Deficiency of c-Jun-NH2-terminal kinase-1 in mice enhances skin tumor development by 12-O-tetradecanoylphorbol-13-acetate

Cancer Research

Volumn 62, Issue 5, 2002, Pages 1343-1348

  She, Qing Bai ^a   Chen, Nanyue ^a   Bode, Ann M ^a   Flavell, Richard A ^b   Dong, Zigang ^a  

^a UNIVERSITY OF MINNESOTA   (United States)

^b YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

MITOGEN ACTIVATED PROTEIN KINASE; PHORBOL 13 ACETATE 12 MYRISTATE; PROTEIN KINASE B; STRESS ACTIVATED PROTEIN KINASE; STRESS ACTIVATED PROTEIN KINASE 1; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CANCER INCIDENCE; CANCER INHIBITION; CONTROLLED STUDY; DNA BINDING; ENZYME ACTIVITY; ENZYME DEFICIENCY; ENZYME PHOSPHORYLATION; MOUSE; NONHUMAN; PRIORITY JOURNAL; SKIN CARCINOGENESIS; SKIN TUMOR;

ANIMALS; DNA; MICE; MITOGEN-ACTIVATED PROTEIN KINASE 8; MITOGEN-ACTIVATED PROTEIN KINASE 9; MITOGEN-ACTIVATED PROTEIN KINASES; PAPILLOMA; PHOSPHORYLATION; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION; SKIN NEOPLASMS; TETRADECANOYLPHORBOL ACETATE; TRANSCRIPTION FACTOR AP-1;

EID: 0036494195     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (62)

