细胞常见信号通路图片.docx

细胞常见信号通路图片.docx

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细胞常见信号通路图片

actin肌丝5

Wnt/LRP6?

信号7

WNT信号转导7

West?

Nile?

西尼罗河病毒8

Vitamin?

C?

维生素C在大脑中的作用10

视觉信号转导11

VEGF，低氧13

TSP-1诱导细胞凋亡15

Trka信号转导16

dbpb调节mRNA17

CARM1甲基化19

CREB转录因子20

TPO信号通路21

Toll-Like?

受体22

TNFR2?

信号通路24

TNFR1信号通路25

IGF-1受体26

TNF/Stress相关信号27

共刺激信号29

Th1/Th2?

细胞分化30

TGF?

beta?

信号转导32

端粒、端粒酶与衰老33

TACI和BCMA调节B细胞免疫35

T辅助细胞的表面受体36

T细胞受体信号通路37

T细胞受体和CD3复合物38

Cardiolipin的合成40

Synaptic突触连接中的蛋白42

HSP在应激中的调节的作用43

Stat3?

信号通路45

SREBP控制脂质合成46

酪氨酸激酶的调节48

Sonic?

Hedgehog?

（SHH）受体ptc1调节细胞周期51

Sonic?

Hedgehog?

（Shh）?

信号53

SODD/TNFR1信号56

AKT/mTOR在骨骼肌肥大中的作用58

G蛋白信号转导59

IL1受体信号转导60

acetyl从线粒体到胞浆过程62

趋化因子chemokine在T细胞极化中的选择性表达63

SARS冠状病毒蛋白酶65

SARS冠状病毒蛋白酶67

Parkin在泛素-蛋白酶体中的作用69

nicotinic?

acetylcholine受体在凋亡中的作用71

线粒体在细胞凋亡中的作用73

MEF2D在T细胞凋亡中的作用74

Erk5和神经元生存75

ERBB2信号转导77

GPCRs调节EGF受体78

BRCA1调节肿瘤敏感性79

Rho细胞运动的信号81

Leptin能逆转胰岛素抵抗82

转录因子DREAM调节疼敏感84

PML调节转录86

p27调节细胞周期88

MAPK信号调节89

细胞因子调节造血细胞分化91

eIF4e和p70?

S6激酶调节92

eIF2调节93

谷氨酸受体调节ck1/cdk594

BAD磷酸化调节95

plk3在细胞周期中的作用96

Reelin信号通路97

RB肿瘤抑制和DNA破坏98

NK细胞介导的细胞毒作用99

Ras信号通路100

Rac?

1细胞运动信号101

PTEN依赖的细胞生长抑制和细胞凋亡103

蛋白激酶A（PKA）在中心粒中的作用104

notch信号通路106

蛋白酶体Proteasome复合物108

Prion朊病毒的信号通路109

早老素Presenilin在notch和wnt信号中的作用110

淀粉样蛋白前体信号112

mRNA的poly（A）形成113

PKC抑制myosin磷酸化114

磷脂酶C（PLC）信号115

巨噬细胞Pertussis?

toxin不敏感的CCR5信号通路116

Pelp1调节雌激素受体的活性117

PDGF信号通路118

p53信号通路120

p38MAPK信号通路121

Nrf2是氧化应激基本表达的关键基因122

OX40信号通路123

hTert转录因子的调节作用124

hTerc转录调节活性图125

AIF在细胞凋亡中的作用126

Omega氧化通路127

核受体在脂质代谢和毒性中的作用129

NK细胞中NO2依赖的IL-12信号通路131

TOR信号通路133

NO信号通路134

NF-kB信号转导通路135

NFAT与心肌肥厚的示意图137

神经营养素及其表面分子139

神经肽VIP和PACAP防止活化T细胞凋亡图141

神经生长因子信号图142

细胞凋亡信号通路144

MAPK级联通路144

MAPK信号通路图145

BCR信号通路146

蛋白质乙酰化示意图147

wnt信号通路148

胰岛素受体信号通路149

细胞周期在G2/M期的调控机理图151

细胞周期G1/S检查点调控机理图152

Jak-STAT关系总表153

Jak/STAT?

信号155

TGFbeta信号156

NFkappaB信号157

p38?

MAPK信号通路159

SAPK/JNK?

信号级联通路160

从G蛋白偶联受体到MAPK161

MAPKpathwayMAPK级联信号图162

eIF-4E和p70?

