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基本情報
登録情報 | ![]() | ||||||||||||
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タイトル | Beta-Arf1 homodimeric interface within AP-1 lattice on narrow membrane tubes | ||||||||||||
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機能・相同性 | ![]() basolateral protein secretion / perturbation by virus of host immune response / negative regulation of CD4 production / mitotic cleavage furrow ingression / endosome to melanosome transport / trans-Golgi Network Vesicle Budding / AP-1 adaptor complex / Lysosome Vesicle Biogenesis / platelet dense granule organization / protein trimerization ...basolateral protein secretion / perturbation by virus of host immune response / negative regulation of CD4 production / mitotic cleavage furrow ingression / endosome to melanosome transport / trans-Golgi Network Vesicle Budding / AP-1 adaptor complex / Lysosome Vesicle Biogenesis / platelet dense granule organization / protein trimerization / Glycosphingolipid transport / regulation of receptor internalization / melanosome assembly / regulation of Arp2/3 complex-mediated actin nucleation / symbiont-mediated suppression of host antigen processing and presentation of peptide antigen via MHC class I / Intra-Golgi traffic / Golgi to vacuole transport / symbiont-mediated suppression of host antigen processing and presentation of peptide antigen via MHC class II / Synthesis of PIPs at the Golgi membrane / Golgi Associated Vesicle Biogenesis / symbiont-mediated suppression of host apoptosis / clathrin adaptor activity / suppression by virus of host autophagy / MHC class II antigen presentation / CD4 receptor binding / Nef Mediated CD4 Down-regulation / thioesterase binding / dendritic spine organization / determination of left/right symmetry / long-term synaptic depression / clathrin-coated vesicle / COPI-dependent Golgi-to-ER retrograde traffic / T cell mediated cytotoxicity directed against tumor cell target / positive regulation of memory T cell activation / Lysosome Vesicle Biogenesis / TAP complex binding / positive regulation of CD8-positive, alpha-beta T cell activation / CD8-positive, alpha-beta T cell activation / clathrin binding / Golgi medial cisterna / positive regulation of CD8-positive, alpha-beta T cell proliferation / Golgi Associated Vesicle Biogenesis / CD8 receptor binding / cell leading edge / MHC class I protein binding / antigen processing and presentation of exogenous peptide antigen via MHC class I / endoplasmic reticulum exit site / host cell Golgi membrane / Synthesis of PIPs at the plasma membrane / antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-dependent / TAP binding / protection from natural killer cell mediated cytotoxicity / intracellular copper ion homeostasis / protein targeting / beta-2-microglobulin binding / COPI-mediated anterograde transport / T cell receptor binding / detection of bacterium / clathrin-coated pit / regulation of calcium-mediated signaling / vesicle-mediated transport / viral life cycle / MHC class II antigen presentation / Neutrophil degranulation / Gene and protein expression by JAK-STAT signaling after Interleukin-12 stimulation / sarcomere / small monomeric GTPase / trans-Golgi network membrane / Nef mediated downregulation of MHC class I complex cell surface expression / antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independent / antigen processing and presentation of endogenous peptide antigen via MHC class Ib / kidney development / Endosomal/Vacuolar pathway / lumenal side of endoplasmic reticulum membrane / Antigen Presentation: Folding, assembly and peptide loading of class I MHC / intracellular protein transport / trans-Golgi