在推理是基于从PANTHER同源性映射。简而言之，将所有涉及的身体性（进入，输出和催化剂）的反应具有映射的原序/级级蛋黄（用于复合物，至少75％的组分必须具有映射）。高水平事件也推断这些事件，以允许更容易的导航。

更多细节及在Reactome事件推理的注意事项。以豹细节也看到： http://www.pantherdb.org/about.jsp ADP-庚糖 ADP-L-β-d-庚糖 ADP-L甘油基d甘露 - 庚糖 Reactome DB_ID: 9645519 cytosol. 基因本体论 去：0005829. ADP-L-glycero-D-manno-heptose (ChEBI: 15915) ADP-L甘油基d甘露 - 庚糖 Chebi. CHEBI：15915 Reactome数据库ID版本77 9645519 数据库标识符。使用此URL连接到Reactome中的此实例的网页://www.joaskin.com/cgi-bin/eventbrowser?DB=gk_current&ID=9645519 反应 r - - 9645519 6. Reactome稳定的标识符。使用此URL连接到Reactome中的此实例的网页://www.joaskin.com/cgi-bin/eventbrowser_st_id?ST_ID=R-ALL-9645519.6 反应 //www.joaskin.com ALPK1 ALPK1 E2R0X4 Reactome DB_ID：10042234 UniProt的：E2R0X4 ALPK1 家犬 NCBI分类 9615 UniProt的 E2R0X4 1 平等的 1244. 平等的 Reactome数据库ID版本77 10042234 数据库标识符。使用此URL连接到该实例的网页中Reactome：//www.joaskin.com/cgi-bin/eventbrowser?DB=gk_current&ID=10042234 反应 R-CFA-9645473 1 Reactome稳定的标识符。使用此URL连接到该实例的网页中Reactome：//www.joaskin.com/cgi-bin/eventbrowser_st_id?ST_ID=R-CFA-9645473.1 ALPK1：ADP庚 Reactome DB_ID: 10042236 1 1 Reactome数据库ID版本77 10042236 数据库标识符。使用此URL连接到该实例的网页中Reactome：//www.joaskin.com/cgi-bin/eventbrowser?DB=gk_current&ID=10042236 反应 r - cfa - 9645521 1 Reactome稳定的标识符。使用此URL连接到该实例的网页中Reactome：//www.joaskin.com/cgi-bin/eventbrowser_st_id?ST_ID=R-CFA-9645521.1 Reactome数据库ID版本77 10042261 数据库标识符。使用此URL连接到该实例的网页中Reactome：//www.joaskin.com/cgi-bin/eventbrowser?DB=gk_current&ID=10042261 反应 R-CFA-9645428 1 Reactome稳定的标识符。使用此URL连接到该实例的网页中Reactome：//www.joaskin.com/cgi-bin/eventbrowser_st_id?ST_ID=R-CFA-9645428.1 在革兰氏阴性菌鉴定植物症（Y.Pseudotublosis）中诱导的21,000个突变体的转座诱变研究表明，携带HLDE突变的细菌转基因诱导核因子Kappa B（NF-κB）途径的活化能力受损人胚胎肾293T细胞系（HEK293T）（周P等人2018）。基因HLDE对于ADP L-甘油-β-D-甘露糖膜（ADP-庚糖）的生物合成至关重要，脂多糖（LPS）生物合成中的细菌代谢中间体，其存在于所有革兰氏阴性和一些革兰中阳性细菌（TANG W ET A。2018）。此外，缺失ADP-庚糖相关的代谢物的生物合成所需的相关基因D-甘油-β-D-甘露庚糖1,7-双磷酸盐（HBP），防止了Y.Pseudotublosis的NF-κB活化（周P等人2018）。此外，合成ADP-庚段但不是HBP，当添加到细胞外空间时，在HEK293T细胞中诱导NF-κB活化和白细胞介素8（IL8或CXCL8）分泌（周P等人。2018）。基于HEK293T NF-κB报告细胞系的基因组 - 宽CRSP-CAS9筛选的荧光激活的细胞分选（FACS），鉴定了α蛋白激酶1（ALPK1），肿瘤坏死因子（TNF-α）受体相关因子（TRAF） - 用叉头关联的域（TIFA）和TRAF6作为由ADP-庚糖或Y.Pseudotuberculosis诱导的NF-KB活化的介质（Zhou P等人2018）。ALPK1 - / - 或TIFA - / - HEK293T细胞显示出废除NF-κB活化和细胞因子表达。通过野生型ALPK1恢复ADP-Heptose治疗的ALPK1-/ - HEK293T细胞中的缺陷NF-κB活化，但不是其激酶 - 活性K1067M突变体（周P等人2018）。此外，ADP-Heptose刺激了TIFA与ALPK1的CIMMUNOPLECIPIPIPIPIPIPIPIPIPIPIPIPIPIPIPIPIPIPIPIPIPIPITIPIPIPITIPITIPIPIPIPIPIPIPIPIPITIPIPITIPITIPIPITIPIPIPIPIPIPIPIPITIPITITIPITITION。此外，在HEK293T细胞中需要ADP-庚糖诱导的TIFA磷酸化所需的ALPK1激酶活性，从而表明ALPK1作用于TIFA的上游（周P等人2018）。 