1. Signal transduction by the c-Jun N-terminal kinase (JNK)-from inflammation to development
2. The JUN kinase/stress-activated protein kinase pathway is required for epidermal growth factor stimulation of growth of human A549 lung carcinoma cells
3. Inhibition of c-Jun N-terminal kinase 2 expression suppresses growth and induces apoptosis of human tumor cells in a p53-dependent manner
4. c-Jun N-terminal kinase is essential for growth of human T98G glioblastoma cells
5. Activation of the JNK pathway is essential for transformation by the met oncogene
6. The Jun kinase 2 isoform is preferentially required for epidermal growth factor-induced transformation of human A549 lung carcinoma cells
7. Requirement of Erk, but not JNK, for arsenite-induced cell transformation
8. JNK activation is required for JB6 cell transformation induced by tumor necrosis factor-α but not by 12-O-tetradecanoylphorbol-13-acetate
9. Platelet-derived growth factor (PDGF) receptor-α activates c-Jun NH2-terminal kinase-1 and antagonizes PDGF receptor-β-induced phenotypic transformation
10. Selective interaction of JNK protein kinase isoforms with transcription factors
11. JNK1: A protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain
12. Transcription factor ATF2 regulation by the JNK signal transduction pathway
13. Induction of c-fos expression through JNK-mediated TCF/Elk-1 phosphorylation
14. p53 is phosphorylated in vitro and in vivo by an ultraviolet radiation-induced protein kinase characteristic of the c-Jun kinase, JNK1
15. JNK2 contains a specificity-determining region responsible for efficient c-Jun binding and phosphorylation
16. c-Jun NH2-terminal kinase regulation of the apoptotic response of small cell lung cancer cells to ultraviolet radiation
17. Preferential activation of the p46 isoform of JNK/SAPK in mouse macrophages by TNF α
18. Dominant-negative c-Jun NH2-terminal kinase 2 sensitizes renal inner medullary collecting duct cells to hypertonicity-induced lethality independent of organic osmolyte transport
19. Inhibition of hypoxia/reoxygenation-induced apoptosis by an antisense oligonucleotide targeted to JNK1 in human kidney cells
20. 2-terminal kinase and caspase- 3
21. Defective T cell differentiation in the absence of Jnk1
22. Differentiation of CD4+ T cells to Thl cells requires MAP kinase JNK2
23. Molecular mechanisms involved in skin tumor initiation, promotion, and progression
24. Multistage carcinogenesis in mouse skin
25. 2-terminal kinase-2-deficient mice
26. ERKs and p38 kinase phosphorylate p53 protein at serine 15 in response to UV radiation
27. Inhibition of tumor promoter-induced activator protein 1 activation and cell transformation by tea polyphenols. (-)-Epigallocatechin gallate, and theaflavins
28. Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis
29. P13K: Downstream AKTion blocks apoptosis
30. Shortage of mitogen-activated protein kinase is responsible for resistance to AP-1 transactivation and transformation in mouse JB6 cells
31. Colorectal carcinomas in mice lacking the catalytic subunit of PI(3)Kγ
32. Elevated phosphorylation of AKT and Stat3 in prostate, breast, and cervical cancer cells
33. Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor
34. The role of Jun, Fos and the AP-1 complex in cell-proliferation and transformation
35. JNK is required for effector T-cell function but not for T-cell activation
36. Insulin-like growth factor-I inhibits the stress-activated protein kinase/c-Jun N-terminal kinase
37. Akt negatively regulates the cJun N-terminal kinase pathway in PC12 cells
38. Pharmacologic or genetic manipulation of glutathione S-transferase P1-1 (GSTpi) influences cell proliferation pathways
39. Glutathione S-transferase P1-1 (GSTP1-1) inhibits c-Jun N-terminal kinase (JNK1) signaling through interaction with the C terminus
40. cDNA cloning and characterization of a ligand for the Cek5 receptor protein-tyrosine kinase
41. Genomic organization and alternatively processed forms of Cek5, a receptor protein-tyrosine kinase of the Eph subfamily
42. Tyrosine phosphorylation of transmembrane ligands for Eph receptors
43. The N-terminal globular domain of Eph receptors is sufficient for ligand binding and receptor signaling
44. The transactivating domain of the c-Jun proto-oncoprotein is required for cotransformation of rat embryo cells
45. Requirement for phosphatidylinositol 3-kinase in epidermal growth factor-induced AP-1 transactivation and transformation in JB6 P+ cells
46. Phosphatidylinositol-3 kinase is necessary for 12-O-tetradecanoylphorbol-13-acetate-induced cell transformation and activated protein 1 activation
47. Expression of dominant negative Erk2 inhibits AP-1 transactivation and neoplastic transformation
48. Blocking activator protein-1 activity, but not activating retinoic acid response element, is required for the antitumor promotion effect of retinoic acid
49. Transgenic mice demonstrate AP-1 (activator protein-1) transactivation is required for tumor promotion
50. Transition from SCLC to NSCLC phenotype is accompanied by an increased TRE-binding activity and recruitment of specific AP-1 proteins
51. Progression of MCF-7 breast cancer cells to antiestrogen-resistant phenotype is accompanied by elevated levels of AP-1 DNA-binding activity
52. c-fos is required for malignant progression of skin tumors
53. A dominant negative mutant of jun blocking 12-O-tetradecanoylphorbol-13-acetate-induced invasion in mouse keratinocytes
54. Stable expression of a c-JUN deletion mutant in two malignant mouse epidermal cell lines blocks tumor formation in nude mice
55. AP-1-mediated invasion requires increased expression of the hyaluronan receptor CD44
56. The role and regulation of the Jun proteins in response to phorbol ester and UV light
57. AP1/jun function is differentially induced in promotion-sensitive and resistant JB6 cells
58. Blocking of tumor promoter-induced AP-1 activity inhibits induced transformation in JB6 mouse epidermal cells
59. Inhibition of tumor promoter-induced transformation by retinoids that transrepress AP-1 without transactivating retinoic acid response element
60. The regulation of AP-1 activity by mitogen-activated protein kinases
61. Activation of the B-cell surface receptor CD40 induced A20, a novel zinc finger protein that inhibits apoptosis
62. Failure to regulate TNF-induced NF-κB and cell death responses in A20-deficient mice