Overexpression of insulin receptor substrate-1, but not insulin receptor substrate-2, protects a T cell hybridoma from activation-induced cell death

Journal of Immunology

Volumn 168, Issue 12, 2002, Pages 6215-6223

  Li, Li ^a   Qi, Xiulan ^a   Williams, Mark ^a   Shi, Yufang ^a   Keegan, Achsah D ^a  

^a HOLLAND LABORATORY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

INSULIN RECEPTOR SUBSTRATE 1; INSULIN RECEPTOR SUBSTRATE 2; LUCIFERASE; PHOSPHATIDYLINOSITOL 3 KINASE;

ANIMAL CELL; APOPTOSIS; ARTICLE; CELL DEATH; CELL PROTECTION; ENZYME ACTIVITY; GENE OVEREXPRESSION; HYBRIDOMA; IMMOBILIZED CELL; MOLECULAR CLONING; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FAMILY; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; T LYMPHOCYTE ACTIVATION;

EID: 0037097536     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.168.12.6215     Document Type: Article

References (52)

1. Activation induced cell death (AICD) in T cell hybridomas is due to apoptosis: Morphological aspects and DNA fragmentation
2. T cell antigen-receptor signal transduction
3. Fatal interactions: Fas-induced apoptosis of mature T cells
4. Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation
5. Fas and activation induced Fas ligand mediate apoptosis of T cell hybridomas: Inhibition of Fas ligand expression by retinioic acid and glucocorticoids
6. Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome
7. Potential involvement of Fas and its ligand in the pathogenesis of Hashimoto's thyroiditis
8. Melanoma cell expression of Fas(Apo-1/CD95) ligand: Implications for tumor immune escape
9. Lymphocyte responses and cytokines
10. Differential ability of Th1 and Th2 T cells to express Fas ligand and to undergo activation-induced cell death
11. Expression of the Fas ligand in cells of T cell lineage
12. Unequal death in T helper cell (Th)1 and Th2 effectors: Th1, but not Th2, effectors undergo rapid Fas/FasL-mediated apoptosis
13. Differential ability of T cell subsets to undergo activation-induced cell death
14. The IL-4 receptor: Signaling mechanisms and biologic functions
15. Interleukin-4 signals two related pathways
16. Impaired interleukin-4 signaling in T helper type I cells
17. Role of IRS-2 in insulin and cytokine signalling
18. The IRS-2 gene on murine chromosome 8 encodes a unique signaling adapter for insulin and cytokine action
19. 307
20. IRS-4 mediates protein kinase B signaling during insulin stimulation without promoting anti-apoptosis
21. Differential signaling by insulin receptor substrate 1 (IRS-1) and IRS-2 in IRS-1-deficient cells
22. YMXM motifs and signaling by an insulin receptor substrate 1 molecule without tyrosine phosphorylation sites
23. Interleukins 2, 4, 7, and 15 stimulate tyrosine phosphorylation of insulin receptor substrates 1 and 2 in T cells: Potential role of JAK kinases
24. Differential association of phosphatidylinositol 3-kinase with insulin receptor substrate (IRS)-1 and IRS-2 in human thymocytes in response to IL-7
25. NF-ΚB/Rel participation in the lymphokine-dependent proliferation of T lymphoid cells
26. Stat6 and IRS-2 cooperate in interleukin 4 (IL-4)-induced proliferation and differentiation but are dispensable for IL-4-dependent rescue from apoptosis
27. Alternative pathway of insulin signalling in mice with targeted disruption of the IRS-1 gene
28. Insulin receptor substrate 3 is not essential for growth or glucose homeostasis
29. Disruption of IRS-2 causes type 2 diabetes in mice
30. Protein kinase C regulates Fas (CD95/Apo-1) expression
31. Differential regulation of the expression of CD95L, RANKL, TRAIL, and TNFα during T cell activation
32. IL-4 protects cells from apoptosis via the insulin receptor substrate pathway and a second independent signaling pathway
33. Cyclosporin-A sensitive transcription factor Egr-3 regulates fas ligand expression Mol
34. Role of Egr-2 in up-regulation of Fas ligand in normal T cells and aberrant double-negative lpr and gld T cells
35. Target cell lysis by CTL granule exocytosis is independent of ICE/Ced-3 family proteases
36. Sequential involvement of NFAT and Egr transcription factors in FasL regulation
37. Dominant negative mutant of c-Jun inhibits NF-AT transcriptional activity and prevents IL-2 gene transcription
38. IRS-2 coordinates IGF-I receptor-mediated β-cell development and peripheral insulin signalling
39. Insulin receptor substrate 1 overexpression in human hepatocellular carcinoma cells prevents transforming growth factor beta1 induced apoptosis
40. Overexpression of human insulin receptor substrate 1 induces cellular transformation with activation of mitogen activated protein kinases
41. Transforming potential of the insulin receptor substrate 1
42. Enhanced expression of the insulin receptor substrate-2 docking protein in human pancreatic cancer
43. Regulation of CD95 (Fas) ligand expression by TCR mediated signaling events
44. DNA damaging agents induce expression of Fas ligand and subsequent apoptosis in T lymphocytes via the activation of NFΚB and AP-1
45. A newly identified response element in the CD95 ligand promoter contributes to optimal inducibility in activated T lymphocytes
46. The NFΚB signaling pathway is not required for Fas ligand gene induction but mediates protection from activation-induced cell death
47. 2-terminal kinase
48. Stress-induced Fas ligand expression in T cells is mediated through a MEK kinase-1-regulated response element in the Fas ligand promoter
49. c-Jun-dependent CD95-L expression is a rate-limiting step in the induction of apoptosis by alkylating agents
50. IRS-2 pathways integrate female reproduction and energy homeostasis
51. Gene expression elicited by NFAT in the presence or absence of cooperative recruitment of Fos and Jun
52. Differential expression of Fas ligand in Th1 and Th2 cells is regulated by early growth response gene and NFAT family members