いんしT-bet而促进I型がた辅助T细胞(Th1细胞)的てき分化ぶんか。

干ひ扰素-γがんま是ぜI型がた辅助T细胞(Th1细胞)的てき标志性せい的てき细胞因子いんし。II型がた辅助T细胞(Th2细胞)释放白しろ细胞介かい素もと-4（IL-4）和白わじろ细胞介かい素もと-13（IL-13）。自然しぜん杀伤细胞和わCD8⁺T细胞也产生せい干ひ扰素-γがんま。干ひ扰素-γがんま通どおり过迅速そく降くだ解かいRANK-RANKL信号しんごう通路つうろ的てきTRAF6而抑制よくせい破やぶ骨ほね细胞形成けいせい。

治ち疗用途ようと[编辑]

干ひ扰素可か以用来らい治ち疗传染病びょう，但ただし也能促成そくせい自體じたい免疫めんえき。在ざい接受せつじゅ干ひ扰素伽とぎ玛治疗的病びょう人中ひとなか，多た达19%的てき病人びょうにん会かい有ゆう自體じたい免疫めんえき.

干ひ擾素IFNγがんま用よう於豬生殖せいしょく與あずか呼吸こきゅう道どう綜合そうごう症しょうPRRSV的てき治療ちりょう上じょう，有ゆう試驗しけん發現はつげん干ひ擾素IFNγがんま能のう活かつ化か先天せんてん免疫めんえき細胞さいぼう，進しん而達到いた抑制よくせい病毒びょうどく數量すうりょう的てき效果こうか。^[6]

A型がた流感りゅうかん的てき治療ちりょう上じょう，也有やゆう小しょう鼠ねずみ試驗しけん表ひょう現出げんしゅつ當とう缺かけ失しつ干ひ擾素後ご，流感りゅうかん感染かんせん小しょう鼠ねずみ死亡しぼう率りつ大幅おおはば提ひさげ升ます且體內病毒びょうどく數量すうりょう維持いじ高だか濃度のうど水平すいへい；相しょう較之下か，體たい內有干ひ擾素存在そんざい的てき小しょう鼠ねずみ，流感りゅうかん病毒びょうどく數量すうりょう隨ずい著ちょ干ひ擾素的てき生成せいせい而逐漸やや下降かこう。^[7]

参考さんこう文献ぶんけん[编辑]

^ PDB 1FG9; Thiel DJ, le Du MH, Walter RL, D'Arcy A, Chène C, Fountoulakis M, Garotta G, Winkler FK, Ealick SE. Observation of an unexpected third receptor molecule in the crystal structure of human interferon-gamma receptor complex. Structure. September 2000, 8 (9): 927–36. PMID 10986460. doi:10.1016/S0969-2126(00)00184-2.
^ Gray PW, Goeddel DV. Structure of the human immune interferon gene. Nature. 1982 Aug 26;298(5877):859-63.
^ Gray PW, Goeddel DV. Structure of the human immune interferon gene. Nature. August 1982, 298 (5877): 859–63. PMID 6180322. doi:10.1038/298859a0.
^ Ealick SE, et al., Three-dimensional structure of recombinant human interferon-gamma. Science. 1991 May 3;252(5006):698-702.
^ Schroder K, Hertzog PJ, Ravasi T, Hume DA. Interferon-gamma: an overview of signals, mechanisms and functions. J Leukoc Biol. 2004 Feb;75(2):163-89.
^ Bautista, E. M.; Molitor, T. W. IFNγがんま inhibits porcine reproductive and respiratory syndrome virus replication in macrophages. Archives of Virology. 1999-06, 144 (6): 1191–1200. ISSN 0304-8608. doi:10.1007/s007050050578.
^ Hoshino, Akinori; Takenaka, Hiroshi; Mizukoshi, Osamu; Imanishi, Jiro; Kishida, Tsunataro; Tovey, Michael G. Effect of anti-interferon serum of influenza virus infection in mice. Antiviral Research. 1983-03, 3 (1): 59–65. ISSN 0166-3542. doi:10.1016/0166-3542(83)90015-3.

