細胞常見信號通路圖片合集

1、· ·NGF信號通路 (2004-8-16) · ·TGF beta 信號轉(zhuǎn)導(dǎo) (2004-8-16) · ·細胞凋亡信號 (2004-8-16) · ·線粒體輸入信號 (2004-8-16) · ·ROS信號 (2004-8-16) · ·Toll-Like 受體家族 (2004-8-16) · ·Toll-Like 受體 (2004-8-16) · ·actin肌絲 (2004-8-16) &

2、#183; ·Wnt/LRP6 信號 (2004-8-16) · ·WNT信號轉(zhuǎn)導(dǎo) (2004-8-16) · ·West Nile 西尼羅河病毒 (2004-8-16) · ·Vitamin C 維生素C在大腦中的作用 (2004-8-16) · ·視覺信號轉(zhuǎn)導(dǎo) (2004-8-16) · ·VEGF，低氧 (2004-8-16) · ·TSP-1誘導(dǎo)細胞凋亡 (2004-8-16) · ·Tr

3、ka信號轉(zhuǎn)導(dǎo) (2004-8-16) · ·dbpb調(diào)節(jié)mRNA (2004-8-16) · ·CARM1甲基化 (2004-8-16) · ·CREB轉(zhuǎn)錄因子 (2004-8-16) · ·TPO信號通路 (2004-8-16) · ·Toll-Like 受體 (2004-8-16) · ·TNFR2 信號通路 (2004-8-16) · ·TNFR1信號通路 (2004-8-16) · ·TNF/Stress相關(guān)

4、信號 (2004-8-16) · ·IGF-1受體 (2004-8-16) · ·共刺激信號 (2004-8-16) · ·Th1/Th2 細胞分化 (2004-8-16) · ·TGF beta 信號轉(zhuǎn)導(dǎo) (2004-8-16) · ·端粒、端粒酶與衰老 (2004-8-16) · ·TACI和BCMA調(diào)節(jié)B細胞免疫 (2004-8-16) · ·T輔助細胞的表面受體 (2004-8-16) · ·T細胞

5、受體信號通路 (2004-8-16) · ·T細胞受體和CD3復(fù)合物 (2004-8-16) · ·Cardiolipin的合成 (2004-8-16) · ·Synaptic突觸連接中的蛋白 (2004-8-16) · ·HSP在應(yīng)激中的調(diào)節(jié)的作用 (2004-8-16) · ·Stat3 信號通路 (2004-8-16) · ·SREBP控制脂質(zhì)合成 (2004-8-16) · ·酪氨酸激酶的調(diào)節(jié) (2004-8-16) ·

6、83;Sonic Hedgehog (SHH)受體ptc1調(diào)節(jié)細胞周期 (2004-8-16) · ·Sonic Hedgehog (Shh) 信號 (2004-8-16) · ·SODD/TNFR1信號 (2004-8-16) · ·AKT/mTOR在骨骼肌肥大中的作用 (2004-8-16) · ·G蛋白信號轉(zhuǎn)導(dǎo) (2004-8-16) · ·肝細胞生長因子受體信號 (2004-8-16) · ·IL1受體信號轉(zhuǎn)導(dǎo) (20

7、04-8-16) · ·acetyl從線粒體到胞漿過程 (2004-8-16) · ·趨化因子chemokine在T細胞極化中的選擇性表 (2004-8-16) · ·SARS冠狀病毒蛋白酶 (2004-8-16) · ·Parkin在泛素-蛋白酶體中的作用 (2004-8-16) · ·nicotinic acetylcholine受體在凋亡中的作用 (2004-8-16) · ·線粒體在細胞凋亡中的作用 (2004-8-16) · ·MEF2

8、D在T細胞凋亡中的作用 (2004-8-16) · ·Erk5和神經(jīng)元生存 (2004-8-16) · ·ERBB2信號轉(zhuǎn)導(dǎo) (2004-8-16) · ·GPCRs調(diào)節(jié)EGF受體 (2004-8-16) · ·BRCA1調(diào)節(jié)腫瘤敏感性 (2004-8-16) · ·Rho細胞運動的信號 (2004-8-16) · ·Leptin能逆轉(zhuǎn)胰島素抵抗 (2004-8-16) · ·轉(zhuǎn)錄因子DREAM調(diào)節(jié)疼敏感 (2004-8-16) · ·

