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NFIB  -  nuclear factor I/B

Homo sapiens

Synonyms: CCAAT-box-binding transcription factor, CTF, HMGIC/NFIB, NF-I/B, NF1-B, ...
 
 
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Disease relevance of NFIB

 

High impact information on NFIB

  • Among transcription factors that are important in multiple members of this gene family are the C/EBPs, Sp1,USF, and AP1, HNF-1, CTF/NF-1, glucocorticoid, and retinoic acid receptors, and several as-yet unidentified negative elements, are important in at least one of the genes [5].
  • Thus, each of the three functional upstream regions, as defined by transfection assays, was shown to interact with five factors: Sp1 and CTF/NF-I at the upstream site, two unidentified proteins at the central site, and SRF at the most proximal site [6].
  • Since DAPT treatment resulted in increased beta2-CTF levels, we also tested whether beta2-CTFs or beta2-ICDs would directly affect cell migration by overexpressing recombinant proteins [7].
  • In the present report, we examine the disposition of PS NTF and CTF assemblies in stable mouse N2a neuroblastoma cell lines expressing human PS polypeptides [8].
  • PS1 and PS2 are polytopic membrane proteins that undergo endoproteolytic cleavage to generate stable NH2- and COOH-terminal derivatives (NTF and CTF, respectively) [8].
 

Biological context of NFIB

  • Coexpression of NFI-B3 with other isoforms of the NFI-B, -C, and -X family, however, led to a strong reduction of transcriptional activation compared with the expression of these factors alone [9].
  • 3'-RACE analysis of a primary adenoma with an apparently normal karyotype revealed an HMGIC fusion transcript containing ectopic sequences derived from the human NFIB gene, previously mapped to chromosome band 9p24 [1].
  • Nucleotide sequence analysis of the fusion transcripts indicated that the genetic aberration in both tumors resulted in the replacement of a carboxy-terminal segment of HMGIC by the last five amino acids of NFIB [1].
  • Transfection analyses revealed that the function of NF1-B on the transcriptional regulation differed between NF1-B isoforms and was affected by the factor(s) that bind to the promoter regions [10].
  • An in-frame fusion transcript, combining the four first exons of HMGA2 with exon 8 of NFIB, was detected in one case [4].
 

Anatomical context of NFIB

 

Associations of NFIB with chemical compounds

  • In addition, we identified the transcriptional regulatory domain of NF1-B, which is enriched with proline and serine residues [10].
  • We have previously purified NF1-A and NF1-B from rat liver as factors that bind to the silencer in the glutathione transferase P gene, and have also reported the repression domain of NF1-A [10].
  • The Nuclear Factor I (NFI) family of site-specific DNA-binding proteins (also known as CTF or CAAT box transcription factor) functions both in viral DNA replication and in the regulation of gene expression [14].
  • Proliferative activity was significantly (P < 0.05) more strongly inhibited in kelfib than in nfib under HePC treatment, whereas their phosphatidylcholine synthesis was inhibited to a similar extent [13].
  • We show that aspartate-mutant holoprotein presenilins are not incorporated into the high molecular weight, NTF/CTF-containing complexes [15].
 

Other interactions of NFIB

  • Purified CCAAT box-binding transcription factor CTF/NF-I and Sp1 were shown to interact with the far-upstream regulatory element at -410, and footprint analysis showed extensive overlap of these two sites [6].
  • The reciprocal NFIB/HMGIC fusion transcript, however, could not be detected in any of these tumors [1].
 

Analytical, diagnostic and therapeutic context of NFIB

  • EXPERIMENTAL DESIGN: Polymeric microspheres made of poly(lactic-co-glycolic acid) (PLGA) were loaded with very low amounts of PEX and PF-4/CTF [12].
  • A single local s.c. injection of PLGA microspheres loaded with low amounts of PEX or PF-4/CTF resulted in an 88% and 95% reduction in glioma tumor volume 30 days post-treatment [12].
  • The insertion of a chest tube was required in only one (2%) procedure using the CTF technique, while this was needed in four (10%) using the conventional technique [16].
  • These data correlate well with the heterogeneity of the DiGeorge syndrome and variable results seen with human CTF transplantation [17].