S6激酶调控蛋白质翻译163

eif2蛋白质翻译164

蛋白质翻译示意图165

线粒体凋亡通路167

死亡受体信号通路168

凋亡抑制通路170

细胞凋亡综合示意图171

Akt/Pkb信号通路172

MAPK/ERK信号通路174

哺乳动物MAPK信号通路175

Pitx2多步调节基因转录176

IGF-1R导致BAD磷酸化的多个凋亡路径177

多重耐药因子179

mTOR信号通路180

Msp/Ron受体信号通路181

单核细胞和其表面分子182

线粒体的肉毒碱转移酶（CPT）系统183

METS影响巨噬细胞的分化184

Anandamide，内源性大麻醇的代谢186

黑色素细胞（Melanocyte）发育和信号187

DNA甲基化导致转录抑制的机理图188

蛋白质的核输入信号图190

PPARa调节过氧化物酶体的增殖192

对乙氨基酚（Acetaminophen）的活性和毒性机理194

mCalpain在细胞运动中的作用196

MAPK信号图198

MAPK抑制SMRT活化200

苹果酸和天门冬酸间的转化201

低密度脂蛋白（LDL）在动脉粥样硬化中的作用202

LIS1基因在神经细胞的发育和迁移中的作用图204

Pyk2与Mapk相连的信号通路205

galactose代谢通路206

Lectin诱导补体的通路207

Lck和Fyn在TCR活化中的作用208

乳酸合成图209

Keratinocyte分化图210

离子通道在心血管内皮细胞中的作用211

离子通道和佛波脂（Phorbal?

Esters）信号213

内源性Prothrombin激活通路214

Ribosome内化通路216

整合素（Integrin）信号通路217

胰岛素（Insulin）信号通路218

Matrix?

Metalloproteinases219

组氨酸去乙酰化抑制剂抑制Huntington病220

Gleevec诱导细胞增殖222

Ras和Rho在细胞周期的G1/S转换中的作用224

DR3，4，5受体诱导细胞凋亡225

AKT调控Gsk3图226

IL-7信号转导227

IL22可溶性受体信号转导图229

IL-2活化T细胞图230

IL12和Stat4依赖的TH1细胞发育信号通路232

IL-10信号通路233

IL?

6信号通路234

IL?

5信号通路236

actin肌丝

Mammaliancellmotilityrequiresactinpolymerizationinthedirectionofmovementtochangemembraneshapeandextendcytoplasmintolamellipodia.Thepolymerizationofactintodrivecellmovementalsoinvolvesbranchingofactinfilamentsintoanetworkorientedwiththegrowingendsofthefibersnearthecellmembrane.ManipulationofthisprocesshelpsbacterialikeSalmonellagainentryintocellstheyinfect.TwooftheproteinsinvolvedintheformationofYbranchesandincellmotilityareArp2andArp3,bothmembersofalargemultiproteincomplexcontainingseveralotherpolypeptidesaswell.TheArp2/3complexislocalizedattheYbranchjunctionandinducesactinpolymerization.Activityofthiscomplexisregulatedbymultipledifferentcellsurfacereceptorsignalingsystems,activatingWASP,andArp2/3inturntocausechangesincellshapeandcellmotility.WaspanditscousinWave-1interactwiththeArp2/3complexthroughthep21componentofthecomplex.ThecrystalstructureoftheArp2/3complexhasrevealedfurtherinsightsintothenatureofhowthecomplexworks.

ActivationbyWave-1,anothermemberoftheWASPfamily,alsoinducesactinalterationsinresponsetoRac1signalsupstream.Wave-1isheldinaninactivecomplexinthecytosolthatisactivatedtoallowWave-1toassociatewithArp2/3.WhileWASPisactivatedbyinteractionwithCdc42,Wave-1,isactivatedbyinteractionwithRac1andNck.Wave-1activationbyRac1andNckreleasesWave-1withHspc300toactivateactinYbranchingandpolymerizationbyArp2/3.Differentmembersofthisgenefamilymayproducedifferentactincytoskeletalarchitectures.TheimmunologicaldefectsassociatedwithmutationoftheWASPgene,theWiskott-AldrichsyndromeforwhichWASPwasnamed,indicatestheimportanceofthissystemfornormalcellularfunction.

CoryGO,RidleyAJ.Cellmotility:

brakingWAVEs.Nature.2002Aug15;418（6899）:

732-3.Noabstractavailable.

Eden,S.,etal.（2002）MechanismofregulationofWAVE1-inducedactinnucleationbyRac1andNck.Nature418（6899）,790-3

FaletH,HoffmeisterKM,NeujahrR,HartwigJH.NormalArp2/3complexactivationinplateletslackingWASp.Blood.2002Sep15;100（6）:

2113-22.

Kreishman-DeitrickM,RosenMK,Kreishman-DeltrickM.Ignitionofacellularmachine.NatCellBiol.2002Feb;4

（2）:

E31-3.Noabstractavailable.