network / cytoplasmic vesicle membrane / peptide antigen assembly with MHC class I protein complex / ER to Golgi transport vesicle membrane / MHC class I peptide loading complex / T cell mediated cytotoxicity / antigen processing and presentation of endogenous peptide antigen via MHC class I / positive regulation of T cell cytokine production / cellular response to virus / MHC class I protein complex / SH3 domain binding / virion component / positive regulation of T cell mediated cytotoxicity / recycling endosome membrane / phagocytic vesicle membrane / positive regulation of type II interferon production / peptide antigen binding / Immunoregulatory interactions between a Lymphoid and a non-Lymphoid cell / Interferon gamma signaling / Interferon alpha/beta signaling / E3 ubiquitin ligases ubiquitinate target proteins / early endosome membrane / ATPase binding / presynapse 類似検索 - 分子機能 | ||||||||||||
生物種 | ![]() | ||||||||||||
手法 | サブトモグラム平均法 / クライオ電子顕微鏡法 / 解像度: 9.3 Å | ||||||||||||
![]() | Hooy RM / Hurley JH | ||||||||||||
資金援助 | ![]()
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![]() | ![]() タイトル: Self-assembly and structure of a clathrin-independent AP-1:Arf1 tubular membrane coat. 著者: Richard M Hooy / Yuichiro Iwamoto / Dan A Tudorica / Xuefeng Ren / James H Hurley / ![]() 要旨: The adaptor protein (AP) complexes not only form the inner layer of clathrin coats but also have clathrin-independent roles in membrane traffic whose mechanisms are unknown. HIV-1 Nef hijacks AP-1 to ...The adaptor protein (AP) complexes not only form the inner layer of clathrin coats but also have clathrin-independent roles in membrane traffic whose mechanisms are unknown. HIV-1 Nef hijacks AP-1 to sequester major histocompatibility complex class I (MHC-I), evading immune detection. We found that AP-1:Arf1:Nef:MHC-I forms a coat on tubulated membranes without clathrin and determined its structure. The coat assembles via Arf1 dimer interfaces. AP-1-positive tubules are enriched in cells upon clathrin knockdown. Nef localizes preferentially to AP-1 tubules in cells, explaining how Nef sequesters MHC-I. Coat contact residues are conserved across Arf isoforms and the Arf-dependent AP complexes AP-1, AP-3, and AP-4. Thus, AP complexes can self-assemble with Arf1 into tubular coats without clathrin or other scaffolding factors. The AP-1:Arf1 coat defines the structural basis of a broader class of tubulovesicular membrane coats as an intermediate in clathrin vesicle formation from internal membranes and as an MHC-I sequestration mechanism in HIV-1 infection. | ||||||||||||
履歴 |
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構造の表示
添付画像 |
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ダウンロードとリンク
-EMDBアーカイブ
マップデータ | ![]() | 5.2 MB | ![]() | |
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ヘッダ (付随情報) | ![]() ![]() | 21.2 KB 21.2 KB | 表示 表示 | ![]() |
FSC (解像度算出) | ![]() | 4.7 KB | 表示 | ![]() |
画像 | ![]() | 35.5 KB | ||
マスクデータ | ![]() | 8 MB | ![]() | |
その他 | ![]() ![]() | 7.3 MB 7.4 MB | ||
アーカイブディレクトリ | ![]() ![]() | HTTPS FTP |
-検証レポート
文書・要旨 | ![]() | 626.1 KB | 表示 | ![]() |
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文書・詳細版 | ![]() | 625.7 KB | 表示 | |
XML形式データ | ![]() | 10.7 KB | 表示 | |
CIF形式データ | ![]() | 14 KB | 表示 | |
アーカイブディレクトリ | ![]() ![]() | HTTPS FTP |
-関連構造データ
関連構造データ | ![]() 8d9wMC ![]() 7ux3C ![]() 8d4cC ![]() 8d4dC ![]() 8d4eC ![]() 8d4fC ![]() 8d4gC ![]() 8d9rC ![]() 8d9sC ![]() 8d9tC ![]() 8d9uC ![]() 8d9vC C: 同じ文献を引用 ( M: このマップから作成された原子モデル |
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類似構造データ | 類似検索 - 機能・相同性 ![]() |
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リンク
EMDBのページ | ![]() ![]() |
