信号通路图片大全

信号通路图片大全 aktPathway Ras Signaling Pathway 还有一些，如果大家觉得好的话再贴^^ EGF Signaling Pathway 第五张 (缩略图，点击图片链接看原图) 强烈推荐 Cytokine Network(绝没重复) Notch proteins are synthesized as precursor proteins that are processed by a furin-like convertase in the Golgi before being transported to the cell surface, where they reside as heterodimers. Interaction of Notch receptors with their ligands, such as Delta-like or Jagged, leads to a cascade of proteolytic cleavages. The first cleavage is mediated by TACE (tumour-necrosis factor-α-convering enzyme/metalloproteinase), followed by a second cleavage mediated by the γ-secretase activity of presenilins (PS), which liberates the cytoplasmic domain —Notch intracellular domain (NIC) — of the Notch receptors. The liberat ed NIC enters the nucleus and binds to the transcription factor CSL, which displaces co-repressors (CoR) and recruits co-activators (CoA), leading to transcriptional activation of downstream target genes. This pathway is known as the CSL-dependent pathway. Genetic evidence points to the existence of a CSL-independent pathway that is poorly characterized at present. 第二张 (缩略图，点击图片链接看原图) Integrin Signaling Pathway Integrins are cell surface receptors that interact with the extracellular matrix and mediate intracellular signals in response to the extracellular matrix including cellular shape, mobility, and progression through the cell cycle. Integrins do not themselves possess a kinase domain or enzymatic activity but rely on association with other signaling molecules t o transmit signals. Interactions between the extracellular matrix and the actin cytoskeleton commonly take place at focal adhesions on the cell surface that contain localized concentrations of integrins, signaling molecules, and cytoskeletal elements. Talin forms a direct interaction with the integrin cytoplasmic domain, and interacts with cytoskeletal elements (actin) and signaling factors. Paxillin and CAS also localize in focal adhesions and may serve as a scaffold for other integrin signaling components like FAK and src. Interaction of FAK, CAS and src may be required for integrin regulation of cell cycle progression. The CrkL adaptor protein may regulate downstream integrin signaling. Growth factor signaling pathways and the caveolin receptor exhibit important cross talk with integrin receptors in cellular responses like activation of map kinase, proliferation and motility.[img][/img] NF-kB Signaling Pathway NFkappaB Signaling :)新来的，献上我课 题 快递公司问题件快递公司问题件货款处理关于圆的周长面积重点题型关于解方程组的题及答案关于南海问题 相关的信号通道 Signalling pathway of hepatocyte growth factor action. Diagram of the proposed intracellular signaling pathway involved in hepatocyte growth factor (HGF)-mediated tubulogenesis. Although HGF is perhaps the best-characterized of the growth factors involved in epithelial cell-branching tubulogenesis, very little of its mechanism of action is understood. However, recent evidence has shown that the HGF receptor (c-Met) is associated with G ab-1, a docking protein believed to be involved in signal transduction [ref]. Thus, on binding to c-Met, HGF activates Gab-1-mediated signal transduction, which, by an unknown mechanism, affects changes in cell shape and cell movement or cell-cell-cell-matrix interactions. Ultimately, these alterations lead to epithelial cell-branching tubulogenesis. Growth hormone plays a major role in regulating growth during childhood and adolescence and also regulates metabolism. Defects in growth hormone signaling can result in dwarfism and decreases in growth hormone levels with age have been suggested to play a role in the reduced function of some physiological systems. Growth hormone signals a response in cells through the growth hormone receptor, a member of the cytokine receptor gene family. Growth hormone causes the receptor to dimerize, activating the JAK2 protein kinase. The activity of JAK2 mediates many of the downstream responses to growth hormone through phosphorylation of STAT transcription factors, MAP kinases, other kinase cascades and molecules involved in metabolism like IRS-1. Factors like SOCS and SHP-1 appear to play a role in the down regulation of signaling by growth hormone and cytokines. 