Similarly, ADP‐heptose sensing was ALPK1‐dependent during S. flexneri infection (Garcia-Weber D et al. 2018). These findings are supported by studies showing that cytosolic HBP, found in the bacteria Neisseria meningitidis, Shigella flexneri, Salmonella enterica serovar Typhimurium and Helicobacter pylori (H. pylori), induced activation of ALPK1-TIFA-dependent NF-κB signaling in host cells (Zimmermann S et al. 2017; Milivojevic M et al. 2017; Gaudet RG et al. 2017). In addition, HBP failed to directly activate ALPK1 (Garcia-Weber D et al. 2018; Zhou P et al. 2018); instead, HBP is converted by host-derived adenylyltransferases, such as nicotinamide nucleotide adenylyltransferases, to ADP-heptose 7-P, a substrate which activates ALPK1 and the downstream NF-κB response (Zhou P et al. 2018). ALPK1 contains a kinase domain (KD) and an α-helical domain linked by an unstructured region (Zhou P et al. 2018). Co-expression of the N-terminal domain (NTD) and KD of ALPK1 (ALPK1-NTD (1–473) and ALPK1-KD (959–1244), respectively) in HEK293T cells was sufficient to allow ADP-heptose or Y. pseudotuberculosis to induce activation of NF-κB and phosphorylation of TIFA (Zhou P et al. 2018). High-performance liquid chromatography (HPLC)- mass spectrometry (MS) fractionation of small-molecule extracts from His6–ALPK1-NTD purified from wild-type E. coli coupled with anti-pT9-TIFA immunoblotting and NF-κB luciferase reporter assays in HEK293T identified one active fraction that contained the presumed ADP-heptose ion. Direct binding of E. coli ΔhldE-derived apo-ALPK1-(NTD+KD) complex to ADP-heptose was detected by BioLayer Interferometry (BLI) assay in vitro (Zhou P et al. 2018). The structural studies revealed that a narrow pocket in ALPK1-NTD directly binds ADP-heptose (Zhou P et al. 2018). The ADP-heptose-binding residues are conserved in ALPK1 of other vertebrates. Introducing several mutations in respective residues at the NTD of ALPK1 impaired the ability of ALPK1 to activate NF-κB in response to ADP-heptose (Zhou P et al. 2018). The ADP-heptose binding to ALPK1 is thought to trigger conformational changes and stimulate the kinase domain of ALPK1 to phosphorylate and further activate TIFA, which eventually trigger activation of the downstream NF-κB pathway (Zhou P et al. 2018). Many Gram-negative bacteria induce host cytokine expression in a type III secretion system (T3SS)-dependent manner. T3SS of Y. pseudotuberculosis was required for ADP-heptose induced activation of NF-κB signaling, indicating that a bacterial injection system mediated ADP-heptose translocation to