The Smad3 protein is involved in TGF-β inhibition of class II transactivator and class II MHC expression

Journal of Immunology

Volumn 167, Issue 1, 2001, Pages 311-319

  Dong, Y ^a   Tang, L ^a   Letterio, J J ^a   Benveniste, E N ^a  

^a UNIVERSITY OF ALABAMA AT BIRMINGHAM   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

DNA; GAMMA INTERFERON; MAJOR HISTOCOMPATIBILITY ANTIGEN CLASS 2; MAJOR HISTOCOMPATIBILITY ANTIGEN CLASS 2 TRANSACTIVATOR; SMAD PROTEIN; SMAD3 PROTEIN; STAT1 PROTEIN; TRANSACTIVATOR PROTEIN; TRANSFORMING GROWTH FACTOR BETA; UNCLASSIFIED DRUG;

ANIMAL CELL; ANTIGEN EXPRESSION; ARTICLE; ASTROCYTE; CONTROLLED STUDY; CYTOKINE PRODUCTION; FEMALE; IMMUNOREGULATION; INHIBITION KINETICS; MAJOR HISTOCOMPATIBILITY COMPLEX; MOUSE; NEWBORN; NONHUMAN; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; PROTEIN PROTEIN INTERACTION; RAT; REGULATORY MECHANISM; SIGNAL TRANSDUCTION; TRANSCRIPTION REGULATION;

EID: 0035399833     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.167.1.311     Document Type: Article

References (50)

1. Regulation of class II MHC expression
2. Immune responses in MHC class II-deficient mice
3. Class II MHC genes: A model gene regulatory system with great biologic consequences
4. The class II transactivator CIITA is a transcriptional integrator
5. Class II transactivator: Mastering the art of major histocompatibility complex expression
6. CIITA is a transcriptional coactivator that is recruited to MHC class II promoters by multiple synergistic interactions with an enhanceosome complex
7. 1132
8. Transactivation by CIITA, the type II bare lymphocyte syndrome-associated factor, requires participation of multiple regions of the TATA box binding protein
9. Involvement of CREB binding protein in expression of major histocompatibility complex class II genes via interaction with the class II transactivator
10. 11250
11. Quantitative control of MHC class II expression by the transactivator CIITA
12. Regulation of MHC class II expression by interferon-γ mediated by the transactivator gene CIITA
13. Class II transactivator (CIITA) is sufficient for the inducible expression of major histocompatibility complex class II genes
14. STAT-1α expression is involved in IFN-γ induction of the class II transactivator and class II MHC genes
15. Mice lacking the MHC class II transactivator (CIITA) show tissue-specific impairment of MHC class II expression
16. Expression of MHC class II molecules in different cellular and functional compartments is controlled by differential usage of multiple promoters of the transactivator CIITA
17. IFN-γ regulation of the type IV class II transactivator promoter in astrocytes
18. Differential selectivity of CIITA promoter activation by IFN-γ and IRF-1 in astrocytes and macrophages: CIITA promoter activation is not affected by TNF-α
19. Two distinct γ interferon-inducible promoters of the major histocompatibility complex class II transactivator gene are differentially regulated by STAT1, interferon regulatory factor 1, and transforming growth factor β
20. Identification of distinct regions of 5′ flanking DNA that mediate constitutive. IFN-γ, STAT1, and TGF-β-regulated expression of the class II transactivator gene
21. Activation of the MHC class II transactivator CIITA by interferon-γ requires cooperative interaction between Stat1 and USF-1
22. Role of transforming growth factor β in human disease
23. Regulation of immune responses by TGF-β
24. Production of transforming growth factor β by human T lymphocytes and its potential role in the regulation of T cell growth
25. Pleiotropic effects of transforming growth factor-β on cells of the immune system
26. 1 modulates the expression of class II histocompatibility antigens on human cells
27. 1 repression of the HLA-DRα gene is mediated by conserved proximal promoter elements
28. Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease
29. Autoimmunity associated with TGF-β1-deficiency in mice is dependent on MHC class II antigen expression
30. Manipulation of TGF-β to control autoimmune and chronic inflammatory diseases
31. TGF-β signal transduction
32. Transcriptional control by the TGF-β/Smad signaling system
33. TGF-β signaling from receptors to the nucleus
34. Smad2 role in mesoderm formation, left-right patterning and craniofacial development
35. Failure of egg cylinder elongation and mesoderm induction in mouse embryos lacking the tumor suppressor smad2
36. Targeted disruption of SMAD3 results in impaired mucosal immunity and diminished T cell responsiveness to TGF-β
37. Targeted disruption of Smad3 reveals an essential role in transforming growth factor β-mediated signal transduction
38. TGF-β suppresses IFN-γ induction of class II MHC gene expression by inhibiting class II transactivator messenger RNA expression
39. TGF-β suppression of IFN-γ induced class II MHC gene expression does not involve inhibition of phosphorylation of JAK1, JAK2, or STAT1 α or modification of IFNEX expression
40. Localization of the glial fibrillary acidic protein in astrocytes by immunofluorescence
41. Inhibition of transforming growth factor-β/SMAD signalling by the interferon-γ/STAT pathway
42. Involvement of STAT-1α and its family members in interferon-γ induction of CD40 transcription in macrophages/ microglia
43. Characterization of astrocyte nuclear proteins involved in IFN-γ and TNF-α mediated class II MHC gene expression
44. Identification and functional characterization of a Smad binding element (SBE) in the JunB promoter that acts as a transforming growth factor-β activin, and bone morphogenetic protein-inducible enhancer
45. Maximal activation of transcription by Stat1 and Stat3 requires both tyrosine and serine phosphorylation
46. TGF-β1 inhibition of transin/stromelysin gene expression is mediated through a fos binding sequence
47. A Smad transcriptional corespressor
48. c-Ski acts as a transcriptional co-represser in transforming growth factor-β signaling through interaction with Smads
49. The Ski oncoprotein interacts with the Smad proteins to repress TGFβ signaling
50. Inhibition of E-selectin gene expression by transforming growth factor β in endothelial cells involves coactivator integration of Smad and nuclear factor κB-mediated signals