9、PML調(diào)節(jié)轉(zhuǎn)錄 (2004-8-16) · ·p27調(diào)節(jié)細胞周期 (2004-8-16) · ·MAPK信號調(diào)節(jié) (2004-8-16) · ·細胞因子調(diào)節(jié)造血細胞分化 (2004-8-16) · ·eIF4e和p70 S6激酶調(diào)節(jié) (2004-8-16) · ·eIF2調(diào)節(jié) (2004-8-16) · ·谷氨酸受體調(diào)節(jié)ck1/cdk5 (2004-8-16) · ·plk3在細胞周期中的作用 (2004-8-1) · ·BA

10、D磷酸化調(diào)節(jié) (2004-8-1) · ·Reelin信號通路 (2004-8-1) · ·RB腫瘤抑制和DNA破壞 (2004-8-1) · ·NK細胞介導(dǎo)的細胞毒作用 (2004-8-1) · ·Ras信號通路 (2004-8-1) · ·Rac 1細胞運動信號 (2004-8-1) · ·PTEN依賴的細胞生長抑制和細胞凋亡 (2004-8-1) · ·notch信號通路 (2004-8-1) · ·蛋白激酶A（PKA）

11、在中心粒中的作用 (2004-8-1) · ·蛋白酶體Proteasome復(fù)合物 (2004-8-1) · ·Prion朊病毒的信號通路 (2004-8-1) · ·早老素Presenilin在notch和wnt信號中的作用 (2004-8-1) · ·mRNA的poly(A)形成 (2004-8-1) · ·淀粉樣蛋白前體信號 (2004-8-1) · ·PKC抑制myosin磷酸化 (2004-8-1) · ·磷脂酶C（PLC）信號 (2004-8-1

12、) · ·巨噬細胞Pertussis toxin不敏感的CCR5信號通 (2004-8-1) · ·Pelp1調(diào)節(jié)雌激素受體的活性 (2004-8-1) · ·PDGF信號通路 (2004-8-1) · ·p53信號通路 (2004-8-1) · ·p38MAPK信號通路 (2004-8-1) · ·Nrf2是氧化應(yīng)激基本表達的關(guān)鍵基因 (2004-8-1) · ·OX40信號通路 (2004-8-1) · ·hTerc轉(zhuǎn)錄調(diào)

13、節(jié)活性圖 (2004-8-1) · ·hTert轉(zhuǎn)錄因子的調(diào)節(jié)作用 (2004-8-1) · ·AIF在細胞凋亡中的作用 (2004-8-1) · ·Omega氧化通路 (2004-8-1) · ·核受體在脂質(zhì)代謝和毒性中的作用 (2004-8-1) · ·NK細胞中NO2依賴的IL-12信號通路 (2004-8-1) · ·TOR信號通路 (2004-8-1) · ·NO信號通路 (2004-8-1) · ·NF-kB信號轉(zhuǎn)導(dǎo)通路 (

14、2004-8-1) · ·NFAT與心肌肥厚的示意圖 (2004-8-1) · ·神經(jīng)營養(yǎng)素及其表面分子 (2004-8-1) · ·神經(jīng)肽VIP和PACAP防止活化T細胞凋亡圖 (2004-8-1) · ·神經(jīng)生長因子信號圖 (2004-8-1) · ·線蟲和哺乳動物的MAPK信號比較 (2004-7-17) · ·細胞內(nèi)信號總論 (2004-7-17) · ·細胞凋亡信號通路 (2004-7-17) · ·MAPK級聯(lián)通路 (200