延伸えんしん閱讀[编辑]

Hall, Stephen K. A commotion in the blood: life, death, and the immune system. New York: Henry Holt. 1997. ISBN 0-8050-5841-9.
Ikeda H, Old LJ, Schreiber RD. The roles of IFN gamma in protection against tumor development and cancer immunoediting.. Cytokine Growth Factor Rev. 2002, 13 (2): 95–109. PMID 11900986. doi:10.1016/S1359-6101(01)00038-7.
Chesler DA, Reiss CS. The role of IFN-gamma in immune responses to viral infections of the central nervous system.. Cytokine Growth Factor Rev. 2003, 13 (6): 441–54. PMID 12401479. doi:10.1016/S1359-6101(02)00044-8.
Dessein A, Kouriba B, Eboumbou C, Dessein H, Argiro L, Marquet S, Elwali NE, Rodrigues V, Li Y, Doumbo O, Chevillard C. Interleukin-13 in the skin and interferon-gamma in the liver are key players in immune protection in human schistosomiasis.. Immunol. Rev. 2005, 201: 180–90. PMID 15361241. doi:10.1111/j.0105-2896.2004.00195.x.
Joseph AM, Kumar M, Mitra D. Nef: "necessary and enforcing factor" in HIV infection.. Curr. HIV Res. 2005, 3 (1): 87–94. PMID 15638726. doi:10.2174/1570162052773013.
Copeland KF. Modulation of HIV-1 transcription by cytokines and chemokines.. Mini reviews in medicinal chemistry. 2006, 5 (12): 1093–101. PMID 16375755. doi:10.2174/138955705774933383.
Chiba H, Kojima T, Osanai M, Sawada N. The significance of interferon-gamma-triggered internalization of tight-junction proteins in inflammatory bowel disease.. Sci. STKE. 2006, 2006 (316): pe1. PMID 16391178. doi:10.1126/stke.3162006pe1.
Tellides G, Pober JS. Interferon-gamma axis in graft arteriosclerosis.. Circ. Res. 2007, 100 (5): 622–32. PMID 17363708. doi:10.1161/01.RES.0000258861.72279.29.

参看さんかん[编辑]

外部がいぶ链接[编辑]

MeSH|Interferon+Type+II （页面存そん档备份，存そん于互联网档案あん馆）

[PDB_1FG9-1] PDB 1FG9; Thiel DJ, le Du MH, Walter RL, D'Arcy A, Chène C, Fountoulakis M, Garotta G, Winkler FK, Ealick SE. Observation of an unexpected third receptor molecule in the crystal structure of human interferon-gamma receptor complex. Structure. September 2000, 8 (9): 927–36. PMID 10986460. doi:10.1016/S0969-2126(00)00184-2.

[2] Gray PW, Goeddel DV. Structure of the human immune interferon gene. Nature. 1982 Aug 26;298(5877):859-63.

[pmid6180322-3] Gray PW, Goeddel DV. Structure of the human immune interferon gene. Nature. August 1982, 298 (5877): 859–63. PMID 6180322. doi:10.1038/298859a0.

[4] Ealick SE, et al., Three-dimensional structure of recombinant human interferon-gamma. Science. 1991 May 3;252(5006):698-702.

[5] Schroder K, Hertzog PJ, Ravasi T, Hume DA. Interferon-gamma: an overview of signals, mechanisms and functions. J Leukoc Biol. 2004 Feb;75(2):163-89.

[6] Bautista, E. M.; Molitor, T. W. IFNγがんま inhibits porcine reproductive and respiratory syndrome virus replication in macrophages. Archives of Virology. 1999-06, 144 (6): 1191–1200. ISSN 0304-8608. doi:10.1007/s007050050578.

[7] Hoshino, Akinori; Takenaka, Hiroshi; Mizukoshi, Osamu; Imanishi, Jiro; Kishida, Tsunataro; Tovey, Michael G. Effect of anti-interferon serum of influenza virus infection in mice. Antiviral Research. 1983-03, 3 (1): 59–65. ISSN 0166-3542. doi:10.1016/0166-3542(83)90015-3.

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