叶酸代谢及相关信号途径 This simplified figure illustrates the interconnectedness of folate metabolism and proteins for which functional polymorphisms have been identified. Polymorphisms have been found that are associated with pharmacogenetic outcomes in three key proteins in these pathways: the drug transporter protein reduced folate carrier (RFC); the regulatory enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR); and the drug target thymidylate synthase. Key enzymes are denoted as ovals, substrates as rectangles. Red ovals denote enzymes with genetic polymorphisms that have been investigated in pharmacogenetic studies. Orange ovals denote enzymes for which functional genetic polymorphisms have been described. 5-FU, 5-fluorouracil; AICAR, 5-aminoimidazole-4-carboxamine ribonucleotide; AICARFT, AICAR formyltransferase; CBS, cystathionine-β-synthase; DHF, dihydrofolate; D HFR, DHF reductase; dTMP, deoxythymidine monophosphate; dUMP, deoxyuridine monophosphate; GAR, glycinamide ribonucleotide; GART, phosphoribosylglycinamide formyltransferase; hFR, human folate receptor; MTX, methotrexate; SAH, S-adenosylhomocysteine; SAM, S-adenosylmethionine; SHMT, serine hydroxymethyltransferase; THF, tetrahydrofolate; X, various substrates for methylation. (缩略图，点击图片链接看原图)发一张神经酰胺的信号图 Ceramide Signaling Pathway 不错的图片，希望对大家有用 VEGF, Hypoxia, and Angiogenesis 我也来凑凑热闹吧～ R链接素((3-catenin)是一种多功能胞浆蛋白，既是Wnt信号传导通路的关键调整控点，又是上 皮钙粘附素复合体的重要组分，与肿瘤的发生、浸润和转移密切相关. Science. 2004 Mar 5;303(5663):1483-7. Convergence of Wnt, -Catenin, and Cadherin Pa thways (缩略图，点击图片链接看原图) In the presence of Wnt, the activated Fz transduces the signal to a cytoplasmic protein, known as dishevelled protein (Dvl), which inhibits the serine/threonine kinase glycogen synthase-3b (GSK-3b). The Wnt signal leads to functional inactivation and dissociation of a multi-protein b-catenin destruction complex, which is made up of the tumour suppressor protein adenomatous polyposis coli (APC), GSK-3b and a scaffold of Axin. This results in dephosphorylation and dissociation of b-tenin. Unphosphorylated b-catenin is stabilised and accumulates in the cytoplasm of cells. The b-catenin then associates with the T-cell factor (TCF)/lymphoid enhancer factor (LEF) family of transcription factors in the nucleus leading to the eventual transcription and expression of target genes such as c-myc, c-jun, Fra and cyclin D1 (Fig. 1). In the absence of the Wnt signal, GSK-3b phosphorylates b-catenin. Phosphorylated b-catenin is recognised by the mammalian homologue of Slimb, b-TrCP, which is a component of an E3 ubiquitin ligase. b-TrCP associates with the b-catenin and activates the ubiquination machinery resulting in its degradation in proteasomes. Acute Myocardial Infarction (缩略图，点击图片链接看原图) Angiotensin-converting enzyme 2 regulates heart function Ca++/ Calmodulin-dependent Protein Kinase Activation 氧化应激激活的细胞内信号转导通路和转录因子 补充几张。 (缩略图，点击图片链接看原图) g1 sphase g1 sphase and more! Models of signal transduction through four plant receptor kinases (PRKs). CLV3–CLV1 signalling. The inactive CLAVATA complex is composed of disulfide-bound CLAVATA 1 (CLV1) and CLAVATA 2 (CLV2) proteins. Binding of the ligand CLAVATA 3 (CLV3), perhaps in association with an unknown X factor, induces receptor oligomerization and transphosphorylation followed by phosphorylation of kinase-associated protein phosphatase (KAPP). Rho-GTPase-related protein (Rop), (which might interact directly or via an unknown intermediate with the CLV1–CLV2 complex), might be respon