15、4-7-17) · ·MAPK信號通路圖 (2004-7-17) · ·BCR信號通路 (2004-7-17) · ·蛋白質(zhì)乙?；疽鈭D (2004-7-17) · ·wnt信號通路 (2004-7-17) · ·胰島素受體信號通路 (2004-7-17) · ·細胞周期在G2/M期的調(diào)控機理圖 (2004-7-17) · ·細胞周期G1/S檢查點調(diào)控機理圖 (2004-7-17) · ·Jak-STAT關(guān)系總表 (2004-7-17)

16、 · ·Jak/STAT 信號 (2004-7-17) · ·TGFbeta信號 (2004-7-17) · ·NFkappaB信號 (2004-7-17) · ·p38 MAPK信號通路 (2004-7-17) · ·SAPK/JNK 信號級聯(lián)通路 (2004-7-17) · ·從G蛋白偶聯(lián)受體到MAPK (2004-7-17) · ·MAPK級聯(lián)信號圖 (2004-7-17) · ·eIF-4E和p70

17、 S6激酶調(diào)控蛋白質(zhì)翻譯 (2004-7-17) · ·eif2蛋白質(zhì)翻譯 (2004-7-17) · ·蛋白質(zhì)翻譯示意圖 (2004-7-17) · ·線粒體凋亡通路 (2004-7-17) · ·死亡受體信號通路 (2004-7-17) · ·凋亡抑制通路 (2004-7-17) · ·細胞凋亡綜合示意圖 (2004-7-17) · ·Akt/Pkb信號通路 (2004-7-17) · ·MAPK/ERK信號通路 (200

18、4-7-17) · ·哺乳動物MAPK信號通路 (2004-7-17) · ·Pitx2多步調(diào)節(jié)基因轉(zhuǎn)錄 (2004-7-17) · ·IGF-1R導(dǎo)致BAD磷酸化的多個凋亡路徑 (2004-7-17) · ·多重耐藥因子 (2004-7-17) · ·mTOR信號通路 (2004-7-17) · ·Msp/Ron受體信號通路 (2004-7-17) · ·單核細胞和其表面分子 (2004-7-17) · ·線粒體的肉毒堿轉(zhuǎn)移酶（CPT

19、）系統(tǒng) (2004-7-17) · ·METS影響巨噬細胞的分化 (2004-7-17) · ·Anandamide，內(nèi)源性大麻醇的代謝 (2004-7-17) · ·黑色素細胞（Melanocyte）發(fā)育和信號 (2004-7-17) · ·DNA甲基化導(dǎo)致轉(zhuǎn)錄抑制的機理圖 (2004-7-17) · ·蛋白質(zhì)的核輸入信號圖 (2004-7-17) · ·PPARa調(diào)節(jié)過氧化物酶體的增殖 (2004-7-17) · ·對乙氨基酚（Acetaminophe

20、n）的活性和毒性機 (2004-7-17) · ·mCalpain在細胞運動中的作用 (2004-7-17) · ·MAPK信號圖 (2004-7-17) · ·MAPK抑制SMRT活化 (2004-7-17) · ·蘋果酸和天門冬酸間的轉(zhuǎn)化 (2004-7-17) · ·低密度脂蛋白（LDL）在動脈粥樣硬化中的作用 (2004-7-17) · ·LIS1基因在神經(jīng)細胞的發(fā)育和遷移中的作用圖 (2004-7-17) · ·Pyk2與Mapk相連的信號通路

21、(2004-7-17) · ·galactose代謝通路 (2004-7-17) · ·Lectin誘導(dǎo)補體的通路 (2004-7-17) · ·Lck和Fyn在TCR活化中的作用 (2004-7-17) · ·乳酸合成圖 (2004-7-17) · ·Keratinocyte分化圖 (2004-7-17) · ·離子通道在心血管內(nèi)皮細胞中的作用 (2004-7-17) · ·離子通道和佛波脂（Phorbal Esters）信號 (2004-7-

22、17) · ·內(nèi)源性Prothrombin激活通路 (2004-7-17) · ·Ribosome內(nèi)化通路 (2004-7-17) · ·整合素（Integrin）信號通路 (2004-7-17) · ·胰島素（Insulin）信號通路 (2004-7-17) · ·Matrix Metalloproteinases (2004-7-17) · ·組氨酸去乙酰化抑制劑抑制Huntington病 (2004-7-17) · ·Gleevec誘導(dǎo)細胞

