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Gene Review

Trim28  -  tripartite motif-containing 28

Mus musculus

Synonyms: AA408787, E3 SUMO-protein ligase TRIM28, KAP-1, KRAB-A-interacting protein, KRIP-1, ...
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High impact information on Trim28

  • We show that its obligate corepressor, KAP1, can coordinate all the machinery required for stable gene silencing [1].
  • Thus, KRIP-1 interacts with the KRAB-A region of C2H2 zinc finger proteins and may mediate or modulate KRAB-A transcriptional repressor activity [2].
  • KRIP-1 is a member of the RBCC subfamily of the RING finger, or Cys3HisCys4, family of zinc binding proteins whose other members are known to play important roles in differentiation, oncogenesis, and signal transduction [2].
  • We show that KAP1 is rapidly phosphorylated following DNA damage by members of the phosphatidylinositol-3 kinase-like family of kinases [3].
  • Spatiotemporally controlled ablation of TIF1beta by using a germ cell lineage-specific CreER(T)/loxP system leads to testicular degeneration [4].

Biological context of Trim28


Anatomical context of Trim28


Associations of Trim28 with chemical compounds

  • Second, a specific inhibitor of histone deacetylases, trichostatin A, effectively redistributes KRAZ1 and KAP-1 from centromeric foci and partially relieves their silencing activities [6].

Physical interactions of Trim28

  • Here we report that TIF1beta directly binds to the NRD and negatively regulates the c-Myb-dependent trans-activation [7].
  • KAP-1 directly interacts with heterochromatin protein 1 (HP1), a dose-dependent regulator of heterochromatin-mediated silencing [6].

Other interactions of Trim28

  • Furthermore, the Drosophila TIF1beta homolog, Bonus, negatively regulates Drosophila Myb activity [7].
  • Oncogenic activation of c-Myb correlates with a loss of negative regulation by TIF1beta and Ski [7].
  • These data strongly suggest that KRAB-ZFPs/KAP-1 silence transcription by dynamic recruitment of the target locus to the specific gene silencing compartment, centromeric heterochromatin, in a histone deacetylase-dependent manner [6].


  1. Regulated recruitment of HP1 to a euchromatic gene induces mitotically heritable, epigenetic gene silencing: a mammalian cell culture model of gene variegation. Ayyanathan, K., Lechner, M.S., Bell, P., Maul, G.G., Schultz, D.C., Yamada, Y., Tanaka, K., Torigoe, K., Rauscher, F.J. Genes Dev. (2003) [Pubmed]
  2. A novel member of the RING finger family, KRIP-1, associates with the KRAB-A transcriptional repressor domain of zinc finger proteins. Kim, S.S., Chen, Y.M., O'Leary, E., Witzgall, R., Vidal, M., Bonventre, J.V. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  3. KAP1, a novel substrate for PIKK family members, colocalizes with numerous damage response factors at DNA lesions. White, D.E., Negorev, D., Peng, H., Ivanov, A.V., Maul, G.G., Rauscher, F.J. Cancer Res. (2006) [Pubmed]
  4. Germ cell expression of the transcriptional co-repressor TIF1beta is required for the maintenance of spermatogenesis in the mouse. Weber, P., Cammas, F., Gerard, C., Metzger, D., Chambon, P., Losson, R., Mark, M. Development (2002) [Pubmed]
  5. Mice lacking the transcriptional corepressor TIF1beta are defective in early postimplantation development. Cammas, F., Mark, M., Dollé, P., Dierich, A., Chambon, P., Losson, R. Development (2000) [Pubmed]
  6. Targeting of Krüppel-associated box-containing zinc finger proteins to centromeric heterochromatin. Implication for the gene silencing mechanisms. Matsuda, E., Agata, Y., Sugai, M., Katakai, T., Gonda, H., Shimizu, A. J. Biol. Chem. (2001) [Pubmed]
  7. Oncogenic activation of c-Myb correlates with a loss of negative regulation by TIF1beta and Ski. Nomura, T., Tanikawa, J., Akimaru, H., Kanei-Ishii, C., Ichikawa-Iwata, E., Khan, M.M., Ito, H., Ishii, S. J. Biol. Chem. (2004) [Pubmed]
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