sible for signal transduction downstream of CLV1. Repression of WUSCHEL (WUS) expression enables progression of meristem stem cells toward differentiation. Genetic evidence indicates that dephosphorylation by KAPP downregulates the activated receptor complex. The POLTERGEIST (POL) protein functions as a negative regulator of CLV1 signalling. BR–BRI1–BAK1 signalling. Binding of brassinosteroids (BR), perhaps in association with a sterol binding protein, activates heterodimers of brassinosteroid-insensitive 1 receptor (BRI1) and BRI1-associated receptor kinase 1 (BAK1), leading to mutual transphosphorylation. Signal transduction from the activated receptor c omplex leads to inactivation of the BR-insensitive 2 (BIN2) kinase probably via one or more unknown intermediates. The reduced BIN2 activity in turn leads to an increase in unphosphorylated BRI-EMS-suppressor 2 (BES2) and brassinazole-resistant 1 (BZR1), which move into the nucleus and trigger at least some of the cell responses to flg22–FLS2 signalling. Binding of flagellin 22 (flg22) to flagellin sensing 2 BR. (FLS2) triggers kinase activation. It is not known whether this involves FLS2 oligomerization. FLS2 activation, in turn, triggers a mitogen-activated protein (MAP) kinase cascade, putatively through signal-transduction intermediates. KAPP also interacts with FLS2, probably to downregulate its activity. SCR–SRK signalling. In the basal (unpollinated) state, S-locus receptor kinase (SRK) is present as a monomer and as a homodimer and is maintained in an inactive state by interacting with thioredoxin-hlike (THL). After self-pollination, the ligand, S-locus cysteine-rich (SCR), binds as a dimer either to an SRK homodimer or to a hetetodimer of SRK with extracellular SRK (eSRK) or S-locus glycoprotein (SLG). SCR binding is thought to induce receptor oligomerization and transphosphorylation, followed by phosphorylation of armadillorepeat- containing 1 (ARC1) and KAPP. ARC1 is a positive effector of the self-incompatibility response. KAPP probably dephosphorylates SRK and consequently downregulates the activated SRK complex. Red stars indicate protein phosphorylation. Attenuation of GPCR Signal 前面那TNF受体介导细胞凋亡的信号转导图、文字很多很不错，可惜是 ppt 关于艾滋病ppt课件精益管理ppt下载地图下载ppt可编辑假如ppt教学课件下载triz基础知识ppt 格式，好象不支持 这种格式，抱歉，需要者我发到你们邮箱 PKC-catalyzed phosphorylation of inhibitory phosphoprotein of myosin phosphatase src蛋白质激活图 Cell Cycle Control: G2/M DNA Damage Checkpoint Erk1/Erk2 Mapk Signaling pathway Akt/PKB Signaling PATHWAY DESCRIPTION: Since its discovery as a proto-oncogene nearly ten years ago, the serine/threonine kinase Akt, also known as protein kinase B (PK, has become a major focus of attention b ecause of its critical regulatory role in diverse cellular processes, including cancer progression. The Akt cascade is activated by receptor tyrosine kinases, integrins, B- and T-cell receptors, cytokine receptors, G-protein coupled receptors, and other stimuli that induce the accumulation of phosphatidylinositol 3,4,5 triphosphates, (PtdIns(3,4,5)P3), by the phosphoinositide 3-kinase (PI3K). The three Akt isoforms (Akt1, Akt2 and Akt3) thus mediate many of the downstream events regulated by PI3K. For instance, Akt is a major regulator of insulin signaling and glucose metabolism. Akt controls cell growth through its effects on the mTOR and p70 S6 kinase pathways, as well as the cell cycle and cell proliferation through its direct action on the CDK inhibitors, p21 and p27, and indirectly by affecting the levels of cyclin D1 and p53. Akt is also major mediator of cell survival by directly inhibiting different pro-apoptotic signals such as Bad and the Forkhead family of transcription factors, or indirectly by modulating two central regulators of cell death such as p53 and NF-?eB. Akt signaling in endothelial cells plays also critical roles in the regulation of vascular homeostasis and angiogenesis. These findings have turned Akt/PKB into important therapeutic target for the treatment of cancer, diabetes and stroke. TNFR2 Signaling Pathway TNFR1 Signaling Pathway :)新来的，献上我课题相关的信号通道 again (缩略图，点击图片链接看原图)anti-apoptotic brakes downstream of mitochondria mito_ctrl (缩略图，点击图片链接看原图) 我收集了一些有关信号转导的图片，先发几张，如果同志们觉得不错，我做成压缩文件送给大家。 