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3. Primary coenzyme Q10 nephropathy, a potentially treatable form of steroid-resistant nephrotic syndrome

4. Endothelial cells drive organ fibrosis in mice by inducing expression of the transcription factor SOX9

5. Repression of Sox9 by Jag1 Is Continuously Required to Suppress the Default Chondrogenic Fate of Vascular Smooth Muscle Cells

6. ADCK4 mutations promote steroid-resistant nephrotic syndrome through CoQ10 biosynthesis disruption

7. Abstract GS.06: The Fibrogenic Transcription Factor Sox9 Controls Mesenchymal Activation Of Endothelial Cells And Drives Fibrotic Disease

8. Mitochondrial ROS Triggers KIN Pathogenesis in FAN1-Deficient Kidneys

10. Premature Aging and Reduced Cancer Incidence Associated with Near-Complete Body-WideMycInactivation

11. Premature Aging and Reduced Cancer Incidence Associated With Body-Wide Loss of Myc

14. Mitigation of portal fibrosis and cholestatic liver disease in ANKS6 ‐deficient livers by macrophage depletion

15. BiallelicANKS6mutations cause late-onset ciliopathy with chronic kidney disease through YAP dysregulation

17. COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness

18. Loss of Sox9 in the periotic mesenchyme affects mesenchymal expansion and differentiation, and epithelial morphogenesis during cochlea development in the mouse

20. Mutation analysis of 18 nephronophthisis associated ciliopathy disease genes using a DNA pooling and next generation sequencing strategy

21. Loss ofAnks6leads to YAP deficiency and liver abnormalities

26. Delayed onset of smooth muscle cell differentiation leads to hydroureter formation in mice with conditional loss of the zinc finger transcription factor geneGata2in the ureteric mesenchyme

28. The prepattern transcription factor Irx3 directs nephron segment identity

29. Delayed onset of smooth muscle cell differentiation leads to hydroureter formation in mice with conditional loss of the zinc finger transcription factor gene Gata2 in the ureteric mesenchyme.

30. Whole exome sequencing identifies causative mutations in the majority of consanguineous or familial cases with childhood-onset increased renal echogenicity

31. SDCCAG8 Interacts with RAB Effector Proteins RABEP2 and ERC1 and Is Required for Hedgehog Signaling

32. FAT1 mutations cause a glomerulotubular nephropathy

35. FAT1 mutations cause a glomerulotubular nephropathy

36. Whole exome sequencing identifies causative mutations in the majority of consanguineous or familial cases with childhood-onset increased renal echogenicity

37. DCDC2 mutations cause a renal-hepatic ciliopathy by disrupting Wnt signaling

38. DCDC2 mutations cause a renal-hepatic ciliopathy by disrupting Wnt signaling

39. Defects in the IFT-B Component IFT172 Cause Jeune and Mainzer-Saldino Syndromes in Humans

40. Zebrafish Ciliopathy Screen Plus Human Mutational Analysis Identifies C21orf59 and CCDC65 Defects as Causing Primary Ciliary Dyskinesia

42. DCDC2 Mutations Cause a Renal-Hepatic Ciliopathy by Disrupting Wnt Signaling

43. Renal-Retinal Ciliopathy Gene Sdccag8 Regulates DNA Damage Response Signaling

44. Whole-exome resequencing distinguishes cystic kidney diseases from phenocopies in renal ciliopathies

46. Renal-Retinal Ciliopathy Gene Sdccag8 Regulates DNA Damage Response Signaling

49. Whole-exome resequencing distinguishes cystic kidney diseases from phenocopies in renal ciliopathies

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