&& 查看话题
求大神翻译两段话
1、Ubiquitin-editing enzyme that contains both ubiquitin ligase and deubiquitinase activities. Involved in immune and inflammatory responses signaled by cytokines, such as TNF-alpha and IL-1 beta, or pathogens via Toll-like receptors (TLRs) through terminating NF-kappa-B activity. Essential component of a ubiquitin-editing protein complex, comprising also RNF11, ITCH and TAX1BP1, that ensures the transient nature of inflammatory signaling pathways. In cooperation with TAX1BP1 promotes disassembly of E2-E3 ubiquitin protein ligase complexes in IL-1R and TNFR-1 affected are at least E3 ligases TRAF6, TRAF2 and BIRC2, and E2 ubiquitin-conjugating enzymes UBE2N and UBE2D3. In cooperation with TAX1BP1 promotes ubiquitination of UBE2N and proteasomal degradation of UBE2N and UBE2D3. Upon TNF stimulation, deubiquitinates 'Lys-63'-polyubiquitin chains on RIPK1 and catalyzes the formation of 'Lys-48'-polyubiquitin chains. This leads to RIPK1 proteasomal degradation and consequently termination of the TNF- or LPS-mediated activation of NF-kappa-B. Deubiquitinates TRAF6 probably acting on 'Lys-63'-linked polyubiquitin. Upon T-cell receptor (TCR)-mediated T-cell activation, deubiquitinates 'Lys-63'-polyubiquitin chains on MALT1 thereby mediating disassociation of the CBM (CARD11:BCL10:MALT1) and IKK complexes and preventing sustained IKK activation. Deubiquitinates NEMO/IKBKG; the function is facilitated by TNIP1 and leads to inhibition of NF-kappa-B activation. Upon stimulation by bacterial peptidoglycans, probably deubiquitinates RIPK2. Can also inhibit I-kappa-B-kinase (IKK) through a non-catalytic mechanism which in polyubiquitin promotes association with IKBKG and prevents IKK MAP3K7-mediated phosphorylation. Targets TRAF2 for lysosomal degradation. In vitro able to deubiquitinate 'Lys-11'-, 'Lys-48'- and 'Lys-63' polyubiquitin chains. Inhibitor of programmed cell death. Has a role in the function of the lymphoid system. Required for LPS-induced production of proinflammatory cytokines and IFN beta in LPS-tolerized macrophages.
2、Non-receptor tyrosine-protein kinase that transmits signals from cell surface receptors and plays an important role in the regulation of innate and adaptive immune responses, hematopoiesis, responses to growth factors and cytokines, integrin signaling, but also responses to DNA damage and genotoxic agents. Functions primarily as negative regulator, but can also function as activator, depending on the context. Required for the initiation of the B-cell response, but also for its down-regulation and termination. Plays an important role in the regulation of B-cell differentiation, proliferation, survival and apoptosis, and is important for immune self-tolerance. Acts downstream of several immune receptors, including the B-cell receptor, CD79A, CD79B, CD5, CD19, CD22, FCER1, FCGR2, FCGR1A, TLR2 and TLR4. Plays a role in the inflammatory response to bacterial lipopolysaccharide. Mediates the responses to cytokines and growth factors in hematopoietic progenitors, platelets, erythrocytes, and in mature myeloid cells, such as dendritic cells, neutrophils and eosinophils. Acts downstream of EPOR, KIT, MPL, the chemokine receptor CXCR4, as well as the receptors for IL3, IL5 and CSF2. Plays an important role in integrin signaling. Regulates cell proliferation, survival, differentiation, migration, adhesion, degranulation, and cytokine release. Down-regulates signaling pathways by phosphorylation of immunoreceptor tyrosine-based inhibitory motifs (ITIM), that then serve as binding sites for phosphatases, such as PTPN6/SHP-1, PTPN11/SHP-2 and INPP5D/SHIP-1, that modulate signaling by dephosphorylation of kinases and their substrates. Phosphorylates LIME1 in response to CD22 activation. Phosphorylates BTK, CBL, CD5, CD19, CD72, CD79A, CD79B, CSF2RB, DOK1, HCLS1, LILRB3/PIR-B, MS4A2/FCER1B, PTK2B/PYK2, SYK and TEC. Promotes phosphorylation of SIRPA, PTPN6/SHP-1, PTPN11/SHP-2 and INPP5D/SHIP-1. Required for rapid phosphorylation of FER in response to FCER1 activation. Mediates KIT phosphorylation. Acts as an effector of EPOR (erythropoietin receptor) in controlling KIT expression and may play a role in erythroid differentiation during the switch between proliferation and maturation. Depending on the context, activates or inhibits several signaling cascades. Regulates phosphatidylinositol 3-kinase activity and AKT1 activation. Regulates activation of the MAP kinase signaling cascade, including activation of MAP2K1/MEK1, MAPK1/ERK2, MAPK3/ERK1, MAPK8/JNK1 and MAPK9/JNK2. Mediates activation of STAT5A and/or STAT5B. Phosphorylates LPXN on 'Tyr-72'.
