神経性ウィスコット・アルドリッチ症候群タンパク質、神経性Wiskott-Aldrich症候群タンパク質
WordNet
- a pattern of symptoms indicative of some disease
- a complex of concurrent things; "every word has a syndrome of meanings"
- any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
PrepTutorEJDIC
- (疾患の徴候となる一群の)症徴候,症候群 / (事件・社会的状態などのパターンを示す)徴候形態
- 蛋白(たんばく)質
- 神経単位,神経細胞,ニューロン,ノイロン
UpToDate Contents
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- 1. 肝性脳症：病因 hepatic encephalopathy pathogenesis
- 2. ビタミンB12欠乏や葉酸欠乏の原因と病態生理 causes and pathophysiology of vitamin b12 and folate deficiencies
- 3. ウィスコット・オルドリック症候群 wiskott aldrich syndrome
- 4. 先天性好中球減少症 congenital neutropenia
- 5. T細胞受容体シグナル伝達 t cell receptor signaling
English Journal
- Synthetic polyamines: new compounds specific to actin dynamics for mammalian cell and fission yeast.
- Riveline D1, Thiagarajan R, Lehn JM, Carlier MF.
- Bioarchitecture.Bioarchitecture.2015 Feb 9:1-5. [Epub ahead of print]
- Actin is a major actor in the determination of cell shape. On the one hand, site-directed assembly/disassembly cycles of actin filaments drive protrusive force leading to lamellipodia and filopodia dynamics. Force produced by actin similarly contributes in membrane scission in endocytosis or Golgi r
- PMID 25664996
- Thromboxane-induced actin polymerization in hypoxic neonatal pulmonary arterial myocytes involves Cdc42 signaling.
- Fediuk J1, Sikarwar AS1, Nolette N2, Dakshinamurti S3.
- American journal of physiology. Lung cellular and molecular physiology.Am J Physiol Lung Cell Mol Physiol.2014 Dec 1;307(11):L877-87. doi: 10.1152/ajplung.00036.2014. Epub 2014 Oct 3.
- In hypoxic pulmonary arterial (PA) myocytes, challenge with thromboxane mimetic U46619 induces marked actin polymerization and contraction, phenotypic features of persistent pulmonary hypertension of the newborn (PPHN). Rho GTPases regulate the actin cytoskeleton. We previously reported that U46619-
- PMID 25281640
- Protocadherin-17 mediates collective axon extension by recruiting actin regulator complexes to interaxonal contacts.
- Hayashi S1, Inoue Y1, Kiyonari H2, Abe T2, Misaki K3, Moriguchi H4, Tanaka Y4, Takeichi M5.
- Developmental cell.Dev Cell.2014 Sep 29;30(6):673-87. doi: 10.1016/j.devcel.2014.07.015. Epub 2014 Sep 4.
- In the process of neuronal wiring, axons derived from the same functional group typically extend together, resulting in fascicle formation. How these axons communicate with one another remains largely unknown. Here, we show that protocadherin-17 (Pcdh17) supports this group extension by recruiting a
- PMID 25199687
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★リンクテーブル★
| リンク元 | 「神経性Wiskott-Aldrich症候群タンパク質」「神経性ウィスコット・アルドリッチ症候群タンパク質」 |
| 関連記事 | 「neuronal」「syndrome」「Aldrich syndrome」 |
「神経性Wiskott-Aldrich症候群タンパク質」
「神経性ウィスコット・アルドリッチ症候群タンパク質」
「neuronal」
- 神経細胞の、ニューロンの、神経型の
「syndrome」
- n.