23、增殖 (2004-7-17) · ·Ras和Rho在細胞周期的G1/S轉(zhuǎn)換中的作用 (2004-7-17) · ·DR3，4，5受體誘導(dǎo)細胞凋亡 (2004-7-17) · ·AKT調(diào)控Gsk3圖 (2004-7-17) · ·IL-7信號轉(zhuǎn)導(dǎo) (2004-7-17) · ·IL22可溶性受體信號轉(zhuǎn)導(dǎo)圖 (2004-7-17) · ·IL-2活化T細胞圖 (2004-7-17) · ·IL12和Stat4依賴的TH1細胞發(fā)育信號通路 (2004-7-17)

24、 · ·IL-10信號通路 (2004-7-17) · ·IL 6信號通路 (2004-7-17) · ·IL 5信號通路 (2004-7-17) · ·IL 4信號通路 (2004-7-17) · ·IL 3信號通路 (2004-7-17) · ·IL 2 信號通路 (2004-7-17) · ·IL 18信號通路 (2004-7-17) · ·IL 17

25、信號通路 (2004-7-17) · ·IGF-1信號通路 (2004-7-17) · ·IFN gamma信號通路 (2004-7-17) · ·INF信號通路 (2004-7-17) · ·低氧誘導(dǎo)因子（HIF）在心血管中的作用 (2004-7-17) · ·低氧和P53在心血管系統(tǒng)中的作用 (2004-7-17) · ·人類巨細胞病毒和MAP信號通路 (2004-7-17) · ·孕酮如何促進卵細胞成熟？ (2004-7-17) ·

26、; ·How does salmonella hijack a cell (2004-7-17) · ·Hop通路在心臟發(fā)育中的作用 (2004-7-17) · ·HIV-I Nef:負性調(diào)節(jié)fas和TNF (2004-7-17) · ·HIV-1防止宿主細胞耐受的機理 (2004-7-17) · ·HIV誘導(dǎo)T細胞凋亡圖 (2004-7-17) · ·血紅素的伴侶分子 (2004-7-17) · ·g-S

27、ecretase介導(dǎo)ErbB4信號通路 (2004-7-17) · ·生物激素信號 (2004-7-17) · ·Granzyme A介導(dǎo)的凋亡信號通路 (2004-7-17) · ·G蛋白偶聯(lián)信號需要Tubby支持 (2004-7-17) · ·糖酵解通路 (2004-7-17) · ·Ghrelin：食物吸收和能量平衡的調(diào)控者 (2004-7-17) · ·PS1能產(chǎn)生beta淀粉樣蛋白導(dǎo)致老年性癡呆 (2004-7-17) · ·GATA3

28、部分參與TH2細胞因子基因的表達 (2004-7-17) · ·GABA受體的代謝圖 (2004-7-17) · ·FXR和LXR調(diào)節(jié)膽固醇代謝 (2004-7-17) · ·SLRP在骨骼中的作用 (2004-7-17) · ·自由基誘導(dǎo)細胞凋亡信號 (2004-7-17) · ·FOSB與藥物成癮 (2004-7-17) · ·fMLP誘導(dǎo)趨化因子基因表達 (2004-7-17) · ·Fibrinolysis通路 (2004-7-17) ·

29、 ·糖酵解通路 (2004-7-17) · ·Fc Epsilon Receptor I信號 (2004-7-17) · ·FAS信號通路 (2004-7-17) · ·外源性Prothrombin激活通路 (2004-7-17) · ·真核細胞蛋白質(zhì)翻譯示意圖 (2004-7-17) · ·雌激素反應(yīng)蛋白EFP控制乳腺癌細胞的細胞周期 (2004-7-17) · ·EPO介導(dǎo)神經(jīng)保護作用與NF-kB相關(guān) (2004-7-17)