References

  1. Identification of NFIB as recurrent translocation partner gene of HMGIC in pleomorphic adenomas. Geurts, J.M., Schoenmakers, E.F., Röijer, E., Aström, A.K., Stenman, G., van de Ven, W.J. Oncogene (1998) [Pubmed]
  2. Comparison of molecular markers in a cohort of patients with chronic myeloproliferative disorders. Kralovics, R., Buser, A.S., Teo, S.S., Coers, J., Tichelli, A., van der Maas, A.P., Skoda, R.C. Blood (2003) [Pubmed]
  3. A novel amplicon at 9p23 - 24 in squamous cell carcinoma of the esophagus that lies proximal to GASC1 and harbors NFIB. Yang, Z.Q., Imoto, I., Pimkhaokham, A., Shimada, Y., Sasaki, K., Oka, M., Inazawa, J. Jpn. J. Cancer Res. (2001) [Pubmed]
  4. Fusion of the HMGA2 and NFIB genes in lipoma. Nilsson, M., Panagopoulos, I., Mertens, F., Mandahl, N. Virchows Arch. (2005) [Pubmed]
  5. Regulation of the mammalian alcohol dehydrogenase genes. Edenberg, H.J. Prog. Nucleic Acid Res. Mol. Biol. (2000) [Pubmed]
  6. Identification of multiple proteins that interact with functional regions of the human cardiac alpha-actin promoter. Gustafson, T.A., Kedes, L. Mol. Cell. Biol. (1989) [Pubmed]
  7. Presenilin/gamma-secretase-mediated cleavage of the voltage-gated sodium channel beta2-subunit regulates cell adhesion and migration. Kim, D.Y., Ingano, L.A., Carey, B.W., Pettingell, W.H., Kovacs, D.M. J. Biol. Chem. (2005) [Pubmed]
  8. Evidence that intramolecular associations between presenilin domains are obligatory for endoproteolytic processing. Saura, C.A., Tomita, T., Davenport, F., Harris, C.L., Iwatsubo, T., Thinakaran, G. J. Biol. Chem. (1999) [Pubmed]
  9. NFI-B3, a novel transcriptional repressor of the nuclear factor I family, is generated by alternative RNA processing. Liu, Y., Bernard, H.U., Apt, D. J. Biol. Chem. (1997) [Pubmed]
  10. Expression, DNA-binding specificity and transcriptional regulation of nuclear factor 1 family proteins from rat. Osada, S., Matsubara, T., Daimon, S., Terazu, Y., Xu, M., Nishihara, T., Imagawa, M. Biochem. J. (1999) [Pubmed]
  11. The 30-kDa rat liver transcription factor nuclear factor 1 binds the rat growth-hormone proximal silencer. Roy, R.J., Guérin, S.L. Eur. J. Biochem. (1994) [Pubmed]
  12. Continuous delivery of endogenous inhibitors from poly(lactic-co-glycolic acid) polymeric microspheres inhibits glioma tumor growth. Benny, O., Duvshani-Eshet, M., Cargioli, T., Bello, L., Bikfalvi, A., Carroll, R.S., Machluf, M. Clin. Cancer Res. (2005) [Pubmed]
  13. The phospholipid analogue hexadecylphosphocholine (HePC) inhibits proliferation of keloid fibroblasts in vitro and modulates their fibronectin and integrin synthesis. Blume-Peytavi, U., Geilen, C.C., Sommer, C., Almond-Roesler, B., Orfanos, C.E. Arch. Dermatol. Res. (1997) [Pubmed]
  14. Roles of the NFI/CTF gene family in transcription and development. Gronostajski, R.M. Gene (2000) [Pubmed]
  15. Mutation of conserved aspartates affect maturation of presenilin 1 and presenilin 2 complexes. Yu, G., Chen, F., Nishimura, M., Steiner, H., Tandon, A., Kawarai, T., Arawaka, S., Supala, A., Song, Y.Q., Rogaeva, E., Holmes, E., Zhang, D.M., Milman, P., Fraser, P., Haass, C., St George-Hyslop, P. Acta Neurol. Scand., Suppl. (2000) [Pubmed]
  16. Accuracy and complications in computed tomography fluoroscopy-guided needle biopsies of lung masses. Heck, S.L., Blom, P., Berstad, A. European radiology. (2006) [Pubmed]
  17. Transplantation of cultured thymic fragments: results in nude mice. IV. Effect of amount of thymic tissue. Manning, J.K., Hong, R. Thymus (1983) [Pubmed]
 
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