細胞常見信號通路圖片合集

1、目錄actin肌絲5Wnt/LRP6 信號7WNT信號轉(zhuǎn)導(dǎo)7West Nile 西尼羅河病毒8Vitamin C 維生素C在大腦中的作用10視覺信號轉(zhuǎn)導(dǎo)11VEGF，低氧13TSP-1誘導(dǎo)細胞凋亡15Trka信號轉(zhuǎn)導(dǎo)16dbpb調(diào)節(jié)mRNA17CARM1甲基化19CREB轉(zhuǎn)錄因子20TPO信號通路21Toll-Like 受體22TNFR2 信號通路24TNFR1信號通路25IGF-1受體26TNF/Stress相關(guān)信號27共刺激信號29Th1/Th2 細胞分化30TGF beta 信號轉(zhuǎn)導(dǎo)32端

2、粒、端粒酶與衰老33TACI和BCMA調(diào)節(jié)B細胞免疫35T輔助細胞的表面受體36T細胞受體信號通路37T細胞受體和CD3復(fù)合物38Cardiolipin的合成40Synaptic突觸連接中的蛋白42HSP在應(yīng)激中的調(diào)節(jié)的作用43Stat3 信號通路45SREBP控制脂質(zhì)合成46酪氨酸激酶的調(diào)節(jié)48Sonic Hedgehog (SHH)受體ptc1調(diào)節(jié)細胞周期51Sonic Hedgehog (Shh) 信號53SODD/TNFR1信號56AKT/mTOR在骨骼肌肥大中的作用58G蛋白信號轉(zhuǎn)導(dǎo)59IL1受體信號轉(zhuǎn)導(dǎo)60acetyl從線

3、粒體到胞漿過程62趨化因子chemokine在T細胞極化中的選擇性表達63SARS冠狀病毒蛋白酶65SARS冠狀病毒蛋白酶67Parkin在泛素-蛋白酶體中的作用69nicotinic acetylcholine受體在凋亡中的作用71線粒體在細胞凋亡中的作用73MEF2D在T細胞凋亡中的作用74Erk5和神經(jīng)元生存75ERBB2信號轉(zhuǎn)導(dǎo)77GPCRs調(diào)節(jié)EGF受體78BRCA1調(diào)節(jié)腫瘤敏感性79Rho細胞運動的信號81Leptin能逆轉(zhuǎn)胰島素抵抗82轉(zhuǎn)錄因子DREAM調(diào)節(jié)疼敏感84PML調(diào)節(jié)轉(zhuǎn)錄86p27調(diào)節(jié)細胞周期88MAPK信號調(diào)節(jié)89細胞因子調(diào)節(jié)造血細胞分化91eIF4e和p7

4、0 S6激酶調(diào)節(jié)92eIF2調(diào)節(jié)93谷氨酸受體調(diào)節(jié)ck1/cdk594BAD磷酸化調(diào)節(jié)95plk3在細胞周期中的作用96Reelin信號通路97RB腫瘤抑制和DNA破壞98NK細胞介導(dǎo)的細胞毒作用99Ras信號通路100Rac 1細胞運動信號101PTEN依賴的細胞生長抑制和細胞凋亡103蛋白激酶A（PKA）在中心粒中的作用104notch信號通路106蛋白酶體Proteasome復(fù)合物108Prion朊病毒的信號通路109早老素Presenilin在notch和wnt信號中的作用110淀粉樣蛋白前體信號112mRNA的poly(A)形成113PKC抑制myosin磷酸化1

5、14磷脂酶C（PLC）信號115巨噬細胞Pertussis toxin不敏感的CCR5信號通路116Pelp1調(diào)節(jié)雌激素受體的活性117PDGF信號通路118p53信號通路120p38MAPK信號通路121Nrf2是氧化應(yīng)激基本表達的關(guān)鍵基因122OX40信號通路123hTert轉(zhuǎn)錄因子的調(diào)節(jié)作用124hTerc轉(zhuǎn)錄調(diào)節(jié)活性圖125AIF在細胞凋亡中的作用126Omega氧化通路127核受體在脂質(zhì)代謝和毒性中的作用129NK細胞中NO2依賴的IL-12信號通路131TOR信號通路133NO信號通路134NF-kB信號轉(zhuǎn)導(dǎo)通路135NFAT與心肌肥厚的示意圖137神經(jīng)營養(yǎng)素及其表面分子