在发几张把 Insulin like growth factor 1 (IGF-1) and its receptor (IGF-1R) provide a potent proliferative signaling system that stimulates growth in many different cell types and blocks apoptosis. In vivo IGF-1 acts as an intermediate of many growth hormone responses, and may stimulate the growth of some types of cancer. IGF-1 also provides a mitogenic signal to act as a growth factor for many tissue culture cells. One component of IGF-1 mitogenic signaling is association of the receptor tyrosine kinase with Shc, Grb2, and Sos-1 to activate ras and the Map kinase cascade (raf, Mek, Erk). An endpoint of the Map kinase pathway is modification of transcription factor activity, such as activation of ELK transcription factors. Serum response factor (SRF) and AP-1 contribute to mitogenic signaling by many factors. Phosphorylation of IRS-1 and PI3 kinase activation are also involved in IGF-1 signaling, similar to insulin signaling. The full network is complex and can be divided into five levels: 1) activation of the insulin receptor tyrosine kinase and closely linked events; 2) phosphorylation of a family of substrate proteins; 3) interaction of the receptor and its substrates with several intermediate signaling molecules via SH2 (src homology 2) and other recognition domains; 4) activation of serine and lipid kinases, resulting in a broad range of phosphorylation-dephosphorylation events; and 5) regulation of the final biological effectors of insulin action, such as glucose transport, lipid synthesis, gene expression, and mitogenesis. The SH2 proteins link the insulin receptor substrate (IRS) proteins to a series of cascading reactions involving serine/threonine kinases and phosphatases such as the mitogen-activated protein (MAP) kinases, S6 kinases, and protein phosphatase-1A. These serine kinases act on enzymes such as glycogen synthase, transcription factors, and other proteins to produce many of the final biological effects of the hormone. In adipose tissue and muscle, insulin stimulation also increases glucose uptake by promoting translocation of an intracellular pool of glucose transporters to the plasma membrane. Exactly how this action is linked to the phosphorylation cascade is unknown, but several studies suggest that this important action of insulin, as well as most metabolic effects, is downstream of the enzyme phosphatidylinositol 3-kinase (PI 3-kinase). Other effects of insulin, such as stimulation of glycogen and lipid synthesis, occur through additional intracellular effects to stimulate the enzymes involved in these reactions. ATP—adenosine triphosphate; GAP—GTPase-activ ating protein; GRB2—growth-factor receptor binding protein 2; GTP—guanosine triphosph ate; IGF—insulin-like growth factor; MEK—MAP-Erk kinase; SOS—son-of-seven less protei n. The appropriate signaling through the insulin pathway is critical for the regulation of glucose levels and the avoidance of diabetes. Insulin forms a complex with the Insulin Receptor (IR) and b chains to form the active signaling complex. Through recruitment of adaptor molecules and the activation of RAS, the activated IR can cause transcriptional activation. 3.胰岛素信号通路的多样性 Pleiotropic insulin signaling pathways. CAP—c-Cbl-associated protein; IRS-1—insulin receptor substrate-1; MAPK—mitogenactivated protein kinase; PC-1—plasma cell glycoprotein-1; PDK—phosphoinositide-dependent kinase; PKC—protein kinase C; PI3-K—phosphatidylinositol 3-kinase. 