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「今月の分子」の関連する項目 |
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マップ
ファイル | ![]() | ||||||||||||||||||||
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ボクセルのサイズ | X=Y=Z: 2.1 Å | ||||||||||||||||||||
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対称性 | 空間群: 1 | ||||||||||||||||||||
詳細 | EMDB XML:
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-添付データ
-マスク #1
ファイル | ![]() | ||||||||||||
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投影像・断面図 |
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密度ヒストグラム |
-ハーフマップ: #1
ファイル | emd_27186_half_map_1.map | ||||||||||||
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投影像・断面図 |
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密度ヒストグラム |
-ハーフマップ: #2
ファイル | emd_27186_half_map_2.map | ||||||||||||
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投影像・断面図 |
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密度ヒストグラム |
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試料の構成要素
-全体 : Assembly of AP-1, Arf1 and Nef complexes on narrow membrane tubes
全体 | 名称: Assembly of AP-1, Arf1 and Nef complexes on narrow membrane tubes |
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要素 |
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-超分子 #1: Assembly of AP-1, Arf1 and Nef complexes on narrow membrane tubes
超分子 | 名称: Assembly of AP-1, Arf1 and Nef complexes on narrow membrane tubes タイプ: complex / キメラ: Yes / ID: 1 / 親要素: 0 / 含まれる分子: #1-#8 詳細: Subtomogram average of beta-Arf1 homodimeric interface within AP-1 lattice on narrow membrane tubes |
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由来(天然) | 生物種: ![]() |
-超分子 #2: AP-1 heterotetramer
超分子 | 名称: AP-1 heterotetramer / タイプ: complex / キメラ: Yes / ID: 2 / 親要素: 1 / 含まれる分子: #4-#5, #7-#8 詳細: All four subunits are co-expressed from the same plasmid. Assembly occurs in situ during expression. |
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由来(天然) | 生物種: ![]() |
組換発現 | 生物種: ![]() ![]() |
-実験情報
-構造解析
手法 | クライオ電子顕微鏡法 |
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![]() | サブトモグラム平均法 |
試料の集合状態 | particle |
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試料調製
濃度 | 0.2 mg/mL | |||||||||||||||
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緩衝液 | pH: 7.2 構成要素:
詳細: HEPES/KOAc concentrated stocks are diluted to their final concentrations then pH'd to 7.2 with KOH prior to use in experiments. | |||||||||||||||
グリッド | モデル: EMS Lacey Carbon / 支持フィルム - 材質: CARBON / 支持フィルム - トポロジー: LACEY / 支持フィルム - Film thickness: 50.0 nm | |||||||||||||||
凍結 | 凍結剤: ETHANE / チャンバー内湿度: 100 % / チャンバー内温度: 298 K / 装置: FEI VITROBOT MARK IV 詳細: 60 second wait, 3-5 second blot, 597 filter paper, 0.5 second drain. Sample was supplemented with 10nm BSA-gold fiducials. 3.5ul of the mixture was double-side blotted.. |
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電子顕微鏡法
顕微鏡 | FEI TITAN KRIOS |
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特殊光学系 | エネルギーフィルター - スリット幅: 25 eV |
撮影 | フィルム・検出器のモデル: GATAN K3 BIOQUANTUM (6k x 4k) デジタル化 - サイズ - 横: 5760 pixel / デジタル化 - サイズ - 縦: 4092 pixel / 撮影したグリッド数: 1 / 平均露光時間: 3.0 sec. / 平均電子線量: 3.0 e/Å2 詳細: Tilt images were collected in movie-mode. Each movie/tilt consisted of 3-4 frames each |
電子線 | 加速電圧: 300 kV / 電子線源: ![]() |
電子光学系 | 照射モード: FLOOD BEAM / 撮影モード: BRIGHT FIELD / Cs: 2.7 mm / 最大 デフォーカス(公称値): 4.5 µm / 最小 デフォーカス(公称値): 1.5 µm / 倍率(公称値): 42000 |
試料ステージ | 試料ホルダーモデル: FEI TITAN KRIOS AUTOGRID HOLDER ホルダー冷却材: NITROGEN |
実験機器 | ![]() モデル: Titan Krios / 画像提供: FEI Company |
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画像解析
-原子モデル構築 1
精密化 | プロトコル: RIGID BODY FIT |
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得られたモデル | ![]() PDB-8d9w: |