6、139神經(jīng)肽VIP和PACAP防止活化T細胞凋亡圖141神經(jīng)生長因子信號圖142細胞凋亡信號通路144MAPK級聯(lián)通路144MAPK信號通路圖145BCR信號通路146蛋白質(zhì)乙?；疽鈭D147wnt信號通路148胰島素受體信號通路149細胞周期在G2/M期的調(diào)控機理圖151細胞周期G1/S檢查點調(diào)控機理圖152Jak-STAT關(guān)系總表153Jak/STAT 信號155TGFbeta信號156NFkappaB信號157p38 MAPK信號通路159SAPK/JNK 信號級聯(lián)通路160從G蛋白偶聯(lián)受體到MAPK161MAPK pathwayMAPK級聯(lián)信號圖162eI

7、F-4E和p70 S6激酶調(diào)控蛋白質(zhì)翻譯163eif2蛋白質(zhì)翻譯164蛋白質(zhì)翻譯示意圖165線粒體凋亡通路167死亡受體信號通路168凋亡抑制通路170細胞凋亡綜合示意圖171Akt/Pkb信號通路172MAPK/ERK信號通路174哺乳動物MAPK信號通路175Pitx2多步調(diào)節(jié)基因轉(zhuǎn)錄176IGF-1R導(dǎo)致BAD磷酸化的多個凋亡路徑177多重耐藥因子179mTOR信號通路180Msp/Ron受體信號通路181單核細胞和其表面分子182線粒體的肉毒堿轉(zhuǎn)移酶（CPT）系統(tǒng)183METS影響巨噬細胞的分化184Anandamide，內(nèi)源性大麻醇的代謝186黑色素細胞（Melanocyt

8、e）發(fā)育和信號187DNA甲基化導(dǎo)致轉(zhuǎn)錄抑制的機理圖188蛋白質(zhì)的核輸入信號圖190PPARa調(diào)節(jié)過氧化物酶體的增殖192對乙氨基酚（Acetaminophen）的活性和毒性機理194mCalpain在細胞運動中的作用196MAPK信號圖198MAPK抑制SMRT活化200蘋果酸和天門冬酸間的轉(zhuǎn)化201低密度脂蛋白（LDL）在動脈粥樣硬化中的作用202LIS1基因在神經(jīng)細胞的發(fā)育和遷移中的作用圖204Pyk2與Mapk相連的信號通路205galactose代謝通路206Lectin誘導(dǎo)補體的通路207Lck和Fyn在TCR活化中的作用208乳酸合成圖209Keratinocyte分化圖210離

9、子通道在心血管內(nèi)皮細胞中的作用211離子通道和佛波脂（Phorbal Esters）信號213內(nèi)源性Prothrombin激活通路214Ribosome內(nèi)化通路216整合素（Integrin）信號通路217胰島素（Insulin）信號通路218Matrix Metalloproteinases219組氨酸去乙?；种苿┮种艸untington病220Gleevec誘導(dǎo)細胞增殖222Ras和Rho在細胞周期的G1/S轉(zhuǎn)換中的作用224DR3，4，5受體誘導(dǎo)細胞凋亡225AKT調(diào)控Gsk3圖226IL-7信號轉(zhuǎn)導(dǎo)227IL22可溶性受體信號轉(zhuǎn)導(dǎo)圖229IL-2活化T細胞圖230

10、IL12和Stat4依賴的TH1細胞發(fā)育信號通路232IL-10信號通路233IL 6信號通路234IL 5信號通路236actin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

11、 of actin filaments into a network oriented with the growing 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, b

12、oth members of a large multiprotein complex containing several 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,

13、and Arp2/3 in turn to cause changes in cell shape and cell 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

14、Wave-1, another member of the WASP family, also induces 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

15、interaction with Rac1 and Nck. Wave-1 activation by Rac1 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 o

16、f the WASP gene, the Wiskott-Aldrich syndrome for which 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 regula

17、tion of WAVE1-induced actin nucleation by Rac1 and Nck. 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