30、83; ·Erythrocyte分化通路 (2004-7-17) · ·Erk1/Erk2 Mapk 信號通路 (2004-7-17) · ·Erk和PI-3K在細胞外間質(zhì)中的作用 (2004-7-17) · ·內(nèi)質(zhì)網(wǎng)相關(guān)的蛋白質(zhì)降解通路示意圖 (2004-7-17) · ·EPO售轉(zhuǎn)導(dǎo)機制圖 (2004-7-17) · ·血小板凝聚示意圖 (2004-7-17) · ·NDK動力學(xué) (2004-7-17) · ·線粒體的電子

31、傳遞鏈?zhǔn)疽鈭D (2004-7-17) · ·Eicosanoid代謝 (2004-7-17) · ·EGF信號通路 (2004-7-17) · ·calcineurin對Keratinocyte分化的影響 (2004-7-17) · ·E2F1信號通路 (2004-7-17) · ·MTA-3在雌激素不敏感性乳腺癌中下調(diào) (2004-7-17) · ·雙鏈RNA誘導(dǎo)基因表達示意圖 (2004-7-17) · ·Dicer信號通路（RNAi機理） (2004

32、-7-17) · ·CDK5在老年性癡呆中的調(diào)節(jié)作用 (2004-7-17) · ·樹突狀細胞調(diào)節(jié)TH1和TH2發(fā)育示意圖 (2004-7-17) · ·RAR和RXR被蛋白酶體降解通路 (2004-7-17) · ·D4-GDI信號通路示意圖 (2004-7-17) · ·細胞因子和炎癥反應(yīng)示意圖 (2004-7-9) · ·細胞因子網(wǎng)絡(luò)調(diào)控圖 (2004-7-9) · ·CFTR和beta 2腎上腺素受體通路 (2004-7-9) ·

33、; ·Cyclin和細胞周期調(diào)控圖 (2004-7-9) · ·Ran核質(zhì)循環(huán)轉(zhuǎn)運圖 (2004-7-9) · ·Cyclin E降解通路圖 (2004-7-9) · ·CXCR4信號通路圖 (2004-7-9) · ·CTL介導(dǎo)的免疫反應(yīng)圖 (2004-7-9) · ·CTCF：第一個多價核因子 (2004-7-9) · ·皮質(zhì)激素和心臟保護 (2004-7-9) · ·骨骼肌的成肌信號圖 (2004-7-9) · 

34、3;VitD調(diào)控基因表達信號圖 (2004-7-9) · ·補體信號通路 (2004-7-9) · ·線粒體和過氧化物酶體中氧化的比較圖 (2004-7-9) · ·經(jīng)典的補體信號通路圖 (2004-7-9) · ·心律失常的分子機制圖 (2004-7-9) · ·hSWI/SNF ATP依賴的染色體重塑 (2004-7-9) · ·碳水化合物和cAMP調(diào)節(jié)ChREBP圖 (2004-7-9) · ·分子伴侶調(diào)節(jié)干擾素信號圖 (2004-7-9)

35、 · ·Ceramide信號圖 (2004-7-9) · ·局部急性感染的細胞與分子信號 (2004-7-9) · ·細胞與細胞粘附信號 (2004-7-9) · ·細胞周期G2/M調(diào)控點信號調(diào)節(jié) (2004-7-9) · ·細胞周期 G1/S調(diào)控點信號圖 (2004-7-9) · ·CDK調(diào)節(jié)DNA復(fù)制 (2004-7-9) · ·cdc25和chk1在DNA破壞中的作用圖 (2004-7-9) · ·CD40L信號通路圖

36、(2004-7-9) · ·CCR3信號圖 (2004-7-9) · ·CBL下調(diào)EGF受體的信號轉(zhuǎn)導(dǎo)圖 (2004-7-9) · ·一些氨基酸的代謝通路圖 3 (2004-7-9) · ·一些氨基酸的代謝通路圖 2 (2004-7-9) · ·一些氨基酸的代謝通路圖 (2004-7-9) · ·Catabolic pathway for asparagine and asp (2004-7-9) 

