Siegmund Daniela相关文献与解析，生知库 | 链接生命科学的每一步

Biallelic RIPK1 mutations in humans cause severe immunodeficiency, arthritis, and intestinal inflammation

人类RIPK1双等位基因突变会导致严重的免疫缺陷、关节炎和肠道炎症。

Cuchet-Lourenço, Delphine; Eletto, Davide; Wu, Changxin; Plagnol, Vincent; Papapietro, Olivier; Curtis, James; Ceron-Gutierrez, Lourdes; Bacon, Chris M; Hackett, Scott; Alsaleem, Badr; Maes, Mailis; Gaspar, Miguel; Alisaac, Ali; Goss, Emma; AlIdrissi, Eman; Siegmund, Daniela; Wajant, Harald; Kumararatne, Dinakantha; AlZahrani, Mofareh S; Arkwright, Peter D; Abinun, Mario; Doffinger, Rainer; Nejentsev, Sergey

肠炎

Fibroblast growth factor inducible (Fn14)-specific antibodies concomitantly display signaling pathway-specific agonistic and antagonistic activity

成纤维细胞生长因子诱导型（Fn14）特异性抗体同时表现出信号通路特异性激动剂和拮抗剂活性。

期刊:Journal of Biological Chemistry

影响因子:3.9

doi:10.1074/jbc.M112.435917

Salzmann, Steffen; Seher, Axel; Trebing, Johannes; Weisenberger, Daniela; Rosenthal, Alevtina; Siegmund, Daniela; Wajant, Harald

Signaling active CD95 receptor molecules trigger co-translocation of inactive CD95 molecules into lipid rafts.

激活的 CD95 受体分子会触发非活性 CD95 分子共转位到脂筏中

期刊:Journal of Biological Chemistry

影响因子:3.9

doi:10.1074/jbc.M111.328211

Lang Isabell, Fick Andrea, SchÃ¤fer Viktoria, Giner Tina, Siegmund Daniela, Wajant Harald

Cellular FLICE-inhibitory protein (cFLIP) isoforms block CD95- and TRAIL death receptor-induced gene induction irrespective of processing of caspase-8 or cFLIP in the death-inducing signaling complex

细胞FLICE抑制蛋白（cFLIP）亚型可阻断CD95和TRAIL死亡受体诱导的基因表达，而与死亡诱导信号复合物中caspase-8或cFLIP的加工无关。

期刊:Journal of Biological Chemistry

影响因子:3.9

doi:10.1074/jbc.M110.148585

Kavuri, Shyam M; Geserick, Peter; Berg, Daniela; Dimitrova, Diana Panayotova; Feoktistova, Maria; Siegmund, Daniela; Gollnick, Harald; Neumann, Manfred; Wajant, Harald; Leverkus, Martin

Death receptor-induced signaling pathways are differentially regulated by gamma interferon upstream of caspase 8 processing.

死亡受体诱导的信号通路受到 caspase 8 加工上游的 γ 干扰素的差异性调控

期刊:Molecular and Cellular Biology

影响因子:2.7

doi:10.1128/MCB.25.15.6363-6379.2005

Siegmund Daniela, Wicovsky Andreas, Schmitz Ingo, Schulze-Osthoff Klaus, Kreuz Sebastian, Leverkus Martin, Dittrich-Breiholz Oliver, Kracht Michael, Wajant Harald

信号转导

发表日期：2005

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Downregulation of mutant p53 and severe growth inhibition mediated by antisense-oligonucleotides in pancreatic tumor cells indicate a ‘gain of function’—Type of mutation

胰腺肿瘤细胞中突变型p53的下调以及反义寡核苷酸介导的严重生长抑制表明存在“功能获得性”突变——突变类型

期刊:Molecular Medicine

影响因子:6.4

doi:10.1007/BF02571967

Siegmund, Daniela; Hadwiger, Philipp; Pfizenmaier, Klaus; Vornlocher, Hans-Peter; Wajant, Harald; Fiedler, A; Franke, Y; Büsing, B; Röder, C; Lüttges, J; Bleicher, K; Maier, M; Kalthoff, H

Fn14 and TNFR2 as regulators of cytotoxic TNFR1 signaling

Fn14 和 TNFR2 作为细胞毒性 TNFR1 信号的调节因子

TNF Receptor Associated Factor 2 (TRAF2) Signaling in Cancer

肿瘤坏死因子受体相关因子2 (TRAF2) 信号通路在癌症中的作用

Biallelic RIPK1 mutations in humans cause severe immunodeficiency, arthritis, and intestinal inflammation

人类RIPK1双等位基因突变会导致严重的免疫缺陷、关节炎和肠道炎症。

Fibroblast growth factor inducible (Fn14)-specific antibodies concomitantly display signaling pathway-specific agonistic and antagonistic activity

成纤维细胞生长因子诱导型（Fn14）特异性抗体同时表现出信号通路特异性激动剂和拮抗剂活性。

Signaling active CD95 receptor molecules trigger co-translocation of inactive CD95 molecules into lipid rafts.

激活的 CD95 受体分子会触发非活性 CD95 分子共转位到脂筏中

Cellular FLICE-inhibitory protein (cFLIP) isoforms block CD95- and TRAIL death receptor-induced gene induction irrespective of processing of caspase-8 or cFLIP in the death-inducing signaling complex

细胞FLICE抑制蛋白（cFLIP）亚型可阻断CD95和TRAIL死亡受体诱导的基因表达，而与死亡诱导信号复合物中caspase-8或cFLIP的加工无关。

Death receptor-induced signaling pathways are differentially regulated by gamma interferon upstream of caspase 8 processing.

死亡受体诱导的信号通路受到 caspase 8 加工上游的 γ 干扰素的差异性调控

Downregulation of mutant p53 and severe growth inhibition mediated by antisense-oligonucleotides in pancreatic tumor cells indicate a ‘gain of function’—Type of mutation

胰腺肿瘤细胞中突变型p53的下调以及反义寡核苷酸介导的严重生长抑制表明存在“功能获得性”突变——突变类型