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Gene Review

Litaf  -  LPS-induced TN factor

Mus musculus

Synonyms: 3222402J11Rik, C85531, Estrogen-enhanced transcript protein, LITAF-like protein, LPS-induced TNF-alpha factor homolog, ...
 
 
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Disease relevance of Litaf

  • Using these cells, we now show that LITAF expression can be induced after challenge either with LPS from Porphyromonas gingivalis via agonism at TLR-2, or with LPS from Escherichia coli via agonism at TLR-4, both requiring functional MyD88 [1].
  • TBX1 is the major candidate gene for DiGeorge syndrome (DGS) [2].
  • Thyroid dysgenesis related to Tbx1 inactivation may explain an overrepresentation of hypothyroidism occurring in patients with the 22q11DS [3].
  • Using the growth delay assay, the therapeutic response was enhanced by prior TBX: for example, in mice receiving 3000 rad TBX 1 day before fibrosarcoma cell inoculation, the growth delay from 8 to 12 mm produced by CY (150 mg/kg) was 18.8 days compared with 9.4 days without prior TBX [4].
 

High impact information on Litaf

  • We conclude that LITAF is an important mediator of the LPS-induced inflammatory response that can be distinguished from NF-kappaB pathway and that p38alpha is the specific kinase involved in the pathway linking LPS/MyD88/LITAF to TNF [1].
  • Previously we identified a transcription factor, LPS-Induced TNF-alpha Factor (LITAF), mediating inflammatory cytokine expression in LPS-induced processes [1].
  • To further identify LITAF signaling pathways, we tested mouse TLR-2(-/-), -4(-/-), and -9(-/-) and WT peritoneal macrophages exposed to LPS [1].
  • Tbx1 is a transcription factor, the mutation of which is sufficient to cause most of the physical features of 22q11DS, but the gene had not been previously associated with the behavioral/psychiatric phenotype [5].
  • The 22q11 deletion syndrome candidate gene Tbx1 determines thyroid size and positioning [3].
 

Biological context of Litaf

 

Anatomical context of Litaf

 

Associations of Litaf with chemical compounds

 

Regulatory relationships of Litaf

  • Moreover, we disclosed that mEET inhibited the production of SDF-1alpha by its suppression of NF-kappaB translocation into nucleus [10].
 

Other interactions of Litaf

  • Conversely, inactivation of the mEET gene substantially augmented MCP-1 expression [6].
  • Activation of the mEET gene markedly attenuated activity of nuclear NF-kappaB [6].
 

Analytical, diagnostic and therapeutic context of Litaf

References

  1. LPS-induced TNF-{alpha} factor (LITAF)-deficient mice express reduced LPS-induced cytokine: Evidence for LITAF-dependent LPS signaling pathways. Tang, X., Metzger, D., Leeman, S., Amar, S. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  2. Tbx1 mutation causes multiple cardiovascular defects and disrupts neural crest and cranial nerve migratory pathways. Vitelli, F., Morishima, M., Taddei, I., Lindsay, E.A., Baldini, A. Hum. Mol. Genet. (2002) [Pubmed]
  3. The 22q11 deletion syndrome candidate gene Tbx1 determines thyroid size and positioning. Fagman, H., Liao, J., Westerlund, J., Andersson, L., Morrow, B.E., Nilsson, M. Hum. Mol. Genet. (2007) [Pubmed]
  4. Modification of tumor response to cyclophosphamide and irradiation by preirradiation of the tumor bed: prolonged growth delay but reduced curability. Ito, H., Barkley, T., Peters, L.J., Milas, L. Int. J. Radiat. Oncol. Biol. Phys. (1985) [Pubmed]
  5. Tbx1 haploinsufficiency is linked to behavioral disorders in mice and humans: implications for 22q11 deletion syndrome. Paylor, R., Glaser, B., Mupo, A., Ataliotis, P., Spencer, C., Sobotka, A., Sparks, C., Choi, C.H., Oghalai, J., Curran, S., Murphy, K.C., Monks, S., Williams, N., O'Donovan, M.C., Owen, M.J., Scambler, P.J., Lindsay, E. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  6. Negative regulation of monocyte chemoattractant protein-1 gene expression by a mouse estrogen-enhanced transcript. Xie, L.P., Fu, W.X., Jin, C., Dong, X.Y., Chen, W.F. Eur. J. Immunol. (2002) [Pubmed]
  7. TBX1 is required for inner ear morphogenesis. Vitelli, F., Viola, A., Morishima, M., Pramparo, T., Baldini, A., Lindsay, E. Hum. Mol. Genet. (2003) [Pubmed]
  8. A genetic link between Tbx1 and fibroblast growth factor signaling. Vitelli, F., Taddei, I., Morishima, M., Meyers, E.N., Lindsay, E.A., Baldini, A. Development (2002) [Pubmed]
  9. The 22q11.2 deletion syndrome: a gene dosage perspective. Baldini, A. ScientificWorldJournal (2006) [Pubmed]
  10. SDF-1alpha production is negatively regulated by mouse estrogen enhanced transcript in a mouse thymus epithelial cell line. Jin, C., Fu, W.X., Xie, L.P., Qian, X.P., Chen, W.F. Cell. Immunol. (2003) [Pubmed]
  11. Mesodermal expression of Tbx1 is necessary and sufficient for pharyngeal arch and cardiac outflow tract development. Zhang, Z., Huynh, T., Baldini, A. Development (2006) [Pubmed]
  12. Molecular cloning and characterization of mouse LITAF cDNA: role in the regulation of tumor necrosis factor-alpha (TNF-alpha) gene expression. Bolcato-Bellemin, A.L., Mattei, M.G., Fenton, M., Amar, S. J. Endotoxin Res. (2004) [Pubmed]
  13. Dissection of Tbx1 and Fgf interactions in mouse models of 22q11DS suggests functional redundancy. Aggarwal, V.S., Liao, J., Bondarev, A., Schimmang, T., Lewandoski, M., Locker, J., Shanske, A., Campione, M., Morrow, B.E. Hum. Mol. Genet. (2006) [Pubmed]
 
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