37、3; ·Caspase 信號級聯(lián)通路在細胞凋亡中的作用 (2004-7-9) · ·CARM1和雌激素的信號轉(zhuǎn)導(dǎo)調(diào)控 (2004-7-9) · ·抗氧自由基的心臟保護作用信號轉(zhuǎn)導(dǎo)圖 (2004-7-9) · ·乙肝病毒中的鈣信號調(diào)控 (2004-7-9) · ·鎘誘導(dǎo)巨噬細胞的DNA合成和增殖 (2004-7-9) · ·Ca2+/CaM依賴的激活 (2004-7-9) · ·B細胞活化機理圖 (2004-6-9) · ·BTG家族蛋白

38、和細胞周期的調(diào)節(jié) (2004-6-9) · ·BRCA1作用機理 (2004-6-9) · ·骨重塑示意圖 (2004-6-9) · ·Botulinum Toxin阻斷神經(jīng)遞質(zhì)釋放示意圖 (2004-6-9) · ·纈氨酸的生物合成圖 (2004-6-9) · ·Tryptophan在植物和細菌內(nèi)的生物合成 (2004-6-9) · ·蘇氨酸和蛋氨酸的體內(nèi)合成示意圖 (2004-6-9) · ·sphingolipids生物合成 (2004-6

39、-9) · ·spermidine和spermine生物合成 (2004-6-9) · ·細菌體內(nèi)合成脯氨酸的示意圖 (2004-6-9) · ·苯丙氨酸和酪氨酸的生物合成 (2004-6-9) · ·神經(jīng)遞質(zhì)的合成示意圖 (2004-6-9) · ·賴氨酸生物合成圖 (2004-6-9) · ·亮氨酸的體內(nèi)生物合成圖 (2004-6-9) · ·異亮氨酸的生物合成圖 (2004-6-9) · ·甘氨酸和色氨酸的生物合成 (2004-6

40、-9) · ·Cysteine在哺乳動物中的合成圖 (2004-6-9) · ·Cysteine在細菌和植物內(nèi)生物合成圖 (2004-6-9) · ·Chorismate在細菌和植物內(nèi)的生物合成 (2004-6-9) · ·Arginine在細菌內(nèi)的生物合成 (2004-6-9) · ·生物活性肽誘導(dǎo)的通路 (2004-6-9) · ·脂肪酸的氧化通路 (2004-6-9) · ·BCR信號通路示意圖 (2004-6-9) · ·SUM

41、Oylation基本機理 (2004-6-9) · ·PPAR影響基因表達的基本信號機制圖 (2004-6-9) · ·B淋巴細胞表面分子示意圖 (2004-6-9) · ·B細胞生存信號通路 (2004-6-5) · ·B細胞信號通路的復(fù)雜性 (2004-6-5) · ·GPCR信號的衰減的機理 (2004-6-4) · ·ATM信號通路 (2004-6-4) · ·阿斯匹林的抗凝機理 (2004-6-4) · ·細胞凋亡信號調(diào)節(jié)DN

42、A片段化 (2004-6-4) · ·細胞凋亡DNA片段化與組織穩(wěn)態(tài)的機理 (2004-6-4) · ·反義核酸的作用機理-RNA polymerase III  (2004-6-4) · ·抗原遞呈與處理信號圖 (2004-6-4) · ·Antigen依賴的B細胞激活 (2004-6-4) · ·Anthrax Toxin Mechanism of Action (2004-6-4) · ·血管緊張素轉(zhuǎn)

43、換酶2調(diào)節(jié)心臟功能 (2004-6-4) · ·Angiotensin II 介導(dǎo)JNK信號通路的激活 (2004-6-4) · ·Alternative Complement Pathway (2004-6-4) · ·Alpha-synuclein和Parkin在怕金森病中的作用 (2004-6-4) · ·ALK在心肌細胞中的功能圖 (2004-6-4) · ·AKT信號通路 (2004-6-4) · ·AKAP95在有絲分裂中的