1、泛素编辑酶既包含泛素连接酶活性又包含去泛素酶活性。泛素编辑酶参与由肿瘤坏死因子α（TNFα）和白细胞介素-1β（IL-1β）等细胞因子，或病原体通过Toll样受体（TLRs）等引起的免疫和炎性反应，这些作用是通过终止NK-kB的活性而完成的。泛素编辑酶蛋白复合体的基本组成还包括RNF11， ITCH和TAX1BP1，后者保证了炎性反应的瞬时特性。在IL-1R和TNFR-1信号通路中，通过与TAX1BP1的协作而促进E2-E3泛素蛋白连接酶复合物的解体；受其影响的至少包括E3连接酶TRAF6， TRAF2和BIRC2,以及E2泛素连接酶UBE2N和UBE2D3。通过与TAX1BP1的协作而促使UBE2N的泛素化以及UBE2N和UBE2D3的蛋白酶降解过程。在TNF刺激下，RIPK1中的Lys-63(即K63)-多聚体泛素链发生去泛素化，进而催化Lys-48（即K48）多聚体泛素链的形成。由此引起RIPK1的蛋白酶降解过程，进而终止由TNF-或内毒素（LPS)-介导的NK-kB的激活过程。TRAF6的去泛素化可能发生在K63链接的泛素化。当T细胞经TCR激活后，MALT1 K63型多聚泛素链的去泛素化介导了CBM（CARD11:BCL10:MALT1）以及IKK复合体的解离，从而防止了IKK的持续激活。NEMO/IKBKG的去泛素化由TNIP1促成并引起对NF-B激活的抑制作用。在细菌肽聚糖刺激条件下，RIPK2可能被去泛素化。同样可以通过一种非催化机制以致IKK的作用，该机制包括多聚体泛素化，该泛素化促进其与IKBKG的相互作用，进而防止IKK MAP3K7介导的磷酸化。引起TRAF2的溶酶体降解过程。体外条件下可以引起K11型、K48型和K63型多聚体泛素链的去泛素化。程序死亡的抑制剂。在淋巴系统中具有某种功能。在内毒素耐受巨噬细胞中，是内毒素介导产生前炎性反应细胞因子和干扰素α（IFNα）所必需的。
2、非受体酪氨酸激酶，通过细胞表面受体传递信号，在天然免疫和获得性免疫反应、血细胞生产、对细胞因子、整合素信号等反应，以及在对DNA损伤和基因毒性物质的反应中发挥重要作用。基本功能是一种负性调节因子，但根据周围情况也可以是一种激活因子。对B细胞应答所必需，同时对其向下调节和终止也是需要的。在B细胞分化、增生、存活及凋亡的调节中发挥重要作用，同时对免疫自耐受也非常重要。在数个免疫受体的下游发挥作用，这些受体包括B细胞受体，CD79A, CD79B, CD5, CD19, CD22, FCER1, FCGR2, FCGR1A, TLR2和TLR4。在有细菌脂质体引起的炎性反应中发挥某种作用。介导造血干细胞、血小板、红细胞，以及树突状细胞、中性粒细胞和嗜酸性粒细胞等成熟髓细胞对细胞因子和生长因子的反应。在EPOR， KIT， MPL，化学因子受体CXCR4，以及IL3，IL5和CSF2受体下游发挥作用。调节细胞增生、存活、分化、迁移、粘附、脱颗粒以及细胞因子的释放。通过调节免疫受体基于酪氨酸异质性构型（ITIM）的磷酸化而向下调节信号通路，ITIM被磷酸化后可以作为PTPN6/SHP-1, PTPN11/SHP-2和INPP5D/SHIP-1等磷酸酶的结合位点，进而通过影响蛋白激酶及其底物的脱磷酸化而调制信号通路。CD22激活可以引起LIME1的磷酸化。另外还可以磷酸化BTK, CBL, CD5, CD19, CD72, CD79A, CD79B, CSF2RB, DOK1, HCLS1, LILRB3/PIR-B, MS4A2/FCER1B, PTK2B/PYK2, SYK和TEC。促进SIRPA, PTPN6/SHP-1, PTPN11/SHP-2和INPP5D/SHIP-1的磷酸化。在FCER1激活时对FER的快速磷酸化是必需的。介导KIT的磷酸化。作为促红细胞生成素受体（EPOR）的效应物可以控制KIT的表达，并在红细胞有增生转为成熟的分化过程中发挥某种作用。根据具体情况，可以激活或抑制数个信号通路瀑布。解决磷酸甘油肌醇3激酶活性和AKT1的激活。调节MAP激酶信号通路瀑布的激活，包括激活MAP2K1/MEK1, MAPK1/ERK2, MAPK3/ERK1, MAPK8/JNK1 and MAPK9/JNK2等。介导STAT5A和/或STAT5B的激活。在72位酪氨酸位点上磷酸化LPXN。 楼主竟然跟我头像一样:sweat: : Originally posted by 燕大侠 at
楼主竟然跟我头像一样:sweat: 从哪里弄的图:jok:画图问题 求大神帮忙改改 对画图了解甚微啊
[问题点数：100分，结帖人huang]
画图问题 求大神帮忙改改 对画图了解甚微啊
[问题点数：100分，结帖人huang]
不显示删除回复
显示所有回复
显示星级回复
显示得分回复
只显示楼主
相关推荐：
2014年 总版技术专家分年内排行榜第三
2012年 总版技术专家分年内排行榜第四
匿名用户不能发表回复！|
每天回帖即可获得10分可用分！小技巧：
你还可以输入10000个字符
(Ctrl+Enter)
请遵守CSDN，不得违反国家法律法规。
转载文章请注明出自“CSDN（www.csdn.net）”。如是商业用途请联系原作者。}