induce activation of ALPK1 upon Y. pseudotuberculosis infection (Zhou P et al. 2018). However, sensing of ADP-heptose by ALPK1 is not just limited to bacteria with T3SS. Burkholderia cenocepacia, enterotoxigenic E. coli, and diffuse-adhering E. coli, also stimulated NF-κB activation through the ALPK1-TIFA axis in an hldE-dependent manner in HEK293T cells (Zhou P et al. 2018). Further, TIFAsome formation and NF-kB activation could be triggered by H. pylori’s component secreted in a type IV secretion system (T4SS)-dependent fashion (Zimmermann S et al. 2017; Stein SC et al. 2017). Animal studies indicate that injection of ADP-heptose induced massive neutrophil recruitment with increased production of several NF-κB-dependent cytokines and chemokines in wild type (WT), but not in Alpk1-/- mice. On infection with B. cenocepacia, which triggers lung inflammation in WT, but not Alpk1-/- mice showed increased expression of NF-κB-dependent cytokines and chemokines in the lungs, which led to higher bacterial load in the lungs of Alpk-/-, but not WT, mice (Zhou P et al. 2018). Thus, in vitro and in vivo studies identified ADP-heptose as a bona fide bacterial immunomodulator which is sensed by cytosolic innate immune receptor ALPK1. 29483275 Pubmed 2018 d景天庚酮糖-7-磷酸为septacidin和潮霉素B的庚糖的共同前体 唐,魏 郭争艳 曹珍菊 王珉 李蓬威 孟，湘西 赵学金 谢，Zhoujie 王钊 周，爱华 娄，李春波 陈艺华 Proc。Natl。阿卡。SCI。U.S.A. 115：2818年至2823年 28877472 Pubmed 2017 ALPK1-和TIFA依赖先天免疫应答由幽门螺杆菌IV型分泌系统触发 齐默尔曼,斯蒂芬妮 Pfannkuch，伦纳特 铝泽尔，一个穆尼尔 Bartfeld，新浪 科赫，曼努埃尔 刘,来自广州 雷希纳，辛迪 Soerensen, Meike 索科洛娃，奥尔加 Zamyatina，阿拉 Kosma，保罗 毛雷尔,安德烈P Glowinski，Frithjof PLEISSNER，克劳斯 - 彼得· 施密德,莫妮卡 布林克曼，沃尔克 Karlas，亚历山大 瑙曼，迈克尔· 罗瑟，马里昂 Machuy,尼古拉斯 迈耶,托马斯·F 细胞报道20：2384至2395年 30111836 Pubmed 2018 阿尔法激酶1是用于细菌ADP-庚糖胞质先天性免疫受体 周，P 她，杨 咚,Na 李，彭 他,Huabin 博里奥，阿莱西奥 吴，轻脆 路，山 丁，晓军 曹颙 徐,岳 高，文清 董，孟秋 丁，京津 王，大成 Zamyatina，阿拉 邵,冯 自然561:122 - 126 28222186 Pubmed 2017 ALPK1控制对革兰阴性菌的庚糖-1,7-二磷酸TIFA / TRAF6依赖性先天免疫 Milivojevic，米莉察 唐夏,创作的 卡斯帕，克里斯托夫·亚历山大 Tschon，泰蕾兹 Emmenlauer，马里奥 皮克，克劳迪 Schnupf,帕梅拉 Guignot，朱莉 Arrieumerlou，塞西尔 公共科学图书馆Pathog。13:e1006224 28715499 Pubmed 2017 幽门螺杆菌通过脂多糖内芯七糖生物合成的中间代谢物cagt4ss依赖易位调节宿主细胞的反应 Stein Saskia C 麦嘉华,尤金尼亚 蝙蝠，西蒙^ h 穆里略，塔蒂亚娜 SPEIDEL，伊冯娜 库姆斯，尼娜 Josenhans，恭 PLOS POAROG。13：e1006514 30455202 Pubmed 2018 ADP-庚糖是新鉴定的病原相关分子模式的痢疾杆菌的 加西亚 - 韦伯，迭戈 唐夏,创作的 Cornil,约翰 泰国，琳达 Rytter的，HELOISE Zamyatina，阿拉 Mulard，劳伦斯一 Arrieumerlou，塞西尔 EMBO众议员19： 26068852 Pubmed 2015 先天免疫。细菌代谢物HBP的胞质检测激活TIFA依赖性先天免疫 德特，瑞安g ^ Sintsova,安娜 Buckwalter，卡罗琳中号 梁莉 科克伦，阿伦 李建军 考克斯，安德鲁·d 莫法特，杰森 格雷 - 欧文，斯科特·d 科学348：1251-5 从电子注释推断 证据法典 ECO：0000203