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Gene Review

KLF13  -  Kruppel-like factor 13

Homo sapiens

Synonyms: BTE-binding protein 3, BTEB3, Basic transcription element-binding protein 3, FKLF-2, FKLF2, ...
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Disease relevance of KLF13

  • The expression of FKLF-2 messenger RNA (mRNA) is up-regulated after induction of mouse erythroleukemia cells [1].

High impact information on KLF13

  • While Rel proteins play the dominant role in RANTES gene expression in fibroblasts, RFLAT-1 is a strong transactivator for RANTES in T cells [2].
  • Using expression cloning, we identified the first "late" T lymphocyte associated transcription factor and named it "RANTES Factor of Late Activated T Lymphocytes-1" (RFLAT-1) [2].
  • RFLAT-1 is a novel, phosphorylated, zinc finger transcription factor that is expressed in T cells 3 days after activation, coincident with RANTES expression [2].
  • Physical and functional interaction with GATA-4, a dosage-sensitive cardiac regulator, provides a mechanistic explanation for KLF13 action in the heart [3].
  • FKLF-2 activates the gamma promoter predominantly by interacting with the gamma CACCC box, and to a lesser degree through interaction with the TATA box or its surrounding DNA sequences [1].

Biological context of KLF13


Anatomical context of KLF13

  • RFLAT-1/KLF13, a member of the Krüppel-like family of transcription factors, was identified as a transcription factor expressed 3-5 days after T lymphocyte activation [7].
  • By Northern blot hybridization, the human homologue of FKLF-2 is expressed in the bone marrow and striated muscles and not in 12 other human tissues analyzed [1].

Physical interactions of KLF13

  • The Sp1-like protein BTEB3 inhibits transcription via the basic transcription element box by interacting with mSin3A and HDAC-1 co-repressors and competing with Sp1 [8].

Regulatory relationships of KLF13


Other interactions of KLF13


Analytical, diagnostic and therapeutic context of KLF13


  1. FKLF-2: a novel Krüppel-like transcriptional factor that activates globin and other erythroid lineage genes. Asano, H., Li, X.S., Stamatoyannopoulos, G. Blood (2000) [Pubmed]
  2. RFLAT-1: a new zinc finger transcription factor that activates RANTES gene expression in T lymphocytes. Song, A., Chen, Y.F., Thamatrakoln, K., Storm, T.A., Krensky, A.M. Immunity (1999) [Pubmed]
  3. The Kruppel-like transcription factor KLF13 is a novel regulator of heart development. Lavall??e, G., Andelfinger, G., Nadeau, M., Lefebvre, C., Nemer, G., Horb, M.E., Nemer, M. EMBO J. (2006) [Pubmed]
  4. Identification of KLF13 and KLF14 (SP6), novel members of the SP/XKLF transcription factor family. Scohy, S., Gabant, P., Van Reeth, T., Hertveldt, V., Drèze, P.L., Van Vooren, P., Rivière, M., Szpirer, J., Szpirer, C. Genomics (2000) [Pubmed]
  5. Functional interaction between coactivators CBP/p300, PCAF, and transcription factor FKLF2. Song, C.Z., Keller, K., Murata, K., Asano, H., Stamatoyannopoulos, G. J. Biol. Chem. (2002) [Pubmed]
  6. A novel functional interaction between the Sp1-like protein KLF13 and SREBP-Sp1 activation complex underlies regulation of low density lipoprotein receptor promoter function. Natesampillai, S., Fernandez-Zapico, M.E., Urrutia, R., Veldhuis, J.D. J. Biol. Chem. (2006) [Pubmed]
  7. Functional domains and DNA-binding sequences of RFLAT-1/KLF13, a Krüppel-like transcription factor of activated T lymphocytes. Song, A., Patel, A., Thamatrakoln, K., Liu, C., Feng, D., Clayberger, C., Krensky, A.M. J. Biol. Chem. (2002) [Pubmed]
  8. The Sp1-like protein BTEB3 inhibits transcription via the basic transcription element box by interacting with mSin3A and HDAC-1 co-repressors and competing with Sp1. Kaczynski, J., Zhang, J.S., Ellenrieder, V., Conley, A., Duenes, T., Kester, H., van Der Burg, B., Urrutia, R. J. Biol. Chem. (2001) [Pubmed]
  9. Functional analysis of basic transcription element (BTE)-binding protein (BTEB) 3 and BTEB4, a novel Sp1-like protein, reveals a subfamily of transcriptional repressors for the BTE site of the cytochrome P4501A1 gene promoter. Kaczynski, J.A., Conley, A.A., Fernandez Zapico, M., Delgado, S.M., Zhang, J.S., Urrutia, R. Biochem. J. (2002) [Pubmed]
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