18、machine. Nat Cell Biol. 2002 Feb;4(2):E31-3. No abstract 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

19、 Arp2/3 complex. Science 294(5547), 1679-84 Weeds A, Yeoh 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-ty

20、pe seven-transmembrane-domain receptors (Frz) to stabilize 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) i

21、s a member of the Flaviviridae, a plus-stranded virus family 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

22、 Europe. WNV has rapidly spread across the United States 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 cap

23、sid protein likely contributes to the WNV-associated deadly 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 embedd

24、ed in a lipid bilayer). The virus binds to a specific cell 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 endocyt

25、osis. Once inside the cell, the genome RNA is released into 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

26、 cleavage, which include three structural components and 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-st

27、randed genomic RNAs. Once viral E, preM and C proteins have 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 (ascorbi

28、c acid) was first identified by virtue of the essential 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 r

29、educes the metal ion prosthetic groups of many enzymes, 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

30、ascorbate transporters for vitamin C import into tissues 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 inte

31、stine, upregulated in cellular models for intestinal epithelium 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 transport

32、ed to tissues to play a variety of roles. Svct2 imports 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 vitami

33、n C in neurons of the developing brain may help protect 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

34、 transport significant quantities of ascorbic acid in vivo.視覺信號轉(zhuǎn)導(dǎo)The signal transduction cascade responsible for sensing light in vertebrates is one of the best studied signal transduction processes, and is initiated by rhodopsin in rod cells, a member of the G-protein coupled receptor gene family.

35、Rhodopsin remains the only GPCR whose structure has been resolved at high resolution. Rhodopsin in the discs of rod cells contains a bound 11-cis retinal chromophore, a small molecule derived from Vitamin A that acts as the light sensitive portion of the receptor molecule, absorbing light to initiat

36、e the signal transduction cascade. When light strikes 11-cis retinal and is absorbed, it isomerizes to all-trans retinal, changing the shape of the molecule and the receptor it is bound to. This change in rhodopsin抯 shape alters its interaction with transducin, the member of the G-protein gene famil

37、y that is specific in its role in visual signal transduction. Activation of transducin causes its alpha subunit to dissociate from the trimer and exchange bound GDP for GTP, activating in turn a membrane-bound cyclic-GMP specific phosphodiesterase that hydrolyzes cGMP. In the resting rod cell, high

38、levels of cGMP associate with a cyclic-GMP gated sodium channel in the plasma membrane, keeping the channels open and the membrane of the resting rod cells depolarized. This is distinct from synaptic generation of action potentials, in which stimulation induces opening of sodium channels and depolar

39、ization. When cGMP gated channels in rod cells open, both sodium and calcium ions enter the cell, hyperpolarizing the membrane and initiating the electrochemical impulse responsible for conveying the signal from the sensory neuron to the CNS. The rod cell in the resting state releases high levels of

40、 the inhibitory neurotransmitter glutamate, while the release of glutamate is repressed by the hyperpolarization in the presence of light to trigger a downstream action potential by ganglion cells that convey signals to the brain. The calcium which enters the cell also activates GCAP, which activate

41、s guanylate cyclase (GC-1 and GC-2) to rapidly produce more cGMP, ending the hyperpolarization and returning the cell to its resting depolarized state. A protein called recoverin helps mediate the inactivation of the signal transduction cascade, returning rhodopsin to its preactivated state, along w

42、ith the rhodopsin kinase Grk1. Phosphorylation of rhodopsin by Grkl causes arrestin to bind, helping to terminate the receptor activation signal. Dissociation and reassociation of retinal, dephosphorylation of rhodopsin and release of arrestin all return rhodopsin to its ready state, prepared once a

43、gain to respond to light.VEGF，低氧Vascular endothelial growth factor (VEGF) plays a key role in physiological blood vessel formation and pathological angiogenesis such as tumor growth and ischemic diseases. Hypoxia is a potent inducer of VEGF in vitro. The increase in secreted biologically active VEGF

44、 protein from cells exposed to hypoxia is partly because of an increased transcription rate, mediated by binding of hypoxia-inducible factor-1 (HIF1) to a hypoxia responsive element in the 5'-flanking region of the VEGF gene. bHLH-PAS transcription factor that interacts with the Ah receptor nucl

