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3. Proximal colon–derived O-glycosylated mucus encapsulates and modulates the microbiota

4. Intestinal Enteroendocrine Lineage Cells Possess Homeostatic and Injury-Inducible Stem Cell Activity

5. From Inflammation to Oncogenesis: Tracing Serum DCLK1 and miRNA Signatures in Chronic Liver Diseases.

9. ZIP4 Promotes Muscle Wasting and Cachexia in Mice With Orthotopic Pancreatic Tumors by Stimulating RAB27B-Regulated Release of Extracellular Vesicles From Cancer Cells

16. Supplementary Figure 1 from DCLK1-Isoform2 Alternative Splice Variant Promotes Pancreatic Tumor Immunosuppressive M2-Macrophage Polarization

18. Supplementary Figure 5 from DCLK1-Isoform2 Alternative Splice Variant Promotes Pancreatic Tumor Immunosuppressive M2-Macrophage Polarization

20. Supplementary Figure 3 from DCLK1-Isoform2 Alternative Splice Variant Promotes Pancreatic Tumor Immunosuppressive M2-Macrophage Polarization

21. Supplementary Figure 4 from DCLK1-Isoform2 Alternative Splice Variant Promotes Pancreatic Tumor Immunosuppressive M2-Macrophage Polarization

22. Supplementrary Figure 2 from DCLK1-Isoform2 Alternative Splice Variant Promotes Pancreatic Tumor Immunosuppressive M2-Macrophage Polarization

23. Data from Survival of Patients with Gastrointestinal Cancers Can Be Predicted by a Surrogate microRNA Signature for Cancer Stem–like Cells Marked by DCLK1 Kinase

24. Supplementary table 1 from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism

25. Supplemental Figures and Table from Survival of Patients with Gastrointestinal Cancers Can Be Predicted by a Surrogate microRNA Signature for Cancer Stem–like Cells Marked by DCLK1 Kinase

26. Supplementary figures from ZIP4 Promotes Pancreatic Cancer Progression by Repressing ZO-1 and Claudin-1 through a ZEB1-Dependent Transcriptional Mechanism

27. Supplemental Figure Legends from Survival of Patients with Gastrointestinal Cancers Can Be Predicted by a Surrogate microRNA Signature for Cancer Stem–like Cells Marked by DCLK1 Kinase

28. Data from DCAMKL-1 Regulates Epithelial–Mesenchymal Transition in Human Pancreatic Cells through a miR-200a–Dependent Mechanism

30. Supplementary Figure 3 from Activation of Apoptosis by 1-Hydroxy-5,7-Dimethoxy-2-Naphthalene-Carboxaldehyde, a Novel Compound from Aegle marmelos

31. Supplementary Figure 4 from Activation of Apoptosis by 1-Hydroxy-5,7-Dimethoxy-2-Naphthalene-Carboxaldehyde, a Novel Compound from Aegle marmelos

33. Supplementary Figure 2 from Activation of Apoptosis by 1-Hydroxy-5,7-Dimethoxy-2-Naphthalene-Carboxaldehyde, a Novel Compound from Aegle marmelos

34. Supplementary Legends 1-4 and Materials from Activation of Apoptosis by 1-Hydroxy-5,7-Dimethoxy-2-Naphthalene-Carboxaldehyde, a Novel Compound from Aegle marmelos

36. Supplementary Figure 1 from Activation of Apoptosis by 1-Hydroxy-5,7-Dimethoxy-2-Naphthalene-Carboxaldehyde, a Novel Compound from Aegle marmelos

37. Supplementary Materials and Methods from DCAMKL-1 Regulates Epithelial–Mesenchymal Transition in Human Pancreatic Cells through a miR-200a–Dependent Mechanism

38. Supplementary Figure Legends 1-4, Table Legend from DCAMKL-1 Regulates Epithelial–Mesenchymal Transition in Human Pancreatic Cells through a miR-200a–Dependent Mechanism

39. Supplementary Figures 1-4 from DCAMKL-1 Regulates Epithelial–Mesenchymal Transition in Human Pancreatic Cells through a miR-200a–Dependent Mechanism

43. Supplementary Table 1 from DCAMKL-1 Regulates Epithelial–Mesenchymal Transition in Human Pancreatic Cells through a miR-200a–Dependent Mechanism

49. Acetyl-Coenzyme A Synthetase 2 Potentiates Macropinocytosis and Muscle Wasting Through Metabolic Reprogramming in Pancreatic Cancer

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