44、作用圖 (2004-6-4) · ·Ahr信號轉(zhuǎn)導(dǎo)圖 (2004-6-4) · ·Agrin突觸后的功能圖 (2004-6-4) · ·ADP-Ribosylation 因子 (2004-6-4) · ·淋巴細胞粘附分子信號圖 (2004-6-4) · ·Adhesion and Diapedesis of Lymphocytes (2004-6-4) · ·Adhesion and Diapedesis&

45、#160;of Granulocytes (2004-6-4) · ·急性心肌梗死信號轉(zhuǎn)導(dǎo)圖 (2004-6-4) · ·src蛋白質(zhì)激活圖 (2004-6-4) · ·PKC與G蛋白耦聯(lián)受體的關(guān)系 (2004-6-4) · ·cAMP依賴的CSK抑制T細胞功能示意圖 (2004-6-4) · ·PKA功能示意圖 (2004-6-4) · ·一氧化氮（NO）在心臟中的功能示意圖 (2004-6-4) · ·RelA 在細胞核內(nèi)乙?；腿?/p>

46、乙?；?(2004-6-4) actin肌絲Mammalian cell motility requires actin polymerization in the direction of movement to change membrane shape and extend cytoplasm into lamellipodia. The polymerization of actin to drive cell movement also involves branching of actin filaments into a network oriented with the gro

47、wing ends of the fibers near the cell membrane. Manipulation of this process helps bacteria like Salmonella gain entry into cells they infect. Two of the proteins involved in the formation of Y branches and in cell motility are Arp2 and Arp3, both members of a large multiprotein complex containing s

48、everal other polypeptides as well. The Arp2/3 complex is localized at the Y branch junction and induces actin polymerization. Activity of this complex is regulated by multiple different cell surface receptor signaling systems, activating WASP, and Arp2/3 in turn to cause changes in cell shape and ce

49、ll motility. Wasp and its cousin Wave-1 interact with the Arp2/3 complex through the p21 component of the complex. The crystal structure of the Arp2/3 complex has revealed further insights into the nature of how the complex works.Activation by Wave-1, another member of the WASP family, also induces

50、actin alterations in response to Rac1 signals upstream. Wave-1 is held in an inactive complex in the cytosol that is activated to allow Wave-1 to associate with Arp2/3. While WASP is activated by interaction with Cdc42, Wave-1, is activated by interaction with Rac1 and Nck. Wave-1 activation by Rac1

51、 and Nck releases Wave-1 with Hspc300 to activate actin Y branching and polymerization by Arp2/3. Different members of this gene family may produce different actin cytoskeletal architectures. The immunological defects associated with mutation of the WASP gene, the Wiskott-Aldrich syndrome for which

52、WASP was named, indicates the importance of this system for normal cellular function. Cory GO, Ridley AJ. Cell motility: braking WAVEs. Nature. 2002 Aug 15;418(6899):732-3. No abstract available. Eden, S., et al. (2002) Mechanism of regulation of WAVE1-induced actin nucleation by Rac1 and Nck.

53、Nature 418(6899), 790-3 Falet H, Hoffmeister KM, Neujahr R, Hartwig JH. Normal Arp2/3 complex activation in platelets lacking WASp. Blood. 2002 Sep 15;100(6):2113-22. Kreishman-Deitrick M, Rosen MK, Kreishman-Deltrick M. Ignition of a cellular machine. Nat Cell Biol. 2002 Feb;4(2):E31-3. No abstract

54、 available. Machesky, L.M., Insall, R.H. (1998) Scar1 and the related Wiskott-Aldrich syndrome protein, WASP, regulate the actin cytoskeleton through the Arp2/3 complex. Curr Biol 8(25), 1347-56 Robinson, R.C. et al. (2001) Crystal structure of Arp2/3 complex. Science 294(5547), 1679-84 Weeds A, Yeo

55、h S. Structure. Action at the Y-branch. Science. 2001 Nov 23;294(5547):1660-1. No abstract available. Wnt/LRP6 信號Wnt glycoproteins play a role in diverse processes during embryonic patterning in metazoa through interaction with frizzled-type seven-transmembrane-domain receptors (Frz) to stabili