45、ear translocator (Arnt), and its predicted amino acid sequence exhibits significant similarity to the hypoxia-inducible factor 1alpha (HIF1a) product. HLF mRNA expression is closely correlated with that of VEGF mRNA. The high expression level of HLF mRNA in the O2 delivery system of developing embry

46、os and adult organs suggests that in a normoxic state, HLF regulates gene expression of VEGF, various glycolytic enzymes, and others driven by the HRE sequence, and may be involved in development of blood vessels and the tubular system of lung. VEGF expression is dramatically induced by hypoxia due

47、in large part to an increase in the stability of its mRNA. HuR binds with high affinity and specificity to the VRS element that regulates VEGF mRNA stability by hypoxia. In addition, an internal ribosome entry site (IRES) ensures efficient translation of VEGF mRNA even under hypoxia. The VHL tumor s

48、uppressor (von Hippel-Lindau) regulates also VEGF expression at a post-transcriptional level. The secreted VEGF is a major angiogenic factor that regulates multiple endothelial cell functions, including mitogenesis. Cellular and circulating levels of VEGF are elevated in hematologic malignancies and

49、 are adversely associated with prognosis. Angiogenesis is a very complex, tightly regulated, multistep process, the targeting of which may well prove useful in the creation of novel therapeutic agents. Current approaches being investigated include the inhibition of angiogenesis stimulants (e.g., VEG

50、F), or their receptors, blockade of endothelial cell activation, inhibition of matrix metalloproteinases, and inhibition of tumor vasculature. Preclinical, phase I, and phase II studies of both monoclonal antibodies to VEGF and blockers of the VEGF receptor tyrosine kinase pathway indicate that thes

51、e agents are safe and offer potential clinical utility in patients with hematologic malignancies.TSP-1誘導(dǎo)細胞凋亡As tissues grow they require angiogenesis to occur if they are to be supplied with blood vessels and survive. Factors that inhibit angiogenesis might act as cancer therapeutics by blocking ves

52、sel formation in tumors and starving cancer cells. Thrombospondin-1 (TSP-1) is a protein that inhibits angiogenesis and slows tumor growth, apparently by inducing apoptosis of microvascular endothelial cells that line blood vessels. TSP-1 appears to produce this response by activating a signaling pa

53、thway that begins with its receptor CD36 at the cell surface of the microvascular endothelial cell. The non-receptor tyrosine kinase fyn is activated by TSP-1 through CD36, activating the apoptosis inducing proteases like caspase-3 and p38 protein kinases. p38 is a mitogen-activated kinase that also

54、 induces apoptosis in some conditions, perhaps through AP-1 activation and the activation of genes that lead to apoptosis.Trka信號轉(zhuǎn)導(dǎo)Nerve growth factor (NGF) is a neurotrophic factor that stimulates neuronal survival and growth through TrkA, a member of the trk family of tyrosine kinase receptors that

55、 also includes TrkB and TrkC. Some NGF responses are also mediated or modified by p75LNTR, a low affinity neurotrophin receptor. Binding of NGF to TrkA stimulates neuronal survival, and also proliferation. Pathways coupled to these responses are linked to TrkA through association of signaling factor

56、s with specific amino acids in the TrkA cytoplasmic domain. Cell survival through inhibition of apoptosis is signaled through activation of PI3-kinase and AKT. Ras-mediated signaling and phospholipase C both activate the MAP kinase pathway to stimulate proliferation.dbpb調(diào)節(jié)mRNAEndothelial cells respo

57、nd to treatment with the protease thrombin with increased secretion of the PDGF B-chain. This activation occurs at the transcriptional level and a thrombin response element was identified in the promoter of the PDGF B-chain gene. A transcription factor called the DNA-binding protein B (dbpB) mediate

58、s the activation of PDGF B-chain transcription in response to thrombin treatment. DbpB is a member of the Y box family of transcription factors and binds to both RNA and DNA. In the absence of thrombin, endothelial cells contain a 50 kD form of dbpB that binds RNA in the cytoplasm and may play a role as a chaperone for mRNA. The 50 kD version of dbpB also binds DNA to regulate genes containing Y box elements in their promoters. Thrombin activation results in the cleavage of dbpB to a 30 kD form. The pr