细胞常见信号通路图片Word格式文档下载.docx
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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
（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
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.
信号
Wntglycoproteinsplayaroleindiverseprocessesduringembryonicpatterninginmetazoathroughinteractionwithfrizzled-typeseven-transmembrane-domainreceptors（Frz）tostabilizeb-catenin.LDL-receptor-relatedprotein6（LRP6）,aWntco-receptor,isrequiredforthisinteraction.Dikkopf（dkk）proteinsarebothpositiveandnegativemodulatorsofthissignaling
WNT信号转导
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.
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
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