Apoptosis and JNK activation are differentially regulated by Fas expression level in renal tubular epithelial cells

Kidney International

Volumn 60, Issue 1, 2001, Pages 65-76

  Khan, Shenaz ^a   Koepke, Alexandra ^a   Jarad, George ^a   Schlessman, Katie ^a   Cleveland, Ronald P ^a   Wang, Bingcheng ^a   Konieczkowski, Martha ^a   Schelling, Jeffrey R ^a  

^a METROHEALTH MEDICAL CENTER   (United States)

Author keywords

CD95; Cell death; Inflammatory mediators; Progressive renal disease; Protein kinases; Signal transduction

Indexed keywords

FAS ANTIGEN; LIPOCORTIN 5; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; STRESS ACTIVATED PROTEIN KINASE;

ANTIGEN EXPRESSION; APOPTOSIS; ARTICLE; CHRONIC INFLAMMATION; CONTROLLED STUDY; ENZYME ACTIVATION; ENZYME ACTIVITY; HUMAN; HUMAN CELL; KIDNEY DISEASE; KIDNEY TUBULE EPITHELIUM; NICK END LABELING; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; STRESS;

EID: 0034963549     PISSN: 00852538     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1523-1755.2001.00771.x     Document Type: Article

References (44)

1. Relationship between renal function and histological changes found in renal-biopsy specimens from patients with persistent glomerular nephritis
2. Structural-functional correlations in renal disease
3. Pathogenesis of chronic renal failure in the primary glomerulopathies, renal vasculopathies, and chronic interstitial nephritides
4. Morphologic, biochemical, and molecular evidence of apoptosis during reperfusion phase after brief periods of renal ischemia
5. Apoptosis and loss of renal tissue in polycystic kidney diseases
6. Fas-dependent fratricidal apoptosis is a mechanism of tubular epithelial cell deletion in chronic renal failure
7. Hypoxia induces renal tubular epithelial cell apoptosis in chronic renal disease
8. Constitutive and induced expression of APO-1, a new member of the nerve growth factor/tumor necrosis factor receptor superfamily, in normal and neoplastic cells
9. Regulation of Fas and Fas ligand expression in cultured murine renal cells and in the kidney during endotoxemia
10. Role of Fas (CD95) in tubulointerstitial disease induced by unilateral ureteric obstruction
11. Expression and function of Fas (CD95) on human renal tubular epithelial cells
12. Apoptosis by death factor
13. Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule
14. Downregulation of Fas ligand by shedding
15. Caspase inhibitors
16. Social controls on cell survival and cell death
17. The death domain: A module shared by proteins with diverse cellular functions
18. Fas ligand-induced apoptosis as a mechanism of immune privilege
19. Fas ligand expression in islets of Langerhans does not confer immune privilege and instead targets them for rapid destruction
20. Regulation of the proinflammatory effects of Fas ligand (CD95L)
21. Essential roles of the Fas-Fas ligand pathway in the development of pulmonary fibrosis
22. Dissection of TNF receptor 1 effector functions: JNK activation is not linked to apoptosis while NF-κB activation prevents cell death
23. MAP3K-related kinase involved in NF-κB induction by TNF, CD95 and IL-1
24. Stress-signaling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3
25. Lack of a role for Jun kinase and AP-1 in Fas-induced apoptosis
26. Dominant-negative FADD inhibits TNFR60-, Fas/Apo1- and TRAIL- R/Apo2-mediated cell death but not gene induction
27. Cell lines with extended in vitro growth potential from human renal proximal tubule: Characterization, response to inducers, and comparison with established cell lines
28. Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis
29. 2-terminal kinase regulation of the apoptotic response of small cell lung cancer cells to ultraviolet radiation
30. Annexin II inhibition of G protein-regulated inositol trisphosphate formation in rat aortic smooth muscle
31. Interleukin-1 stimulates Jun N-terminal/stress-activated protein kinase by an arachidonate-dependent mechanism in mesangial cells
32. Cell death: The significance of apoptosis
33. Major DNA fragmentation is a late event in apoptosis
34. Self-association of the 'death domains' of the p55 tumor necrosis factor (TNF) receptor and Fas/APO1 prompts signaling for TNF and Fas/APO1 effects
35. MEK kinase 1, a substrate for DEVD-directed caspases, is involved in genotoxin-induced apoptosis
36. Fas activates the JNK pathway in human colonic epithelial cells: Lack of a direct role in apoptosis
37. JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain
38. The role of c-Jun N-terminal kinase (JNK) in apoptosis induced by ultraviolet C and gamma radiation - Duration of JNK activation may determine cell death and proliferation
39. Fas-induced proteolytic activation and intracellular redistribution of the stress-signaling kinase MEKK1
40. Signal transduction by the c-Jun N-terminal kinase (JNK) - From inflammation to development
41. Early activation of c-Jun N-terminal kinase and p38 kinase regulate cell survival in response to tumor necrosis factor α
42. Dissecting Fas signaling with an altered-specificity death-domain mutant: Requirement of FADD binding for apoptosis but not Jun-terminal kinase activation
43. Cross-talk in cell death signaling
44. L