第四张 (缩略图，点击图片链接看原图) 日月雨请注意，MAPK的信号转导图 MAPKinase Signaling Pathway (缩略图，点击图片链接看原图) Figure 1 | The mitogen-activated protein kinase signalling pathway. Following ligand binding, growth-factor receptor tyrosine kinases such as the platelet-derived growth factor receptor (PDGFR), the vascular endothelial growth factor receptor (VEGFR), the receptor ERBB, and the fibroblast growth factor receptor (FGFR) become activated. This induces the binding of adaptor proteins such as growth-factor-receptor-bound protein 2 (GRB2) that bind to specific phosphorylated residues on the cytoplasmic tails of activated receptors. In cooperation with GRB2, the guanine-nucleotide exchange factor SOS activates RAS, by catalysing the replacement of GDP with GTP. In its GTP-bound form, RAS activates the kinase activity of RAF and its downstream signalling cascade. RAF phosphorylates the mitogen-activated protein kinase (MAPK) kinase (MEK), which phosphorylates and activates MAPK/extracellular signal-regulated kinase (ERK). There exist several negative regulators of this pathway. These regulatory molecules include RAF kinase inhibitor protein (RKIP), which interferes with MEK phosphorylation81; RAS and RAB interactor 1 (RIN1), which competes with RAF for binding to activated RAS82; IMP (impedes mitogenic signal propagation), which interacts with kinase suppressor of RAS (KSR) to prevent recruitment of MEK to activated RAF83; and the MKP (MKP1,3) family of MAPK phosphatases, which reduce the activation state of the RAF–MEK–ERK module84,85. Other negative regula tors include both AKT and serum/glucocorticoid inducible kinase (SGK), which can phosphorylate BRAF86,87. Positive regulators of RAF activity, such as protein kinase C (PKC), SRC, p21-activated kinase (PAK) and 14-3-3, activate RAF in a RAS-independent manner. This pathway can also become activated by adhesion of integrins to specific extracellular-matrix molecules. These interactions activate focal adhesion kinase (FAK) and phosphatidylinositol 3-kinase (PI3K). PI3K is also activated by RAS. Stimulation of this pathway leads to activation of the GTPbinding protein RAC, which interacts with the NCK–PAK com plex, thereby leading to PAK,and subsequently RAF, activation. 日月雨请注意，G-Protein Coupled Receptors Signaling to MAPK/ERK 俺也做点贡献 第三张 (缩略图，点击图片链接看原图) jak_stat singaling (缩略图，点击图片链接看原图) TLR信号通路补充。 BCR Signaling Pathway B Cell Survival Pathway Proximal BCR signaling. (A) The resting BCR is outside lipid rafts. BLNK, Fyn, and Syk associate with the resting BCR, and Lyn and Cbp are in the rafts. ( After the BCR binds antigen, it translocates into lipid rafts. Both Src kinases and Syk phosphorylate the C-termainal ITAM tyrosine, recruiting Syk. Syk phosphorylates itself, ITAM tyrosines, and possibly phosphorylates Y204. Lyn phosphorylates raft-localized CD19. PI3K is activated, recruiting Btk to lipid rafts. (C) Syk phosphorylates BLNK and BCAP, creating binding sites for PLCγ2/Vav/Btk and PI3K, respectively. PI3K produces phosphatidylinositol compounds and assists in the recruitment of PLCγ2/Vav/Btk. The SH2 domains of PI3K also bind to CD19, fully activating PI3K. Lyn phosphorylates and activates Btk. (D) PLCγ2, Btk, and Vav all bind to BLNK via their SH2 domains. Syk and Btk phosphorylate PLCγ2, triggering calcium flux and Ras-mediated ERK activation. Syk and Src kinases phosphorylate Vav, leading to JNK activation. Lyn, meanwhile, phosphorylates Cbp and CD22, creating binding sites for the negative regulators Csk and SHP-1, respectively. (E) Csk, after being recruited to Cbp, phosphorylates Src kinases on the negative regulatory tyrosine. SHP-1 is recruited to the phosphorylated ITIM tyrosines on CD22, as well as to BLNK itself, and dephosphorylates Syk, BLNK, PLCγ2, Src kinases, and possibly Igα and Igβ. SHIP and PTEN inactivate PI3K by dephosphorylating PI3K products. T lymphocyte activation pathways