42 results on '"Hall, Gentzon"'
Search Results
2. Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome
3. Genetic insights into the mechanisms of proliferative glomerulonephritis.
4. JAK inhibitor blocks COVID-19 cytokine–induced JAK/STAT/APOL1 signaling in glomerular cells and podocytopathy in human kidney organoids
5. IL-1 receptor signaling in podocytes limits susceptibility to glomerular damage
6. Steroid-sensitive nephrotic syndrome candidate gene CLVS1 regulates podocyte oxidative stress and endocytosis
7. Mechanisms of Proteinuria in HIV
8. Twist1 in podocytes ameliorates podocyte injury and proteinuria by limiting CCL2-dependent macrophage infiltration
9. IL-1 receptor signaling in podocytes limits susceptibility to glomerular damage.
10. TRPC6 Enhances Angiotensin II-induced Albuminuria
11. TRPC Channels in Proteinuric Kidney Diseases
12. SP001A Novel Heterozygous Missense Mutation of Wilms’ Tumor 1 May Cause FSGS Through Dysregulated Expression of ARHGAP24
13. FO068The LMX1βR246Q Mutation Induces Podocyte Injury Through Dysregulation of Cholesterol Transport Gene Expression
14. Genetic Testing for Steroid-Resistant-Nephrotic Syndrome in an Outbred Population
15. TRPC Channels in Proteinuric Kidney Diseases.
16. The Human FSGS-Causing ANLN R431C Mutation Induces Dysregulated PI3K/AKT/mTOR/Rac1 Signaling in Podocytes
17. Losing their footing: Rac1 signaling causes podocyte detachment and FSGS
18. Dysregulation of WTI (−KTS) is Associated with the Kidney-Specific Effects of the LMX1B R246Q Mutation
19. Variability in phenotype induced by the podocin variant R229Q plus a single pathogenic mutation
20. Translating genetic findings in hereditary nephrotic syndrome: the missing loops
21. HLA-DQA1 and PLCG2 Are Candidate Risk Loci for Childhood-Onset Steroid-Sensitive Nephrotic Syndrome
22. A Novel Missense Mutation of Wilms’ Tumor 1 Causes Autosomal Dominant FSGS
23. Rare hereditary COL4A3/COL4A4 variants may be mistaken for familial focal segmental glomerulosclerosis
24. Abstract 601: A Biased AT1 Receptor Agonist Stimulates COX2 Expression In Intercalated Cells
25. Mutations in the Gene That Encodes the F-Actin Binding Protein Anillin Cause FSGS
26. Phosphodiesterase 5 inhibition ameliorates angiontensin II-induced podocyte dysmotility via the protein kinase G-mediated downregulation of TRPC6 activity
27. TNXB Mutations Can Cause Vesicoureteral Reflux
28. Inverted formin 2 mutations with variable expression in patients with sporadic and hereditary focal and segmental glomerulosclerosis
29. Hepatorenal Correction in Murine Glycogen Storage Disease Type I With a Double-stranded Adeno-associated Virus Vector
30. Translating genetic findings in hereditary nephrotic syndrome: the missing loops.
31. Human mesenchymal stem cells exert potent antitumorigenic effects in a model of Kaposi's sarcoma
32. Inhibitor-κB kinase-β regulates LPS-induced TNF-α production in cardiac myocytes through modulation of NF-κB p65 subunit phosphorylation
33. Endotoxin stress-response in cardiomyocytes: NF-κB activation and tumor necrosis factor-α expression
34. Pregnancy and estradiol decrease GTPase activity in the guinea pig uterine artery
35. Phosphodiesterase 5 inhibition ameliorates angiontensin II-induced podocyte dysmotility via the protein kinase G-mediated downregulation of TRPC6 activity.
36. Human mesenchymal stem cells exert potent antitumorigenic effects in a model of Kaposi's sarcoma.
37. Endotoxin stress-response in cardiomyocytes: NF-κ B activation and tumor necrosis factor-α expression.
38. FO068 The LMX1βR246Q Mutation Induces Podocyte Injury Through Dysregulation of Cholesterol Transport Gene Expression.
39. Abstract 601.
40. Dysregulation of WTI (-KTS) is Associated with the Kidney-Specific Effects of the LMX1B R246Q Mutation.
41. Inhibitor-kappaB kinase-beta regulates LPS-induced TNF-alpha production in cardiac myocytes through modulation of NF-kappaB p65 subunit phosphorylation.
42. Endotoxin stress-response in cardiomyocytes: NF-kappaB activation and tumor necrosis factor-alpha expression.
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