56、ze b-catenin. LDL-receptor-related protein 6 (LRP6), a Wnt co-receptor, is required for this interaction. Dikkopf (dkk) proteins are both positive and negative modulators of this signalingWNT信號轉(zhuǎn)導(dǎo)West Nile 西尼羅河病毒W(wǎng)est Nile virus (WNV) is a member of the Flaviviridae, a plus-stranded virus fa

57、mily that includes St. Louis encephalitis virus, Kunjin virus, yellow fever virus, Dengue virus, and Japanese encephalitis virus. WNV was initially isolated in 1937 in the West Nile region of Uganda and has become prevalent in Africa, Asia, and Europe. WNV has rapidly spread across the United States

58、 through its insect host and causes neurological symptoms and encephalitis, which can result in paralysis or death. Since 1999 about 3700 cases of West Nile virus (WNV) infection and 200 deaths have been recorded in United States. The viral capsid protein likely contributes to the WNV-associated dea

59、dly inflammation via apoptosis induced through the mitochondrial pathway. WNV particles (50 nm in diameter) consist of a dense core (viral protein C encapsidated virus RNA genome) surrounded by a membrane envelope (viral E and M proteins embedded in a lipid bilayer). The virus binds to a specific ce

60、ll surface protein (not yet identified), an interaction thought to involve E protein with highly sulfated neperan sulfate (HSHS) residues that are present on the surfaces of many cells and enters the cell by a process similar to that of endocytosis. Once inside the cell, the genome RNA is released i

61、nto the cytoplasm via endosomal release, a fusion process involving acidic pH induced conformation change in the E protein. The RNA genome serves as mRNA and is translated by ribosomes into ten mature viral proteins are produced via proteolytic cleavage, which include three structural components and

62、 seven different nonstructural components of the virus. These proteins assemble and transcribe complimentary minus strand RNAs from the genomic RNA. The complimentary minus strand RNA in turns serves as template for the synthesis of positive-stranded genomic RNAs. Once viral E, preM and C proteins h

63、ave accumulated to sufficient level, they assemble with the genomic RNA to form progeny virions, which migrate to the cell surface where they are surrounded with lipid envelop and released.Vitamin C 維生素C在大腦中的作用 Vitamin C (ascorbic acid) was first identified by virtue of the essential

64、role it plays in collagen modification, preventing the nutritional deficiency scurvy. Vitamin C acts as a cofactor for hydroxylase enzymes that post-translationally modify collagen to increase the strength and elasticity of tissues. Vitamin C reduces the metal ion prosthetic groups of many enzymes,

65、maintaining activity of enzymes, also acts as an anti-oxidant. Although the prevention of scurvy through modification of collagen may be the most obvious role for vitamin C, it is not necessarily the only role of vitamin C. Svct1 and Svct2 are ascorbate transporters for vitamin C import into tissues

66、 and into cells. Both of these transporters specifically transport reduced L-ascorbic acid against a concentration gradient using the intracellular sodium gradient to drive ascorbate transport. Svct1 is expressed in epithelial cells in the intestine, upregulated in cellular models for intestinal epi

67、thelium and appears to be responsible for the import of dietary vitamin C from the intestinal lumen. The vitamin C imported from the intestine is present in plasma at approximately 50 uM, almost exclusively in the reduced form, and is transported to tissues to play a variety of roles. Svct2 imports

68、reduced ascorbate from the plasma into very active tissues like the brain. Deletion in mice of the gene for Svct2 revealed that ascorbate is required for normal development of the lungs and brain during pregnancy. A high concentration of vitamin C in neurons of the developing brain may help protect

69、the developing brain from free radical damage. The oxidized form of ascorbate, dehydroascorbic acid, is transported into a variety of cells by the glucose transporter Glut-1. Glut-1, Glut-3 and Glut-4 can transport dehydroascorbate, but may not transport significant quantities of ascorbic acid in vivo.視覺信號轉(zhuǎn)導(dǎo)信息來源：本站原創(chuàng) 生物谷網(wǎng)站