Machesky,L.M.,Insall,R.H.（1998）Scar1andtherelatedWiskott-Aldrichsyndromeprotein,WASP,regulatetheactincytoskeletonthroughtheArp2/3complex.CurrBiol8（25）,1347-56

Robinson,R.C.etal.（2001）CrystalstructureofArp2/3complex.Science294（5547）,1679-84

WeedsA,YeohS.Structure.ActionattheY-branch.Science.2001Nov23;294（5547）:

1660-1.Noabstractavailable.

Wnt/LRP6?

信号

Wntglycoproteinsplayaroleindiverseprocessesduringembryonicpatterninginmetazoathroughinteractionwithfrizzled-typeseven-transmembrane-domainreceptors（Frz）tostabilizeb-catenin.LDL-receptor-relatedprotein6（LRP6）,aWntco-receptor,isrequiredforthisinteraction.Dikkopf（dkk）proteinsarebothpositiveandnegativemodulatorsofthissignaling

WNT信号转导

West?

Nile?

西尼罗河病毒

WestNilevirus（WNV）isamemberoftheFlaviviridae,aplus-strandedvirusfamilythatincludesSt.Louisencephalitisvirus,Kunjinvirus,yellowfevervirus,Denguevirus,andJapaneseencephalitisvirus.WNVwasinitiallyisolatedin1937intheWestNileregionofUgandaandhasbecomeprevalentinAfrica,Asia,andEurope.WNVhasrapidlyspreadacrosstheUnitedStatesthroughitsinsecthostandcausesneurologicalsymptomsandencephalitis,whichcanresultinparalysisordeath.Since1999about3700casesofWestNilevirus（WNV）infectionand200deathshavebeenrecordedinUnitedStates.TheviralcapsidproteinlikelycontributestotheWNV-associateddeadlyinflammationviaapoptosisinducedthroughthemitochondrialpathway.

WNVparticles（50nmindiameter）consistofadensecore（viralproteinCencapsidatedvirusRNAgenome）surroundedbyamembraneenvelope（viralEandMproteinsembeddedinalipidbilayer）.Thevirusbindstoaspecificcellsurfaceprotein（notyetidentified）,aninteractionthoughttoinvolveEproteinwithhighlysulfatedneperansulfate（HSHS）residuesthatarepresentonthesurfacesofmanycellsandentersthecellbyaprocesssimilartothatofendocytosis.Onceinsidethecell,thegenomeRNAisreleasedintothecytoplasmviaendosomalrelease,afusionprocessinvolvingacidicpHinducedconformationchangeintheEprotein.TheRNAgenomeservesasmRNAandistranslatedbyribosomesintotenmatureviralproteinsareproducedviaproteolyticcleavage,whichincludethreestructuralcomponentsandsevendifferentnonstructuralcomponentsofthevirus.TheseproteinsassembleandtranscribecomplimentaryminusstrandRNAsfromthegenomicRNA.ThecomplimentaryminusstrandRNAinturnsservesastemplateforthesynthesisofpositive-strandedgenomicRNAs.OnceviralE,preMandCproteinshaveaccumulatedtosufficientlevel,theyassemblewiththegenomicRNAtoformprogenyvirions,whichmigratetothecellsurfacewheretheyaresurroundedwithlipidenvelopandreleased.

Vitamin?

C?

维生素C在大脑中的作用

VitaminC（ascorbicacid）wasfirstidentifiedbyvirtueoftheessentialroleitplaysincollagenmodification,preventingthenutritionaldeficiencyscurvy.VitaminCactsasacofactorforhydroxylaseenzymesthatpost-translationallymodifycollagentoincreasethestrengthandelasticityoftissues.VitaminCreducesthemetalionprostheticgroupsofmanyenzymes,maintainingactivityofenzymes,alsoactsasananti-oxidant.AlthoughthepreventionofscurvythroughmodificationofcollagenmaybethemostobviousroleforvitaminC,itisnotnecessarilytheonlyroleofvitaminC.Svct1andSvct2areascorbatetransportersforvitaminCimportintotissuesandintocells.BothofthesetransportersspecificallytransportreducedL-ascorbicacidagainstaconcentrationgradientusingtheintracellularsodiumgradienttodriveascorbatetransport.Svct1isexpressedinepithelialcellsintheintestine,upregulatedincellularmodelsforintestinalepitheliumandappearstoberesponsiblefortheimportofdietaryvitaminCfromtheintestinallumen.ThevitaminCimportedfromtheintestineispresentinplasmaatapproximately50uM,almostexclusivelyinthereducedform,andistransportedtotissuestoplayavarietyofroles.Svct2importsreducedascorbatefromtheplasmaintoveryactivetissueslikethebrain.DeletioninmiceofthegeneforSvct2revealedthatascorbateisrequiredfornormaldevelopmentofthelungsandbrainduringpregnancy.AhighconcentrationofvitaminCinneuronsofthe