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| 1 | Posttranslational modification of mdm2显示文摘 | Meek DW Knippschild U | 2003 | Mol Cancer Res2003，1，14： | 1 |
| 2 | Association of adiponectin levels and insulin demand in critically ill patientsDiabetes,Metabolic Syndrome and Obesity显示文摘 | Hillenbrand A Weiss M Knippschild U | | 0，，01： | 1 |
| 3 | Sepsis induced changes of adipokines and cytokines-septic patients compared to morbidly obese patients显示文摘 | Hillenbrand A Knippschild U Wolf AM | | 0，，： | 1 |
| 4 | Sepsis induced changes of adipokines and cytokines-septic patients compared to morbidly obese patients显示文摘 | Hillenbrand A Knippschild U Wolf MA | | 0，，： | 1 |
| 5 | Segmental chromosomal aberrations and centrosome amplifications:pathogenetic mechanisms in Hodgkin and ReedSternberg cells of classical Hodgkin's lymphoma显示文摘 | Knippschild U Harder L | 2003 | Leukemia2003，17，11： | 1 |
| 6 | Sepsis induced changes of adipokines and cytokines - septic patients compared to morbidly obese patients 显示文摘 | Hillenbrand A Knippschild U Weiss M | 2010 | BMC Surgery2010，10，： | 1 |
| 7 | Sepsis in- duced changes of adipokines and cytokines - septic patients compared to morbidly obese patients 显示文摘 | Hillenbrand A Knippschild U Wolf A M | 2010 | BMC Surg2010，1026，： | 1 |
| 8 | The role of the casein kinase 1(CK1)Family in different signaling pathways linked to cancer development显示文摘 | KNIPPSCHILD U WOLFF S GIAMAS G | 2005 | Onkologie2005，28，10： | 1 |
| 9 | The casein kinase family: participation in multiple cellular processes in eukary- otes显示文摘 | Knippschild U Gocht A Wolff S | 2005 | Cell Signal2005，17，6： | 1 |
| 10 | The casein kinase 1 family:participation in multiple cellular processes in eukaryotes显示文摘 | Knippschild U Gocht A Wolff S | 2005 | Cell Signal2005，17，6： | 1 |
| 11 | The role ofthe casein kinase 1(CK1)family in different signalingpathways linked to cancer development显示文摘 | Knippschild U Wolff S Giamas G | 2005 | Onkologie2005，28，10： | 1 |
| 12 | The casein kinase 1 family: participation in multiple cellular processes in eukaryotes显示文摘 | Knippschild U Gocht A Wolff S | 2005 | Cell Signal2005，17，6： | 1 |
| 13 | Sepsis-induced adipokine change with regard to insulin resistance显示文摘 | Hillenbrand A Weiss M Knippschild U | | 0，，： | 1 |
| 14 | The casein kinase 1 family : Participation in multiple cellular processes in eukaryotes 显示文摘 | Knippschild U Gocht A Wolff S | 2005 | Cellular Signal2005，17，6： | 1 |
| 15 | The casein kinase 1 family:participation in multiple cellular processes in eukaryotes显示文摘 | KNIPPSCHILD U GOCHT A WOLFF S | 2005 | Cell Signal2005，17，6： | 1 |
| 16 | The role of the casein kinase 1 (CK1) family in different signaling pathways linked to cancer development显示文摘 | Knippschild U Wolff S Giamas G | 2005 | Onkologie2005，28，10： | 1 |
| 17 | The role of the ca- sein kinase I(CK1) family in different signaling pathways linked to cancer development显示文摘 | Knippschild U Wolff S Giamas G et at | 2005 | Onkologie2005，28，10： | 1 |
| 18 | The role of the casein kinase 1 ( CK1 ) family in different signaling pathways linked to cancer development 显示文摘 | KNIPPSCHILD U WOLFF S GIAMAS G | 2005 | Onkologie2005，28，： | 1 |
| 19 | The casein kinase 1 family: participation in multiple cellular processes in eukaryotes 显示文摘 | KNIPPSCHILD U GOCHT A WOLFF S | 2005 | Cellular Signalling2005，17，： | 1 |
| 20 | Stress-activated kinases as therapeutic targets in pancreatic cancer显示文摘Pancreatic cancer is a dismal disease with high incidence and poor survival rates.With the aim to improve overall survival of pancreatic cancer patients,new therapeutic approaches are urgently needed.Protein kinases are key regulatory players in basically all stages of development,maintaining physiologic functions but also being involved in pathogenic processes.c-Jun N-terminal kinases(JNK)and p38 kinases,representatives of the mitogen-activated protein kinases,as well as the casein kinase 1(CK1)family of protein kinases are important mediators of adequate response to cellular stress following inflammatory and metabolic stressors,DNA damage,and others.In their physiologic roles,they are responsible for the regulation of cell cycle progression,cell proliferation and differentiation,and apoptosis.Dysregulation of the underlying pathways consequently has been identified in various cancer types,including pancreatic cancer.Pharmacological targeting of those pathways has been the field of interest for several years.While success in earlier studies was limited due to lacking specificity and off-target effects,more recent improvements in small molecule inhibitor design against stress-activated protein kinases and their use in combination therapies have shown promising in vitro results.Consequently,targeting of JNK,p38,and CK1 protein kinase family members may actually be of particular interest in the field of precision medicine in patients with highly deregulated kinase pathways related to these kinases.However,further studies are warranted,especially involving in vivo investigation and clinical trials,in order to advance inhibition of stress-activated kinases to the field of translational medicine. | Benno Traub Aileen Roth Marko Kornmann Uwe Knippschild Joachim Bischof | 2021 | World Journal of Gastroenterology2021，27，30： | 0 |
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